Scientists Find Genetic Difference In Highly-Sensitive People

LOS ANGELES (CBS) Do people say you are highly sensitive whether it be physically or emotionally? While it can feel like a burden, it can also mean a greater capacity for work, love and compassion.

I knew that I was more sensitive, that I took things deeper and harder, Ane Axford said.

I felt things and they were heavy, added Sandra Clifton.

Both women are so sensitive, they say that it has affected every aspect of their lives.

Its a whole different way of being in the world, Axford said.

Now scientists say that they know why some people feel so much more. New research has indicated that hypersensitive people are genetically different than those who feel a normal degree of sensitivity.

Weve done brain activation studies, said Dr. Elaine Aron.

Sensitive people show more activation, both in the secondary intentional areas, Dr. Arthur Aron added.

Clinical Psychologists Elaine and Arthur Aron conducted the studies and ultimately found that a large portion of the population 20 percent is made up of highly-sensitive people (HSPs), as the Arons have categorized them.

Theyre a bit more emotionally reactive. They process things more deeply, Elaine said.

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Senesco to Present SNS01-T, an eIF5A-based Nanoparticle in a Phase 1b/2a Trial to Treat Multiple Myeloma, is Effective …

BRIDGEWATER, N.J.–(BUSINESS WIRE)–

Senesco Technologies, Inc. (Senesco or the Company) (NYSE Amex: SNT), announced today that an oral presentation will be delivered at the 15th Annual Meeting of the American Society of Gene & Cell Therapy. The conference will be held May 16-19th, 2012 at the Pennsylvania Convention Center in Philadelphia, Pennsylvania. The Company will present during the Cancer-Targeted Gene & Cell Therapy Oral Abstract Session, which will begin Thursday, May 17, at 1:15 P.M. Eastern Time. The oral presentation, entitled SNS01-T, an eIF5A-Based Gene Therapy Nanoparticle Designed for the Treatment of Multiple Myeloma, has Anti-Tumoral Activity in Lymphoma, will describe the effectiveness of SNS01-T in B-cell cancers, which is designed to selectively induce programmed cell death. The talk will be delivered by Catherine Taylor who is from Senesco CSO John Thompsons research laboratory at the University of Waterloo in Ontario, Canada.

About Multiple Myeloma

Multiple myeloma is an incurable cancer of plasma cells, a type of white blood cell derived from B-lymphocytes, normally responsible for the production of antibodies, in which abnormal cells accumulate in the bone marrow leading to bone lesions and interfering with the production of normal blood cells. Senesco was previously granted orphan drug status for SNS01-T, the Companys lead drug candidate for treatment of multiple myeloma.

About Senesco Technologies, Inc.

Senesco, a leader in eIF5A technology, is running a clinical study in multiple myeloma with its lead therapeutic candidate SNS01-T, which targets B-cell cancers by selectively inducing apoptosis by modulating eukaryotic translation initiation factor 5A (eIF5A), which is believed to be an important regulator of cell growth and cell death. Accelerating apoptosis may have applications in treating cancer, while delaying apoptosis may have applications in treating certain inflammatory and ischemic diseases. Senesco has already partnered with leading-edge companies engaged in agricultural biotechnology and is entitled to earn research and development milestones and royalties if its gene-regulating platform technology is incorporated into its partners products. www.senesco.com

Forward-Looking Statements

Certain statements included in this press release are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results could differ materially from such statements expressed or implied herein as a result of a variety of factors, including, but not limited to: the ability of the Company to consummate additional financings; the Companys ability to recruit and enroll patients for its clinical trial;the development of the Companys gene technology; the approval of the Companys patent applications; the successful implementation of the Companys research and development programs and collaborations; the success of the Company’s license agreements; the acceptance by the market of the Companys products; the timing and success of the Companys preliminary studies, preclinical research and clinical trials; competition and the timing of projects and trends in future operating performance, the Companys ability to comply with the continued listing standards of the NYSE Amex, as well as other factors expressed from time to time in the Companys periodic filings with the Securities and Exchange Commission (the “SEC”). As a result, this press release should be read in conjunction with the Companys periodic filings with the SEC. The forward-looking statements contained herein are made only as of the date of this press release, and the Company undertakes no obligation to publicly update such forward-looking statements to reflect subsequent events or circumstances.

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Senesco to Present SNS01-T, an eIF5A-based Nanoparticle in a Phase 1b/2a Trial to Treat Multiple Myeloma, is Effective …

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Gamida Cell Closes $10 Million E Financing Round Earmarked to Support the Global Commercialization of the Company’s …

JERUSALEM–(BUSINESS WIRE)–

Gamida Cell announced today that it has closed an internal E financing round of $10 million. All major shareholders participated.

The financing will be used to support the global commercialization of the companys lead cell therapy product, StemEx, in development as an alternative therapeutic treatment for patients with blood cancers, such as leukemia and lymphoma, who can be cured by bone marrow transplantation but do not have a matched bone marrow donor. The company is currently seeking a strategic partner to join in the global commercialization of StemEx.

The financing will also support the continued development of the companys pipeline of products, primarily the NiCord clinical trial for sickle cell disease and thalassemia.

Mr. Reuven Krupik, chairman of the board of Gamida Cell said, The investors were unanimous in their decision to reinvest, understanding the importance of bringing StemEx to market as well as maintaining the companys leadership role in the stem cell industry. Gamida Cell is a game changer.

The international, multi-center, pivotal registration, Phase III clinical trial of StemEx completed enrollment in February 2012. Clinical outcome is expected in Q4/2012. The market launch of StemEx is planned for 2013. StemEx is likely to be the first allogeneic stem cell product in the market. StemEx is being developed by the Gamida Cell-TEVA joint venture.

Dr. Yael Margolin, president and chief executive officer of Gamida Cell said, With the continued support of our shareholders and the analysis of the clinical results of the StemEx trial just around the corner, we are now focused on submitting the BLA.

StemEx is a graft of an expanded population of stem/progenitor cells, derived from part of a single unit of umbilical cord blood and transplanted by IV administration along with the remaining, non-manipulated cells from the same unit. Competing products in development use two units. As the average cost of a cord blood unit in the U.S. is $40K, StemEx is expected to be a significantly less expensive treatment option. StemEx is also expected to be available in the market several years before any of the competing products.

About Gamida Cell

Gamida Cell is a world leader in stem cell population expansion technologies and stem cell therapy products for transplantation and regenerative medicine. The companys pipeline of stem cell therapy products are in development to treat a wide range of conditions including blood cancers, solid tumors, non-malignant hematological diseases such as hemoglobinopathies, neutropenia and acute radiation syndrome, autoimmune diseases and metabolic diseases as well as conditions that can be helped by regenerative medicine. Gamida Cells therapeutic candidates contain populations of adult stem cells, selected from non-controversial sources such as umbilical cord blood, bone marrow and peripheral blood, which are expanded in culture. Gamida Cells current shareholders include: Elbit Imaging, Clal Biotechnology Industries, Israel Healthcare Venture, Teva Pharmaceutical Industries, Amgen, Denali Ventures and Auriga Ventures. For more information, please visit: www.gamida-cell.com.

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Gamida Cell Closes $10 Million E Financing Round Earmarked to Support the Global Commercialization of the Company’s …

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:: 14, May 2012 :: SCIENTISTS MAKE GROUNDBREAKING DISCOVERY OF MUTATION CAUSING GENETIC DISORDER IN HUMANS

MEDIA RELEASE

SCIENTISTS MAKE GROUNDBREAKING DISCOVERY OF MUTATION CAUSING GENETIC DISORDER IN HUMANS

1. Scientists at A*STARs Institute of Medical Biology (IMB), in collaboration with doctors and scientists in Jordan, Turkey, Switzerland and USA, have identified the genetic cause of a birth defect known as Hamamy syndrome[1]. Their groundbreaking findings were published on May13thin the prestigious journal Nature Genetics. The work lends new insights into common ailments such as heart disease, osteoporosis, blood disorders and possibly sterility.

2. Hamamy syndrome is a rare genetic disorder which is marked by abnormal facial features (Annex A) and defects in the heart, bone, blood and reproductive cells. Its exact cause was unknown until now. The international team, led by scientists at IMB, have pinpointed the genetic mistake to be a mutation in a single gene called IRX5.

3. This is the first time that a mutation in IRX5 (and the family of IRX genes) has ever been discovered in man. IRX5 is part of a family of transcription factors that is highly conserved in all animals, meaning that this gene is present not only in humans but also in mice, fish, frogs, flies and even worms. Using a frog model, the scientists demonstrated that Irx5 orchestrates cell movements in the developing foetus which underlie head and gonad formation.

4. Carine Bonnard, a final-year PhD student at IMB and the first author of the paper, said, Because Hamamy syndrome causes a wide range of symptoms, not just in newborn babies but also in the adult, this implies that IRX5 is critical for development in the womb as well as for the function of many organs in our adult body. For example, patients with this disease cannot evacuate tears from their eyes, and they will also go on to experience repetitive bone fractures (Annex A) or progressive myopia as they age. This discovery of the causative gene is a significant finding that will catalyze research efforts into the role of the Irx gene family and greatly increase our understanding of human health, such as bone homeostasis, or gamete formation for instance.

5. We believe that this discovery could open up new therapeutic solutions to common diseases like osteoporosis, heart disease, anaemia which affect millions of people worldwide, said Dr Bruno Reversade, Senior Principle Investigator at IMB. The findings also provide a framework for understanding fascinating evolutionary questions, such as why humans of different ethnicities have distinct facial features and how these are embedded in our genome. IRX genes have been repeatedly co-opted during evolution, and small variation in their activity could underlie fine alterations in the way we look, or perhaps even drastic ones such as the traits seen in an elephant, whale, turtle or frog body pattern.

6. Only a handful of people in the world have been identified with Hamamy Syndrome making it a very rare genetic disorder. Rare genetic diseases, usually caused by mutations in a single gene, provide a unique opportunity to better understand more common disease processes. These “natural” experiments are similar to carefully controlled knockout animal experiments in which the function of single genes are analyzed and often give major insights into general health issues.[2]

7. Prof Birgitte Lane, Executive Director of IMB, said, Understanding how various pathways in the human body function is the foundation for developing new therapeutic targets. This is an important piece of research that I believe will be of great interest to many scientists and clinicians around the world because of the clinical and genetic insights it brings to a large range of diseases.

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:: 14, May 2012 :: SCIENTISTS MAKE GROUNDBREAKING DISCOVERY OF MUTATION CAUSING GENETIC DISORDER IN HUMANS

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Lung cancer molecular subtypes correlate with genetic alterations, patient's response to therapy

Published on May 14, 2012 at 12:51 AM

Cancer therapies targeting specific molecular subtypes of the disease allow physicians to tailor treatment to a patient’s individual molecular profile. But scientists are finding that in many types of cancer the molecular subtypes are more varied than previously thought and contain further genetic alterations that can affect a patient’s response to therapy.

A UNC-led team of scientists has shown for the first time that lung cancer molecular subtypes correlate with distinct genetic alterations and with patient response to therapy. These findings in pre-clinical models and patient tumor samples build on their previous report of three molecular subtypes of non-small cell lung cancer and refines their molecular analysis of tumors.

Their findings were published in the May 10, 2012 online edition of the Public Library of Science One.

Study senior author, Neil Hayes, MD, MPH, associate professor of medicine, says, “It has been known for about a decade of using gene expression arrays that “molecular subtypes” exist. These subtypes have molecular “fingerprints” and frequently have different clinical outcomes. However, the underlying etiologies of the subtypes have not been recognized. Why do tumors form subtypes?

“Our study shows that tumor subtypes have different underlying alterations of DNA as part of the difference. These differences are further evidence of the importance of subtypes and the way we will use them. For example, the mutations are different which may imply much more ability to target than previously recognized. Also, we are starting to get a suggestion that these subtypes may reflect different cells of origin that rely on different cancer pathways. This is further unlocking the diversity of this complex disease.” Hayes is a member of UNC Lineberger Comprehensive Cancer Center.

The team first defined and reported in 2006 on three lung cancer molecular subtypes, named according to their genetic pattern – bronchoid, squamoid and magnoid.

In this PLoS One paper they sought to determine if distinct genetic mutations co-occur with each specific molecular subtypes. They found that specific genetic mutations were associated with each subtype and that these mutations may have independent predictive value for therapeutic response.

Source: University of North Carolina School of Medicine

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Genetic test can accurately predict spread of eye cancer

Researchers at Washington University School of Medicine in St. Louis have developed a genetic test that can accurately predict whether the most common form of eye cancer will spread to other parts of the body, particularly the liver.

In 459 patients with ocular melanoma at 12 centers in the United States and Canada, the researchers found the test could successfully classify tumors more than 97 percent of the time.

The study will appear in an upcoming issue of the journal Ophthalmology, but is now online.

“When the cancer spreads beyond the eye, it’s unlikely any therapy is going to be effective,” says principal investigator J. William Harbour, MD. “But it’s very possible that we can develop treatments to slow the growth of metastatic tumors. The real importance of this test is that by identifying the type of tumor a patient has, we can first remove the tumor from the eye with surgery or radiation and then get those individuals at high risk into clinical trials that might be able to help them live longer.”

Harbour believes the test should allow ocular oncologists to quickly evaluate the risks associated with particular tumors and to begin treatment the moment they can detect any spread of the cancer.

Melanoma of the eye is relatively rare, diagnosed in about 2,000 people in the United States each year. Advances in treatment have allowed surgeons to preserve patients’ vision, but when cancer spreads beyond the eye, it often is deadly.

About a decade ago, Harbour, the Paul A. Cibis Distinguished Professor of Ophthalmology and Visual Sciences, began using gene expression profiling to monitor the activity of thousands of genes in and around ocular melanoma tumors.

“At the time, we were surprised to see that based on these gene expression profiles, the tumors clustered into two groups that corresponded, almost perfectly, to patients whose cancer spread and those whose cancer was confined within the eye,” says Harbour, who directs Washington University’s Center for Ocular Oncology. “Tumors with a class 1 gene expression profile, or ‘signature,’ very rarely spread, but those with a class 2 profile frequently develop into metastatic cancer.”

Initially, Harbour’s group identified differences in approximately 1,000 genes between class 1 and class 2 tumors, but they whittled down that number, hoping to develop a simple test that could be used easily by ophthalmologists. Eventually, they settled on about a dozen genes that could be evaluated in tumor samples collected with a needle biopsy.

“We went through a number of sophisticated algorithms and validations, and we came up with a group of 12 genes,” he says. “We also included three more genes that don’t change whether they are in tumor tissue or healthy tissue. Those genes act as our ‘controls’ in this prognostic test.”

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Genetic test identifies eye cancer tumors likely to spread

Public release date: 14-May-2012 [ | E-mail | Share ]

Contact: Jim Dryden jdryden@wustl.edu 314-286-0110 Washington University School of Medicine

Researchers at Washington University School of Medicine in St. Louis have developed a genetic test that can accurately predict whether the most common form of eye cancer will spread to other parts of the body, particularly the liver.

In 459 patients with ocular melanoma at 12 centers in the United States and Canada, the researchers found the test could successfully classify tumors more than 97 percent of the time.

The study will appear in an upcoming issue of the journal Ophthalmology, but is now online.

“When the cancer spreads beyond the eye, it’s unlikely any therapy is going to be effective,” says principal investigator J. William Harbour, MD. “But it’s very possible that we can develop treatments to slow the growth of metastatic tumors. The real importance of this test is that by identifying the type of tumor a patient has, we can first remove the tumor from the eye with surgery or radiation and then get those individuals at high risk into clinical trials that might be able to help them live longer.”

Harbour believes the test should allow ocular oncologists to quickly evaluate the risks associated with particular tumors and to begin treatment the moment they can detect any spread of the cancer.

Melanoma of the eye is relatively rare, diagnosed in about 2,000 people in the United States each year. Advances in treatment have allowed surgeons to preserve patients’ vision, but when cancer spreads beyond the eye, it often is deadly.

About a decade ago, Harbour, the Paul A. Cibis Distinguished Professor of Ophthalmology and Visual Sciences, began using gene expression profiling to monitor the activity of thousands of genes in and around ocular melanoma tumors.

“At the time, we were surprised to see that based on these gene expression profiles, the tumors clustered into two groups that corresponded, almost perfectly, to patients whose cancer spread and those whose cancer was confined within the eye,” says Harbour, who directs Washington University’s Center for Ocular Oncology. “Tumors with a class 1 gene expression profile, or ‘signature,’ very rarely spread, but those with a class 2 profile frequently develop into metastatic cancer.”

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Given number of inheritors, donor sperm carries risk of genetic harm

In households across the country, children conceived with donated sperm are struggling with serious genetic conditions inherited from men they have never met: heart defects, spinal muscular atrophy, neurofibromatosis type 1 and fragile-X syndrome the most common form of mental retardation in boys and others.

Donated eggs pose a risk as well, but the threat of genetic harm from sperm donation is arguably much greater. Sperm donors are no more likely to carry genetic diseases than anybody else, but they can father a far greater number of children: 50, 100 or even 150, each a potential inheritor of flawed genes.

Sharine and Brian Kretchmar of Yukon, Okla., tried a number of medical treatments to conceive a second child.

After a depressing series of failures, they were advised by a doctor to find a sperm donor. For more than a year, the Kretchmars researched sperm banks and donors. The donor they chose was a family man, a Christian like them, they were told. Most important, he had a clean bill of health. So the Kretchmars jumped in. After artificial insemination, Sharine Kretchmar became pregnant, and in April 2010, she gave birth to a boy they named Jaxon.

But the baby failed to have a bowel movement in the first day or so after birth, a sign to doctors that something was wrong. Doctors returned with terrible news: Jaxon appeared to have cystic fibrosis.

“We were pretty much devastated,” Sharine Kretchmar said.

Genetic testing showed that Jaxon did carry the genes for cystic fibrosis. Sharine Kretchmar, 33, had no idea she was a carrier and was shocked to discover that so, too, was the Kretchmars’ donor.

His sperm, they would discover, was decades old, originally donated at a laboratory halfway across the country and frozen ever since. Whether it was properly tested is a matter of dispute.

Experience not unique

Sadly, the Kretchmars’ experience is not unique.

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New York Stem Cell Foundation scientist grows bone from human embryonic stem cells

Public release date: 14-May-2012 [ | E-mail | Share ]

Contact: David McKeon dmckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation

NEW YORK, NY (May 14, 2012) — Dr. Darja Marolt, an Investigator at The New York Stem Cell Foundation (NYSCF) Laboratory, is lead author on a study showing that human embryonic stem cells can be used to grow bone tissue grafts for use in research and potential therapeutic application. Dr. Marolt conducted this research as a post-doctoral NYSCF Druckenmiller Fellow at Columbia University in the laboratory of Dr. Gordana Vunjak-Novakovic.

The study is the first example of using bone cell progenitors derived from human embryonic stem cells to grow compact bone tissue in quantities large enough to repair centimeter-sized defects. When implanted in mice and studied over time, the implanted bone tissue supported blood vessel ingrowth, and continued development of normal bone structure, without demonstrating any incidence of tumor growth.

Dr. Marolt’s work is a significant step forward in using pluripotent stem cells to repair and replace bone tissue in patients. Bone replacement therapies are relevant in treating patients with a variety of conditions, including wounded military personnel, patients with birth defects, or patients who have suffered other traumatic injury.

Since conducting this work as proof of principle at Columbia University, Dr. Marolt has continued to build upon this research as an Investigator in the NYSCF Laboratory, developing bone grafts from induced pluripotent stem (iPS) cells. iPS cells are similar to embryonic stem cells in that they can also give rise to nearly any type of cell in the body, but iPS cells are produced from adult cells and as such are individualized to each patient. By using iPS cells rather than embryonic stem cells to engineer tissue, Dr. Marolt hopes to develop personalized bone grafts that will avoid immune rejection and other implant complications.

###

The New York Stem Cell Foundation has supported Dr. Marolt’s research throughout her career, first through a NYSCF Druckenmiller Fellowship to fund her post-doctoral work at Columbia University, and now with a NYSCF Helmsley Investigator Award at The New York Stem Cell Foundation Laboratory. “The continuity of funding provided by NYSCF has allowed me to continue my research uninterrupted, making progress more quickly than would have otherwise been possible,” Dr. Marolt said.

The New York Stem Cell Foundation (NYSCF) conducts cutting-edge translational stem cell research in its laboratory in New York City and supports research by stem cell scientists at other leading institutions around the world. More information is available at www.nyscf.org.

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Scientists Discover Clues to Muscle Stem Cell Functions

Study reveals a potential key to new treatment strategies for Muscular Dystrophy

Newswise May 14, 2012 – Oakland, Calif. A study conducted by Childrens Hospital & Research Center Oakland scientists identifies how skeletal muscle stem cells respond to muscle injury and may be stimulated to improve muscle repair in Duchenne Muscular Dystrophy, a severe inherited disease of muscle that causes weakness, disability and, ultimately, heart and respiratory failure.

The study, led by Julie D. Saba, MD, PhD, senior scientist at Childrens Hospital Oakland Research Institute (CHORI), shows that a lipid signaling molecule called sphingosine-1-phosphate or S1P can trigger an inflammatory response that stimulates the muscle stem cells to proliferate and assist in muscle repair. It further shows that mdx mice, which have a disease similar to Duchenne Muscular Dystrophy, exhibit a deficiency of S1P, and that boosting their S1P levels improves muscle regeneration in these mice. A research report describing the study findings will be published online (http://www.plosone.org/article/info%3Adoi %2F10.1371%2Fjournal.pone.0037218) on May 14, 2012 in the journal Public Library of Science ONE (PLoS ONE).

Skeletal muscle is the biggest organ system of the human body. It is important for all human activity. Muscles can be injured by trauma, inactivity, aging and a variety of inherited muscle diseases. Importantly however, skeletal muscle is one of the few tissues of the human body that has the potential to fully repair itself after injury. The ability of muscles to regenerate themselves is attributed to the presence of a form of adult stem cells called satellite cells that are essential for muscle repair. Normally, satellite cells lie quietly at the periphery of the muscle fiber and do not grow, move or become activated. However, after muscle injury, these stem cells wake up through unclear mechanisms and fuse with the injured muscle, stimulating a complicated process that results in the rebuilding of a healthy muscle fiber.

S1P is a lipid signaling molecule that controls the movement and proliferation of many human cell types. Other scientists had shown previously that S1P can activate satellite cells, but they did not know how this occurred.

We have been studying S1P signaling for many years, states Dr. Saba. In 2003, we published a report demonstrating that fruit fly mutants with defective S1P metabolism were unable to fly because they developed a muscle disease or myopathy that led to degeneration of their flight muscles. Based on that observation, I became convinced that S1P signaling played an important role in muscle stability and homeostasis, not just in flies but in mammals, including humans.

Dr. Sabas team has discovered how S1P is able to wake up the stem cells at the time of injury. It involves the ability of S1P to activate S1P receptor 2, one of its five cell surface receptors, leading to downstream activation of an inflammatory pathway controlled by a transcription factor called STAT3. They showed that S1P is rapidly produced in the muscle immediately after injury, leading to an S1P signal. S1P, acting through S1P receptor 2, leads to activation of STAT3, resulting in changes in gene expression that cause the satellite cell to leave its sleeping state and start to proliferate and assist in muscle repair.

These findings are important especially for certain muscle diseases or myopathies that can affect children, states Dr. Saba. The most common and one of the most severe myopathies is Duchenne Muscular Dystrophy, a disease that affects young boys and often leads to death from respiratory and heart failure in a patients twenties. Although patients with Duchenne Muscular Dystrophy start out life with enough satellite cells to repair the patients degenerating muscles, over time the satellite cells fail to keep up with the rate of muscle degeneration. We found that mdx mice, which have a disease similar to Duchenne Muscular Dystrophy, are deficient in S1P. We were able to increase the S1P levels in the mice using a drug that blocks S1P breakdown. This treatment increased the number of satellite cells in the muscles and improved the efficiency of muscle regeneration after injury.

If these findings are also found to be true in humans with Duchenne Muscular Dystrophy, it may be possible to use similar approaches to boost S1P levels in order to improve satellite cell function and muscle regeneration in patients with the disease. Drugs that block S1P metabolism and boost S1P levels are now being tested for the treatment of other human diseases including rheumatoid arthritis. If these studies prove to be relevant in Duchenne patients, it may be possible to use the same drugs to improve muscle regeneration in these patients. Alternatively, new agents that can specifically activate S1P receptor 2 could also be beneficial in recruiting satellite cells and improving muscle regeneration in muscular dystrophy and potentially other diseases of muscle.

This work was supported by grants from the Muscular Dystrophy Association, the National Institutes of Health and a fellowship award from the California Institute of Regenerative Medicine.

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Scientists Discover Clues to Muscle Stem Cell Functions

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Study identifies how skeletal muscle stem cells respond to muscle injury

A study conducted by Children’s Hospital & Research Center Oakland scientists identifies how skeletal muscle stem cells respond to muscle injury and may be stimulated to improve muscle repair in Duchenne Muscular Dystrophy, a severe inherited disease of muscle that causes weakness, disability and, ultimately, heart and respiratory failure.

The study, led by Julie D. Saba, MD, PhD, senior scientist at Children’s Hospital Oakland Research Institute (CHORI), shows that a lipid signaling molecule called sphingosine-1-phosphate or “S1P” can trigger an inflammatory response that stimulates the muscle stem cells to proliferate and assist in muscle repair. It further shows that mdx mice, which have a disease similar to Duchenne Muscular Dystrophy, exhibit a deficiency of S1P, and that boosting their S1P levels improves muscle regeneration in these mice. A research report describing the study findings will be published online (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0037218) on May 14, 2012 in the journal Public Library of Science ONE (PLoS ONE).

Skeletal muscle is the biggest “organ” system of the human body. It is important for all human activity. Muscles can be injured by trauma, inactivity, aging and a variety of inherited muscle diseases. Importantly however, skeletal muscle is one of the few tissues of the human body that has the potential to fully repair itself after injury. The ability of muscles to regenerate themselves is attributed to the presence of a form of adult stem cells called “satellite cells” that are essential for muscle repair. Normally, satellite cells lie quietly at the periphery of the muscle fiber and do not grow, move or become activated. However, after muscle injury, these stem cells “wake up” through unclear mechanisms and fuse with the injured muscle, stimulating a complicated process that results in the rebuilding of a healthy muscle fiber.

S1P is a lipid signaling molecule that controls the movement and proliferation of many human cell types. Other scientists had shown previously that S1P can activate satellite cells, but they did not know how this occurred.

“We have been studying S1P signaling for many years,” states Dr. Saba. “In 2003, we published a report demonstrating that fruit fly mutants with defective S1P metabolism were unable to fly because they developed a muscle disease or “myopathy” that led to degeneration of their flight muscles. Based on that observation, I became convinced that S1P signaling played an important role in muscle stability and homeostasis, not just in flies but in mammals, including humans.”

Dr. Saba’s team has discovered how S1P is able to “wake up” the stem cells at the time of injury. It involves the ability of S1P to activate S1P receptor 2, one of its five cell surface receptors, leading to downstream activation of an inflammatory pathway controlled by a transcription factor called STAT3. They showed that S1P is rapidly produced in the muscle immediately after injury, leading to an S1P “signal.” S1P, acting through S1P receptor 2, leads to activation of STAT3, resulting in changes in gene expression that cause the satellite cell to leave its “sleeping” state and start to proliferate and assist in muscle repair.

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Study identifies how skeletal muscle stem cells respond to muscle injury

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Bone grown from human embryonic stem cells

Washington, May 15 (ANI): In a new study, researchers have shown that human embryonic stem cells can be used to grow bone tissue grafts for use in research and potential therapeutic application.

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Bone grown from human embryonic stem cells

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Stem Cell Market & Cord Blood Banking Industry Research Reports at 10% Discount – Limited Period Offer

DALLAS, May 15, 2012 /PRNewswire/ —

ReportsnReports.com announces a Flat 10% Discount on ALL market research reports by BioInformant WorldWide, LLC through June 20, 2012. Whether stem cells are to be studied functionally or based on source tissues, our database of reports on stem cells is sure to meet your research requirements.

Here is a list of reports on which you get a Flat 10% Discount through June 20, 2012:

The stem cell research products market (excluding stem cell antibodies) was valued at $1.28 billion for the full year 2011 and is projected to increase to $2.10 billion by 2016. The total market for all types of stem cell products – including stem cell research products, stem cell antibodies, and stem cell therapies – was valued at $5.72 billion for the full year 2011. This report identifies, defines, and quantifies each market segment within the stem cell product industry.

This research helps you with data and analysis on rate of entrants to the cord blood banking industry, revenue distinctions among existing banks, effect of new entrants for existing competitors, leveraging global tactics for growth and more.

As of 2012, 510 cord blood banks are active in 97 countries around the world. This database contains nearly 7000 global cord blood industry contacts from top 15 countries and around 9 categories.

This market research report focuses on recent advances in MSC research applications, explores research priorities by market segment, highlights individual labs and end-users of MSC research products, explores the competitive environment for MSC research products, and provides 5-year growth and trend analysis.

This study explores the complex IP landscape affecting development of human embryonic stem cell products, providing clear guidance for companies that want to enter the product area.

Explore information on applications, application priorities, patents, projected 5-years market growth, Competitors covering suppliers of neural stem & progenitor cell products and their products offered, Specialty pharmaceutical companies in neural stem & progenitor cell therapies, Breakdown of stem cell research activity by cell type, Potential end-users of neural stem cell products, Product ideas & suggestions and more.

This report uses end-user surveys of expectant parents and technology-derived data to determine the factors involved in parental-decision making. More than 1,200 expectation parents in the U.S., Canada, Europe and other international regions answered a detailed survey between November 2008 and January 2009.

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Stem Cell Market & Cord Blood Banking Industry Research Reports at 10% Discount – Limited Period Offer

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Human embryonic stem cells can be used to grow bone tissue grafts

Published on May 15, 2012 at 5:02 AM

Dr. Darja Marolt, an Investigator at The New York Stem Cell Foundation (NYSCF) Laboratory, is lead author on a study showing that human embryonic stem cells can be used to grow bone tissue grafts for use in research and potential therapeutic application. Dr. Marolt conducted this research as a post-doctoral NYSCF – Druckenmiller Fellow at Columbia University in the laboratory of Dr. Gordana Vunjak-Novakovic.

The study is the first example of using bone cell progenitors derived from human embryonic stem cells to grow compact bone tissue in quantities large enough to repair centimeter-sized defects. When implanted in mice and studied over time, the implanted bone tissue supported blood vessel ingrowth, and continued development of normal bone structure, without demonstrating any incidence of tumor growth.

Dr. Marolt’s work is a significant step forward in using pluripotent stem cells to repair and replace bone tissue in patients. Bone replacement therapies are relevant in treating patients with a variety of conditions, including wounded military personnel, patients with birth defects, or patients who have suffered other traumatic injury.

Since conducting this work as proof of principle at Columbia University, Dr. Marolt has continued to build upon this research as an Investigator in the NYSCF Laboratory, developing bone grafts from induced pluripotent stem (iPS) cells. iPS cells are similar to embryonic stem cells in that they can also give rise to nearly any type of cell in the body, but iPS cells are produced from adult cells and as such are individualized to each patient. By using iPS cells rather than embryonic stem cells to engineer tissue, Dr. Marolt hopes to develop personalized bone grafts that will avoid immune rejection and other implant complications.

The New York Stem Cell Foundation has supported Dr. Marolt’s research throughout her career, first through a NYSCF – Druckenmiller Fellowship to fund her post-doctoral work at Columbia University, and now with a NYSCF – Helmsley Investigator Award at The New York Stem Cell Foundation Laboratory. “The continuity of funding provided by NYSCF has allowed me to continue my research uninterrupted, making progress more quickly than would have otherwise been possible,” Dr. Marolt said.

Source: New York Stem Cell Foundation

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VistaGen CEO Issues Update Letter to Stockholders

SOUTH SAN FRANCISCO, CA–(Marketwire -05/14/12)- VistaGen Therapeutics, Inc. (OTC.BB: VSTA) (VSTA.OB), a biotechnology company applying stem cell technology for drug rescue, today issued the following letter to its stockholders and the investment community from its CEO, Shawn Singh.

To our valued Stockholders:

Since becoming a public company one year ago, we have progressed to perhaps the most exciting time in our company’s 14-year history. To arrive at this point, more than $45 million, obtained through various strategic collaborations, investments and grant awards, has been carefully employed. We believe our pluripotent stem cell technology platform, Human Clinical Trials in a Test Tube, combined with the network of strategic relationships we have announced, will allow us to secure additional capital and the large market drug rescue opportunities that can deliver value to our stockholders.

Since the beginning of the year, our team has carefully reviewed our Top 10 drug rescue opportunities and narrowed our focus to our Top 5 candidates. Now we intend to launch our initial drug rescue program and secure strategic capital necessary to support it, as well as launch our second drug rescue program by year-end. We also are working on validation of LiverSafe 3D, our bioassay system for drug rescue involving liver toxicity and drug metabolism issues, for launch during the first half of next year.

The pharmaceutical industry continues to face extremely high barriers in bringing new medicine to market. The number of drugs approved by the FDA over the past decade has dropped precipitously, by over 50%, in spite of staggering increases in resources devoted to R&D by pharmaceutical companies. Based on the progress we have made with CardioSafe 3D and our efforts to build our strategic drug rescue ecosystem of collaborators, we believe our core business model — to use our stem cell technology and strategic relationships to develop less toxic variants of drugs that have already been proven in vitro to be effective — is now more commercially promising than at any other point in our history. We believe we will be able to help major pharmaceutical companies avoid the loss of years of time and millions of dollars spent in developing new therapies that have positive efficacy data, but must be discontinued due to later discovery of unsafe toxicity levels for human heart and liver tissue.

Over the past year, we have secured additional intellectual property protection and entered into strategic relationships with leading biotech firms and academic researchers to support development of our stem technology and our drug rescue-based commercialization initiatives:

Over the next 12 months, we have an ambitious agenda to work closely with our advisors and collaborators to secure capital and achieve these transformative milestones:

Our goals are reachable, with strategic financing. We believe we have the right technology, intellectual property, development teams and specialized focus to deliver on our founding mission — “putting humans first” — bringing clinically relevant human biology to the front end of the drug development process, long before standard animal and human testing, and using better cells to make better medicine.

We would like to thank our partners, advisors, employees and each of you, our loyal stockholders, for helping support us in our efforts to deliver long-term value for you.

Sincerely,

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TiGenix Reports Business & Financial Results for the First Quarter 2012

LEUVEN, BELGIUM–(Marketwire -05/15/12)- TiGenix NV (TIG) a leader in the field of cell therapy, today gave a business update and announced the financial results for the first quarter ending March 31, 2012.

Business highlights

Financial highlights

“In the first quarter 2012 we continued to aggressively push our commercial efforts forward,” said Eduardo Bravo, CEO of TiGenix. “As a result sales of ChondroCelect are developing in line with the improved traction we observed in the second part of last year. At the same time we are moving ahead of schedule with most of our clinical adipose stem cell programs. We closed the quarter with almost EUR 17 million cash on hand, which is sufficient to execute on our business plan and reach key inflection points.”

Business update

ChondroCelect sales increase continues apaceThe Company reports net sales growth for the quarter of 123% compared with the same period of last year, and of 62% compared to Q4, 2011, a positive trend reflecting the uptake in Belgium, where we benefit from national reimbursement. In the Netherlands one of the leading private healthcare insurance companies has made treatment with ChondroCelect compulsory for its insured, and no longer reimburses non-ATMP treatments. Similarly, one of the large private insurers in the UK has expressed its intention to routinely reimburse ChondroCelect going forward. Discussions to obtain full national reimbursement keep advancing in the Netherlands, France, Spain and Germany.

Positive outcome of ChondroCelect compassionate use program published in leading journalPositive outcome data from the ChondroCelect compassionate use program (CUP), involving 43 orthopedic centers in 7 European countries, treating 370 patients with ChondroCelect over the span of four years, were published in advance online in Cartilage, the official journal of the International Cartilage Repair Society. The data show that the implantation of ChondroCelect results in a positive benefit/risk ratio when used in an unselected, heterogeneous population, irrespective of the follow-up period, lesion size and type of lesion treated. In addition, the CUP study significantly expands the data set used to obtain approval for ChondroCelect from the European Medicines Agency in 2009, increasing eight-fold, from 43 to 334, the number of patients with long-term follow up data. To date almost 700 patients have been treated with ChondroCelect.

ADMIRE-CD Phase III trial (Cx601) in complex perianal fistula on schedule The ADMIRE-CD (Adipose Derived Mesenchymal stem cells for Induction of REmission in perianal fistulizing Crohn’s Disease) Phase III protocol was submitted to Ethics Committees or Health Authorities in all 8 participating countries, and to date approvals have been received in four of those countries already.

Cx611 Phase IIa in RA passes last safety hurdleOn April 17, upon review of the safety data of the first three patients of the third cohort of the company’s Phase IIa clinical trial in rheumatoid arthritis (Cx611), TiGenix received the go-ahead from the independent Safety Monitoring Board to recruit and dose the remaining patients of this cohort. This fact is of major importance. In RA it ensures that the product will not be held back by any dose-limiting factors and that we will be able to move forward with the optimal treatment dose. Of almost equal importance is that, if required, we can expand the dosing range in other indications that we are exploring as well. With 6 months of follow-up, the current RA trial in 53 patients is expected to report meaningful results in H1 2013.

Last patient treated in Cx621 Phase I clinical trialAll 10 healthy volunteers have been recruited and treated in the Phase I study of Cx621. Cx621 investigates the safety and feasibility of intra-lymphatic administration of stem cells. Intra-lymphatic administration of (all) stem cells is patented by TiGenix. The final report of this trial will be available at the end of June.

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Vet undertakes stem cell surgery

Animal stem cell regenerative therapy is the newest service at the Animal Hospital of Tiffin.

“We are the official first site for the therapy in Ohio,” said veterinarian Bob McClung.

The technology uses an adult animal’s stem cells to heal itself.

Veterinarian Mike Brothers performed the surgery Monday on his dog, Tucker, a 2-year-old labrador retriever. It was the second surgery performed at the clinic.

Brothers said his dog’s joint problems are hereditary and he’s had problems since he was a puppy.

“What we’ve been able to do is slow down the arthritis,” Brothers said. The cause of the degeneration will continue, but the fatty tissue removed from the dog can be used for future treatments.

From a piece of fatty tissue of the size removed from Tucker, McClung estimated $3.2 billion stem cells were harvested.

Each injection uses about 90 million cells, so there will be enough of the material for future treatments.

“We have basically 2 billion cells to bank,” he said. “We use cryo-preservation.”

In the freezing process, the cells are gradually cooled to prevent damage and stored in liquid nitrogen at temperatures of minus 80 to minus 90 degrees Fahrenheit.

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International Stem Cell Corporation Scientists to Present Pre-Clinical Research Results at American Society of Gene …

CARLSBAD, Calif.–(BUSINESS WIRE)–

International Stem Cell Corporation (OTCBB: ISCO.OB – News) (www.internationalstemcell.com) today announced that several of its leading scientists will present experimental results from three of ISCOs pre-clinical therapeutic programs.

Firstly, the application of A9 dopaminergic neurons derived from human parthenogenetic stem cells (hpSC) for the treatment of Parkinsons disease. Demonstrating functional dopaminergic neurons in vivo represents an important milestone towards the goal of creating well characterized populations of cells that could be used to develop a treatment for Parkinsons.

Secondly, the differentiation of hpSC and embryonic stem cells into cornea-like constructs for use in transplantation therapy and the in vitro study of ocular drug absorption. There are approximately ten million people worldwide who are blind as a result of damage to their cornea. Generating human corneas from a pluripotent stem cell source should increase the likelihood that people will receive treatment in the future even in the absence of suitable tissue from eye banks.

Lastly, the in vivo and in vitro characterization of immature hepatocyte derived from hpSC. Such cells could be used to develop a treatment for individuals with a liver that has been damaged by disease or sufferers of genetic disorders that inhibit normal liver function. In both cases, implanting healthy hepatocyte cells could treat the underlying disease and prolong the life of the individual.

These results not only show the progress we have made in these important programs, but also demonstrate the broad application of human parthenogenetic stem cells in the development of treatments for incurable diseases, says Dr. Ruslan Semechkin, Vice President of Research and Development.

The presentations will take place at the 15th Annual Meeting of American Society of Gene and Cell Therapy, in Philadelphia at 3:30 p.m. on Thursday, May 17th.

About International Stem Cell Corporation

International Stem Cell Corporation is focused on the therapeutic applications of human parthenogenetic stem cells (hpSCs) and the development and commercialization of cell-based research and cosmetic products. ISCO’s core technology, parthenogenesis, results in the creation of pluripotent human stem cells from unfertilized oocytes (eggs). hpSCs avoid ethical issues associated with the use or destruction of viable human embryos. ISCO scientists have created the first parthenogenic, homozygous stem cell line that can be a source of therapeutic cells for hundreds of millions of individuals of differing genders, ages and racial background with minimal immune rejection after transplantation. hpSCs offer the potential to create the first true stem cell bank, UniStemCell. ISCO also produces and markets specialized cells and growth media for therapeutic research worldwide through its subsidiary Lifeline Cell Technology (www.lifelinecelltech.com), and stem cell-based skin care products through its subsidiary Lifeline Skin Care (www.lifelineskincare.com). More information is available at www.internationalstemcell.com or follow us on Twitter @intlstemcell.

To receive ongoing corporate communications, please click on the following link: http://www.b2i.us/irpass.asp?BzID=1468&to=ea&s=0

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A Little More Education, a Little Longer Life?

MONDAY, May 14 (HealthDay News) — It's graduation season, and new research offers yet another reason to congratulate someone who has completed at least nine years of education: They're likely to live longer.

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A Little More Education, a Little Longer Life?

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First gene therapy successful against aging-associated decline: Mouse lifespan extended up to 24% with a single …

ScienceDaily (May 14, 2012) A new study consisting of inducing cells to express telomerase, the enzyme which — metaphorically — slows down the biological clock — was successful. The research provides a “proof-of-principle” that this “feasible and safe” approach can effectively “improve health span.”

A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals’ genes permanently from the embryonic stage — an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director Maria Blasco, have demonstrated that the mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal’s genes. And they have done so using gene therapy, a strategy never before employed to combat aging. The therapy has been found to be safe and effective in mice.

The results were recently published in the journal EMBO Molecular Medicine. The CNIO team, in collaboration with Eduard Ayuso and Fatima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autonoma de Barcelona (UAB), treated adult (one-year-old) and aged (two-year-old) mice, with the gene therapy delivering a “rejuvenating” effect in both cases, according to the authors.

Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age-related diseases — like osteoporosis and insulin resistance — and achieving improved readings on aging indicators like neuromuscular coordination.

The gene therapy consisted of treating the animals with a DNA-modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging. Telomerase repairs the extreme ends or tips of chromosomes, known as telomeres, and in doing so slows the cell’s and therefore the body’s biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells.

This study “shows that it is possible to develop a telomerase-based anti-aging gene therapy without increasing the incidence of cancer,” the authors affirm. “Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage,” they add.

‘Resetting’ the biological clock

Telomeres are the caps that protect the end of chromosomes, but they cannot do so indefinitely: each time the cell divides the telomeres get shorter, until they are so short that they lose all functionality. The cell, as a result, stops dividing and ages or dies. Telomerase gets around this by preventing telomeres from shortening or even rebuilding them. What it does, in essence, is stop or reset the cell’s biological clock.

But in most cells the telomerase gene is only active before birth; the cells of an adult organism, with few exceptions, have no telomerase. The exceptions in question are adult stem cells and cancer cells, which divide limitlessly and are therefore immortal — in fact several studies have shown that telomerase expression is the key to the immortality of tumour cells.

It is precisely this risk of promoting tumour development that has set back the investigation of telomerase-based anti-aging therapies.

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Gene therapy dramatically extends mouse lifespan

click here to continue to article cliquez ici pour lire l’article weiter zum Artikel clicca qui per visualizzare l’articolo weiter zum Artikel ir a la noticia klik hier om door te gaan naar het artikel Yazya devam etmek iin tklayn Tovbb a cikkre

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Iowa State, Salk Researchers Make Plant Protein Discovery That Could Boost Bioeconomy

Newswise AMES, Iowa Research groups from Iowa State University and the Salk Institute for Biological Studies have uncovered the function of three plant proteins, a discovery that could help plant scientists boost seed oil production in crops, thereby benefitting the production of food, biorenewable chemicals and biofuels.

The analysis of gene activity (by the Iowa group) and determination of protein structures (by the Salk group) independently identified in the model plant thale cress (Arabidopsis thaliana) three related proteins that appear to be involved in fatty-acid metabolism. The Iowa and Salk researchers then joined forces to test this hypothesis, demonstrating a role of these proteins in regulating the amounts and types of fatty acids accumulated in plants. The researchers also showed that the action of the proteins is very sensitive to temperature and that this feature may play an important role in how plants mitigate temperature stress using fatty acids.

The discovery is published online at nature.com, the website of the journal Nature. Corresponding authors are Eve Syrkin Wurtele, a professor of genetics, development and cell biology at Iowa State; and Joseph Noel, a professor and director of the Jack H. Skirball Center for Chemical Biology and Proteomics at the Salk Institute in La Jolla, Calif., and an investigator with the Howard Hughes Medical Institute.

This work has major implications for modulating the fatty-acid profiles in plants, which is terribly important, not only to sustainable food production and nutrition but now also to biorenewable chemicals and fuels, Noel said.

Because very high-energy molecules such as fatty acids are created in the plant using the energy of the sun, these types of molecules may ultimately provide the most cost-effective and efficient sources for biorenewable products, Wurtele added.

Although the researchers now understand that the three proteins dubbed fatty-acid-binding proteins one, two and three, or FAP1, FAP2 and FAP3 are involved in fatty-acid accumulation in plant tissues such as leaves and seeds, Wurtele said researchers still dont understand the physical mechanism these proteins employ at the molecular level. That knowledge will ultimately allow the two collaborating research groups to predictably engineer better functions in plants.

To identify the proteins function in plants, Wurteles research group used its expertise in molecular biology and bioinformatics (the application of computer technologies to biological studies).

One tool the Iowa State researchers used was MetaOmGraph (http://www.metnetdb.org), software they developed to analyze large sets of public data about the patterns of gene activity under different developmental, environmental and genetic changes. The software revealed that the expression patterns of the FAP genes resemble those of genes encoding enzymes of fatty-acid synthesis. The analyses also showed that the accumulation of two of the proteins is highest in the regions of the plant where the greatest amount of oil is produced. These clues led the researchers to predict that the three FAP proteins are important for fatty-acid accumulation.

The Iowa State researchers then tested this theory experimentally by comparing the fatty acids of mutant plants lacking the FAP proteins to those of normal plants. Despite the healthy appearance of the mutant plants, the overall fatty-acid content is greater than in the normal plants, and the types of fatty acids differ.

Noel and researchers at the Salk Institute used a variety of techniques including X-ray crystallography and biochemistry to characterize the structures of the FAP1, FAP2 and FAP3 proteins, and to determine that the proteins bind fatty acids.

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Iowa State, Salk Researchers Make Plant Protein Discovery That Could Boost Bioeconomy

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Plant protein discovery could boost bioeconomy

ScienceDaily (May 14, 2012) Research groups from Iowa State University and the Salk Institute for Biological Studies have uncovered the function of three plant proteins, a discovery that could help plant scientists boost seed oil production in crops, thereby benefitting the production of food, biorenewable chemicals and biofuels.

The analysis of gene activity (by the Iowa group) and determination of protein structures (by the Salk group) independently identified in the model plant thale cress (Arabidopsis thaliana) three related proteins that appear to be involved in fatty-acid metabolism. The Iowa and Salk researchers then joined forces to test this hypothesis, demonstrating a role of these proteins in regulating the amounts and types of fatty acids accumulated in plants. The researchers also showed that the action of the proteins is very sensitive to temperature and that this feature may play an important role in how plants mitigate temperature stress using fatty acids.

The discovery is published online on the website of the journal Nature. Corresponding authors are Eve Syrkin Wurtele, a professor of genetics, development and cell biology at Iowa State; and Joseph Noel, a professor and director of the Jack H. Skirball Center for Chemical Biology and Proteomics at the Salk Institute in La Jolla, Calif., and an investigator with the Howard Hughes Medical Institute.

“This work has major implications for modulating the fatty-acid profiles in plants, which is terribly important, not only to sustainable food production and nutrition but now also to biorenewable chemicals and fuels,” Noel said.

“Because very high-energy molecules such as fatty acids are created in the plant using the energy of the sun, these types of molecules may ultimately provide the most cost-effective and efficient sources for biorenewable products,” Wurtele added.

Although the researchers now understand that the three proteins — dubbed fatty-acid-binding proteins one, two and three, or FAP1, FAP2 and FAP3 — are involved in fatty-acid accumulation in plant tissues such as leaves and seeds, Wurtele said researchers still don’t understand the physical mechanism these proteins employ at the molecular level. That knowledge will ultimately allow the two collaborating research groups to predictably engineer better functions in plants.

To identify the proteins’ function in plants, Wurtele’s research group used its expertise in molecular biology and bioinformatics (the application of computer technologies to biological studies).

One tool the Iowa State researchers used was MetaOmGraph, software they developed to analyze large sets of public data about the patterns of gene activity under different developmental, environmental and genetic changes. The software revealed that the expression patterns of the FAP genes resemble those of genes encoding enzymes of fatty-acid synthesis. The analyses also showed that the accumulation of two of the proteins is highest in the regions of the plant where the greatest amount of oil is produced. These clues led the researchers to predict that the three FAP proteins are important for fatty-acid accumulation.

The Iowa State researchers then tested this theory experimentally by comparing the fatty acids of mutant plants lacking the FAP proteins to those of normal plants. Despite the healthy appearance of the mutant plants, the overall fatty-acid content is greater than in the normal plants, and the types of fatty acids differ.

Noel and researchers at the Salk Institute used a variety of techniques — including X-ray crystallography and biochemistry — to characterize the structures of the FAP1, FAP2 and FAP3 proteins, and to determine that the proteins bind fatty acids.

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Plant protein discovery could boost bioeconomy

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