Hubert Yin

Arthritis, autoimmune disease discovery could lead to new treatments

Anonymous — Mon, 20 Nov 2017 21:13:07 +0000

Arthritis, autoimmune disease discovery could lead to new treatments Anonymous (not verified) Mon, 11/20/2017 - 14:13

Lisa Marshall

More than 23.5 million Americans suffer from autoimmune diseases like rheumatoid arthritis, scleroderma and lupus, in which an overzealous immune response leads to pain, inflammation, skin disorders and other chronic health problems. The conditions are so common that three of the top five selling drugs in the United States aim to ease their symptoms. But no cure exists, and treatments are expensive and come with side effects.

Now ��񱦵� researchers have discovered a potent, drug-like compound that could someday revolutionize treatment of such diseases by inhibiting a protein instrumental in prompting the body to start attacking its own tissue.

“We have discovered a key to lock this protein in a resting state,” said Hang Hubert Yin, a biochemistry professor in the BioFrontiers Institute and lead author of a paper, published today in Nature Chemical Biology, describing the discovery. “This could be paradigm shifting.”

For years, scientists have suspected that a protein called Toll-like receptor 8 (TLR8) plays a key role in the innate immune response. When it senses the presence of a virus or bacteria, it goes through a series of steps to transform from its passive to active state, triggering a cascade of inflammatory signals to fight off the foreign invader. But, as Yin explained, “it can be a double-edged sword” leading to disease when that response is excessive.

Because TLR8 has a unique molecular structure and is hidden inside the endosome — an infinitesimal bubble inside the cell — rather than on the cell’s surface, it has proven an extremely difficult target for drug development.

“This is a long-sought-after target with very little success,” Yin said.

But his study shows a drug-like molecule called CU-CPT8m binds to and inhibits TLR8 and exerts “potent anti-inflammatory effects” on the tissue of patients with arthritis, osteoarthritis and Still’s disease, a rare autoimmune illness.

For the study, Yin and his co-authors used high-throughput screening to look through more than 14,000 small molecule compounds to determine whether they had the right chemical structure to bind to TLR8. They identified four that shared a similar structure. Using that structure as a model, they chemically synthesized hundreds of novel compounds in an effort to find one that perfectly bound to and inhibited TLR8.

Previous efforts to target the protein have focused on shutting it down when it is in its active state. But the compound Yin discovered prevents it from activating while still in its passive state.

“Before, people were trying to close the open door to shut it down. We found the key to lock the door from the inside so it never opens,” Yin said.

Much more research is necessary, but that could lead to treatments that strike at the root cause of autoimmune diseases, rather than just treating symptoms. With help from CU’s Technology Transfer Office, Yin has already filed a patent application and hopes to move on to animal studies and clinical trials within the next two years.

“Given the prevalence of these diseases, there is a big push for alternatives,” Yin said.

In the meantime, the new compound can serve as a first-of-its kind tool to understand exactly what TLR8 and the other nine toll-like receptors do in the body.

“Our study provides the first small molecule tool to shut this protein down so we can understand its pathogenesis,” Yin said.

The National Institutes of Health funded the study and researchers from the University of Tokyo, Tsinghua University and Peking Union Medical College Hospital in Beijing contributed to it.

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Finding a new strategy for Parkinson's

Anonymous — Tue, 12 May 2015 06:00:00 +0000

Finding a new strategy for Parkinson's Anonymous (not verified) Tue, 05/12/2015 - 00:00

BioFrontiers

If you believe the common adage that you are only using ten percent of your brain, while the other ninety percent remains untapped potential, you are about to be surprised. It’s true that about ten percent of your nervous system is made up of hard-working neurons, diligently delivering messages back and forth between your senses and your brain. Much of the rest of your nervous system is made up of neuroglia (derived from the Greek word “glue”), a mixture of various cell types that spend much of their time supporting neurons so they can continue to support you.

For example, microglia, a type of specialized immune cells, were originally thought to just connect neurons and hold them together. These cells are found all over the brain and spinal cord, responding to damage in the brain and nervous system. While neurons are constantly taking in information about your environment, microglia are hard at work sampling their own environment, patrolling for anything that looks out of place.

BioFrontiers Institute faculty member, Hang Hubert Yin, an Associate Professor of Chemistry and Biochemistry, is eager to tap into that other 90 percent of our nervous system that we’ve been wondering about. In addition to helping protect our brains and nervous system, microglia play an important role in the inflammation that accompanies any damage to your brain. In some cases, though, microglia overreact to perceived damage to the brain and nervous system, introducing inflammation where it should be controlled. Many diseases are associated with these misguided microglia, including Parkinson’s disease, Alzheimer’s disease and Amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease.

Yin’s focus is on toll-like receptors (TLR), specifically TLR1 and TLR 2 that sit on the surface of each microglia and form a macromolecular complex called a heterodimer. These are pattern recognition receptors designed to identify danger signals and activate an immune response. Humans have ten known toll-like receptors in their cells. In some cases, toll-like receptors can be activated to provide a powerful immune response to a disease, harnessing the body’s own ability to fight off illness. In other cases, the immune response from these receptors needs to be managed, like in the case of many autoimmune diseases, which turn the body’s immunity on itself. Yin is seeking ways to control the inflammatory response of microglia through these toll-like receptors.

Yin is looking at the role of toll like receptors in microglia so that he can find a potential cure for these neurodegenerative diseases. Finding a drug that can stop inflammation in the nervous system is no small feat. The blood-brain barrier is highly effective in keeping out anything foreign, including drugs that might be helpful. There are a few TLR1/2 inhibitors in development as drug candidates including RNAs, polypeptides and antibodies. However, none of these biologic drugs can cross the blood-brain barrier to work in the central nervous system due to their large sizes. Yin’s team found a small molecule drug that can penetrate that barrier.

“We used the High-throughput Screening facility at the BioFrontiers Institute to screen 15,000 different compounds to identify a novel chemical entity,” says Yin. “Biological drugs for toll-like receptors exist, but can’t get past the blood-brain barrier, limiting their applications. Ours is the first small molecule that can be used as a specific inhibitor for TLR1/2 in the nervous system.”

In a new paper, published in Science Signaling, part of AAAS Science Journals, Yin and his collaborator, Kathy Maguire-Zeiss of Georgetown University Medical Center, describe a new TLR1/2 inhibitor that was used to better understand the cellular processes of Parkinson’s disease. The inhibitor, called CU-CPT22, is a potent, “drug-like” small molecule suppressant of the TLR1/2-mediated proinflammation signaling. Developed at CU-Boulder by the Yin team, CU-CPT22 binds with toll-like receptors 1 and 2, preventing them from overreacting and causing protein misfolding in the nervous system. The small molecule blocks the receptors and fine-tunes the system, balancing out the overprotective microglia and keeping inflammation at bay. Preventing this inflammation may be the key to controlling neurological diseases like Parkinson’s. CU-CPT22 was recently licensed to Brickell Biotech and commercialized by EMD Millipore, Sigma-Aldrich and Tocris for drug development and research purposes.

“This is exciting for us,” says Yin. “We are suggesting an entirely new strategy for treating Parkinson’s disease – one that we think will be more effective, and one with a potential therapeutic that patients may access in the future.”

Learn more about this research on the Science Signaling Podcast.

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Unlocking toll-like receptors

Anonymous — Fri, 10 Apr 2015 06:00:00 +0000

Unlocking toll-like receptors Anonymous (not verified) Fri, 04/10/2015 - 00:00

BioFrontiers

BioFrontiers’ Hubert Yin is unlocking the power of toll-like receptors

Hubert Yin has been thinking about one type of cell receptor since he joined the BioFrontiers Institute, and it is a receptor worthy of that kind of time. Yin, an Associate Professor of Chemistry and Biochemistry, is focusing much of his research on toll-like receptors. These are pattern recognition receptors designed to identify pathogen signals and activate an immune response within the cell. Humans have ten known toll-like receptors. In some cases, the immune response from these receptors needs to be managed, like in the case of many autoimmune diseases, which turn the body’s immunity on itself. In other cases, toll-like receptors can be activated to provide a powerful immune response to a disease, harnessing the body’s own ability to fight off illness.

Toll-like receptors are becoming popular research subjects in many labs around the world because they are the body’s first-responders to many of the viruses, bacteria and fungi that are trying to find a home in our cells. In 1989, scientists first proposed the idea that cells are using pattern recognition to weed out pathogens and keep them out of healthy cells. Toll-like receptors that used this pattern recognition were identified nearly a decade later. Scientists also discovered toll-like receptors in plants and smaller organisms, pointing to their role in evolution protecting the host organism from disease.

“These toll-like receptors have been a central interest of my group since 2007,” says Yin. “These receptors are leading us to new ideas for the treatment of different diseases.”

Because these toll-like receptors are so important to fighting off disease, Yin is interested in modulating them in order to fight a wide variety of illnesses, from HIV to various cancers. Last year, he received a patent for an inhibitor for toll-like receptor 4 that could effectively help patients with scleroderma, an autoimmune disease affecting connective tissues. The inhibitor is expected to help patients prevent muscle necrosis and the thickening of skin and connective tissues that are hallmarks of the disease.

Toll like receptors 1 and 2 (TLR1/2), the focus of much of Yin’s attention lately, sit on the surface of the cells, like sentries, in order to respond quickly to attacks. In an article in Science Advances, the newest open-access journal from the AAAS Science Journals (Cheng et al. Science Advances 2015, DOI: 10.1126/sciadv.1400139). Yin’s research team details their work on these receptors. The paper introduces a new group of small molecule agents developed by Yin’s team that can harness the immune response to disease provided by TLR1/2, making it more potent and specific.

“Novel compounds like these could potentially lead to a new generation of cancer therapies,” says Yin. “TLR therapies are very exciting right now and pharmaceutical companies are now starting to introduce innovative programs to develop TLR7 regulators. CU-Boulder has already filed a patent for our work on TLR1/2, and the intellectual property for this technology has been licensed for commercialization to both EMD Millipore and Tocris Bioscience by CU’s Office of Technology Transfer. We’re excited to see what comes out of this work.”

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BioFrontiers Faculty Receive BDEG Grants

Anonymous — Thu, 07 Jun 2012 06:00:00 +0000

BioFrontiers Faculty Receive BDEG Grants Anonymous (not verified) Thu, 06/07/2012 - 00:00

BioFrontiers

BioFrontiers faculty receive commercialization grants from the State of Colorado

Ten CU research projects were recently selected to receive grants through Colorado’s Bioscience Discovery Evaluation Grant Program (BDEG-Co). The State of Colorado Office of Economic Development and International Trade began the BDEG program in 2007, providing proof-of-concept grants to move promising CU biotechnologies closer to market readiness, as well as early-stage matching “seed” grants to enable the development and commercial validation of technologies that are licensed from Colorado research institutions by Colorado based start-up companies. Three BioFrontiers faculty members received these awards in the 2011-12 funding cycle:

Christopher Bowman, Department of Chemical and Biological Engineering, CU-Boulder, for inexpensive, highly-efficient synthetic nucleic acids for use in nanoassembly, biodetection and other biofunctional applications.
Heide Ford, Department of Pathology and Department of Obstetrics & Gynecology, and Andrew Thorburn, Department of Pharmacology, CU Anschutz Medical Campus, for a novel biomarker to predict treatment response in solid tumors.
Robert Garcea, BioFrontiers Institute, Department of Molecular, Cellular and Developmental Biology, CU-Boulder, for a next-generation vaccine for human papillomavirus (HPV).
Richard Johnson, Department of Medicine (Renal Diseases & Hypertension), CU Anschutz Medical Campus, for a novel treatment to prevent acute kidney injury following surgery or use of radiocontrast agents.
Malik Kahook, Department of Ophthalmology, CU Anschutz Medical Campus, for an implanted device to reduce intraocular pressure and treat glaucoma.
Uday Kompella, Department of Pharmaceutical Sciences, CU Anschutz Medical Campus, for a new drug to treat “wet” age-related macular degeneration (AMD).
Leslie Leinwand, BioFrontiers Institute, Department of Molecular, Cellular and Developmental Biology, CU-Boulder, for novel drugs to protect from cardiac disease.
David Wagner, Department of Medicine (Pulmonary Sciences & Critical Care Medicine), CU Anschutz Medical Campus, for a drug to prevent/reverse high blood sugar in type-1 diabetes.
Xiao-Jing Wang, Department of Pathology, CU Anschutz Medical Campus, for a drug to treat oral mucositis, a common side effect of radiation therapy.
Hang (Hubert) Yin, BioFrontiers Institute, Department of Chemistry and Biochemistry, CU-Boulder, for more sensitive biomarkers for metastatic cancers and other diseases in body fluids.

“The BDEG award winners this year show an incredible breadth and depth of bioscience research and innovation,” said Tom Cech, Director of CU’s BioFrontiers Institute, an interdisciplinary center designed to explore critical frontiers of unknown biology and translate new knowledge to practical applications. “The BDEG program provides a powerful catalyst to get these ideas out of their academic institutions and into the marketplace.”

The BioFrontiers Institute provided the required matching funds for the grants to Boulder-based researchers Christopher Bowman, Robert Garcea, Leslie Leinwand and Hubert Yin.

About the Technology Transfer Office and the University of Colorado:
The CU Technology Transfer Office (TTO) pursues, protects, packages, and licenses to business the intellectual property generated from research at CU. The TTO provides assistance to faculty, staff, and students, as well as to businesses looking to license or invest in CU technology. Since 2002, 80 companies have been formed based on CU intellectual property; of these, 65 are operational as either stand alone or subsidiary/merged companies.

The University of Colorado is a premier public research university with four campuses: the ��񱦵�, the University of Colorado Colorado Springs, the University of Colorado Denver and the University of Colorado Anschutz Medical Campus. Some 60,000 students are pursuing academic degrees at CU. The National Science Foundation ranks CU seventh among public institutions in federal research expenditures in engineering and science. Academic prestige is marked by the university’s four Nobel laureates, seven MacArthur “genius” Fellows, 18 alumni astronauts and 19 Rhodes Scholars.

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Biofrontiers researcher rethinks morphine's effects

Anonymous — Mon, 07 May 2012 06:00:00 +0000

Biofrontiers researcher rethinks morphine's effects Anonymous (not verified) Mon, 05/07/2012 - 00:00

BioFrontiers

A ��񱦵�-led research team has discovered that two protein receptors in the central nervous system team up to respond to morphine and cause unwanted neuroinflammation, a finding with implications for improving the efficacy of the widely used painkiller while decreasing its abuse potential.

Scientists have known that a particular protein receptor known as toll-like receptor 4, or TLR4, helps to activate inflammation-signaling pathways to attack foreign substances like bacteria and viruses, said Biofrontiers Institute faculty member and CU-Boulder Assistant Professor Hang “Hubert” Yin of the chemistry and biochemistry department. The new study showed opiod analgesics like morphine also trigger such neuroinflammation by first binding to an accessory protein receptor known as a myeloid differentiation protein receptor 2, or MD-2, which then works in concert with TLR4 to respond to morphine in the central nervous system, said Yin, who led the study.

The new findings should help researchers develop new drugs not only to increase the effectiveness of medical opiates like morphine by preventing neuroinflammation that enhances pain by increasing the excitability of neurons in the pain pathway, but also to influence the TLR4/MD-2 protein complex in a way that may help prevent drug abuse. Such pharmaceuticals could be designed to decrease side effects like tolerance, dependence and addiction not only in opiates, but in methamphetamines, cocaine and even alcohol.

“While inflammation is part of the body’s natural defense system to protect it after injury or infection, too much inflammation is unhealthy,” said Yin. “We hope our new findings on how this particular protein complex works can help us to understand morphine-induced inflammation and eventually lead to therapeutics to make morphine work more efficiently with fewer side effects.”

A paper on the subject is being published this week in the Proceedings of the National Academy of Sciences. Co-authors include CU-Boulder researchers Xiaohui Wang, Lisa Loram, Khara Ramos, Armando de Jesus, Kui Cheng and Annireddy Reddy and Linda Watkins, as well as Jacob Thomas, Andrew Somogyi and Mark Hutchison of Australia’s University of Adelaide. The National Institutes of Health funded the study.

MD-2 is a receptor found on human immune cells in the central nervous system known as glial cells and appears to be left over from millions of years of evolution, said Watkins, a distinguished professor in CU-Boulder’s psychology department. When MD-2 bound to morphine in the study, the glial cells -- which normally act as “housekeeper cells” to clean up debris and support proper neuron function -- excited the neurons that transmit pain signals and hindered the ability of morphine to suppress pain.

The heightened excitement of glia cells by opiates and other drugs appears to amplify the rewarding qualities of several commonly abused drugs, according to the research team. Glial cells, which originally were thought by scientists to hold neurons in the brain together somewhat like glue, outnumber neurons by up to 50 to one.

The team members used a multidisciplinary approach that included biochemistry, biophysics and cellular biology to investigate the TLR4/MD-2 protein complex and to pinpoint the relationship between MD-2 and morphine. As part of the study the team used laboratory “knock-out mice” -- genetically engineered mice in which existing genes or proteins are inactivated -- to infer the function of TLR4 and its relationship with morphine-induced analgesia.

“The exciting thing about this research is that we have discovered that there is not just one receptor that detects morphine, there is a second one that nobody knew about before, namely MD-2/TLR4,” said Watkins. “We have shown this protein complex essentially cuts morphine off at the knees, preventing it from doing its job in controlling pain.”

As part of the study, several “small molecule inhibitors” developed and tested by the research team to target and deactivate TLR4/MD-2 demonstrated that the morphine-induced inflammation is exclusively tied to the protein complex.

Millions of Americans suffer from chronic, debilitating pain that makes it extremely painful to perform even the simplest activities like showering and dressing, and which differs from pain associated with injuries, which generally heal. Chronic pain sufferers include victims of cancer and AIDS who have nerve damage.

It is estimated that four out of every 10 people in the United States are likely to be in chronic pain, costing the nation as much as $635 billion annually in lost productivity and health care expenses. The United States is one of the world’s highest users of morphine, which has been around since the 1850s and which ironically was first marketed as a cure for opium and alcohol addiction.

Yin said the CU-Boulder researchers have been working with the University of Colorado Technology Transfer Office, or TTO, and have filed a group of related patents on potential therapeutics for optimizing current pain management therapies. Several of the small molecule inhibitors used in the study to target and inactivate the TLR4/MD-2 protein complex have been exclusively optioned to BioLineRX, a publicly traded drug development company in Israel, through CU’s TTO.

“Using interdisciplinary approaches to look for unconventional drug targets is a central theme in my work,” said Yin. “Even in graduate school, I was attracted to the idea of ‘rational design’ -- using computer simulation and synthetic chemistry to design something useful like cancer drugs. Working across disciplines is where the future of science lies.”

See more on Hubert Yin's research at:

Futurity.org
Nature

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Stopping cancer's knock on the door

Anonymous — Tue, 06 Dec 2011 07:00:00 +0000

Stopping cancer's knock on the door Anonymous (not verified) Tue, 12/06/2011 - 00:00

BioFrontiers

Stopping cancer's knock on the door

As a self-proclaimed “science nerd” in a Beijing high school, Hubert Yin considered biochemistry to be the ultimate in cool. It was the only science, he felt, that was capable of explaining what he thought was the most complex, most beautiful thing on earth– life at the molecular level.

This sense of awe led him to graduate at the top of his class at Peking University in applied chemistry, and then propelled him to the other side of the globe for a doctorate in organic and bioorganic chemistry from Yale, and post-doctoral work at the University of Pennsylvania School of Medicine. Now he is an assistant professor of chemistry and biochemistry, a University of Colorado Cancer Center Investigator, and a Biofrontiers Institute faculty member at the ��񱦵�.

“I was totally amazed by this ‘in depth’ understanding of how life works,” says Yin. “I was attracted to the idea of rational design where we use all of these fun toys, like computer simulation and protein engineering, to design something novel and useful, like cancer drugs.”

Yin is searching for unconventional drug targets: the ones that have been overlooked by drug companies. His focus is on cell membrane proteins, which act as windows and doors to the inner workings of all cells. Some viruses knock on the doors of the cell, hijacking normal cell functions, allowing them to gain entry through the cell membrane and take over the cell. Scientists have yet to discover just how that “knock on the door” occurs.

Yin is studying this process with the Epstein-Barr virus (shown, left), also known as Human Herpesvirus-4 (HHV-4), which was identified in 1964 as a cancer-causing virus. It is one of the most common viruses in humans, affecting approximately 95 percent of the U.S. population by adulthood. It is also infamously known as the virus that causes mononucleosis.

HHV-4 is one of at least six viruses that are known to cause cancer, and it is associated with some of the rare cancers: Hodgkin’s lymphoma, Burkitt’s lymphoma, nasopharyngeal carcinoma and other central nervous system lymphomas. Because it is so common and is associated with so many cancers, HHV-4 is an attractive target for the development of cancer vaccines and treatment.

Computer simulations have allowed Yin to study the process viruses use to knock on the doors of cells. He has rebuilt the Latent Membrane Protein, or LMP-1, down to the last atom using computer simulations in a membrane environment. LMP-1, when activated, induces an inflammatory response to HHV-4, which allows cancers to grow within the cell. Using these computer simulations, he hopes to predict how and why cells open their doors to these dangerous invaders.

“Our strength is bridging ‘in silico’ computer simulations with wet-lab experimental approaches,” says Yin who collaborated with fellow CU-Boulder biochemist and Biofrontiers Institute faculty member, Natalie Ahn, as well as CU-Boulder biologist, Jennifer Martin. Ahn provided her expertise in mass spectroscopy to understand the structure of the LMP-1 molecule. Martin is an expert on the Epstein-Barr virus and contributed her knowledge on the nature of the virus and how it causes cancer.

Yin’s next step is to take the data provided by the computer simulations of the membrane protein and use it to predict how it will react to potential drugs. It is even more difficult than it sounds. These proteins have defied exploration by many scientists before Yin. But these drugs may provide a process for treating HHV-4, and stopping deadly lymphomas in their tracks.

“Trying to achieve something that took nature millions of years to develop is an outstanding intellectual challenge,” says Yin. “And multidisciplinary approaches are the means we must take to approach this problem.”

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Biomarkers light the way to cancer diagnosis

Anonymous — Tue, 13 Sep 2011 06:00:00 +0000

Biomarkers light the way to cancer diagnosis Anonymous (not verified) Tue, 09/13/2011 - 00:00

BioFrontiers

Biomarkers light the way to cancer diagnosis

In an 18-year study released this summer by the National Cancer Institute, widespread screening for ovarian cancer was found to be ineffective in catching the disease. In fact, the screening often did more harm than good, leading women to unnecessary surgery and the complications that often come with it.

Similar issues have been raised about annual mammography screenings increasing breast cancer risk in women with a predisposition to the disease. The low-dose radiation used in the screening ratcheted up the susceptibility to cancer for women who were already at a higher risk—the women who need the screenings the most. Biofrontiers scientist, Hubert Yin, is on the hunt for a better way to find cancer early, without harming patients in the process.

Hubert, an assistant professor in chemistry and biochemistry, is studying biomarkers, which are traceable substances that allow scientists to track a process within the body. Using a biomarker is like tying a balloon to a friend moving through a crowd. Because you can see the balloon above the crowd, you are easily able to locate your friend. In Hubert’s experiments, the balloons are fluorescent molecules called a fluorophores, which chemically attach themselves to cells that indicate cancer is present, glowing so they can be seen and tracked.

Microvesicles are the objects of the fluorophores’ chemical spotlight. They are shed from the surface of cells and can actually help the spread and release of metastatic cancer cells. The presence of microvesicles is a key indicator that cancer is at work, and fortunately, they are easy to find in a simple blood or urine sample. Once Hubert chemically attaches fluorophores to these microvesicles, screening someone for cancer becomes as easy as looking for the glow. A lack of microvesicles means there is nothing for the fluorophores to attach to, which means they don’t glow. And no glow means no cancer.

“This is a great diagnostic concept,” he says. “Biomarkers like fluorophores give us efficient, non-invasive ways to detect cancer before it is diagnosed and after it is treated. Being a smaller, research focused organization gives us an advantage over big pharmaceutical companies when it comes to designing biomedical solutions. It is easier for us to collaborate across labs, and to innovative methods that lead us in the direction of new ways of treating cancer.”

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Thinking out of the box for a cancer cure

Anonymous — Thu, 16 Jun 2011 06:00:00 +0000

Thinking out of the box for a cancer cure Anonymous (not verified) Thu, 06/16/2011 - 00:00

BioFrontiers

CIMB scientist, Hubert Yin, describes how he is stepping out of his comfort zone in search of a better understanding of cancer. Read more in this interview.

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CIMB Researcher receives $750,000 Cancer Research Grant

Anonymous — Wed, 09 Dec 2009 07:00:00 +0000

CIMB Researcher receives $750,000 Cancer Research Grant Anonymous (not verified) Wed, 12/09/2009 - 00:00

BioFrontiers

A University of Colorado cancer researcher secured a $750,000, highly competitive Stand up to Cancer Innovative Research Grants.

Hang "Hubert" Yin, assistant professor of chemistry and biochemistry at CU-Boulder, will receive the grant over a three-year period for his "high-risk, high-reward" research project.

It's high-risk because it challenges the way cancer science is currently being conducted and high-reward for its potential for saving lives, according to the organization.

Richard D. Kolodner, chairman of the Stand Up to Cancer grants review committee, said in a news release that the group asked young researchers to step outside of their comfort zones in their research.

"If these Hang "Hubert" Yin (University of Colorado)
projects come to fruition, some of the ideas could be game-changers in cancer research," he said.

Yin, assistant professor of chemistry and biochemistry at CU and a researcher with the CU Cancer Center, competed against more than 400 U.S. scientists to win one of the 13 grants.

His project will focus on the Epstein-Barr virus, which benignly infects nine out of 10 people. But, it's also at play in various types of lymphomas, including post-transplant or AIDS-related lymphoma, Burkitt's lymphoma and Hodgkin's lymphoma.

More on this story from ��񱦵� News

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Two CU-Boulder Faculty Selected for $40 Million Howard Hughes Medical Institute Research Program

Anonymous — Mon, 24 Aug 2009 06:00:00 +0000

Two CU-Boulder Faculty Selected for $40 Million Howard Hughes Medical Institute Research Program Anonymous (not verified) Mon, 08/24/2009 - 00:00

BioFrontiers

Two University of Colorado at Boulder faculty members are among 33 researchers selected by the Howard Hughes Medical Institute of Chevy Chase, Md., to participate in a $40 million pilot program to pursue large, collaborative and potentially transformative biomedical research.

The Collaborative Innovation Awards to the eight teams of researchers represent a shift for the institute, the first time administrators there are providing direct funding for specific projects. The four-year pilot effort that includes researchers from 16 institutions in the United States and Chile is intended to encourage both HHMI investigators and outside scientists to undertake projects so new and large in scope that they require a team of collaborators with a range of expertise.

"We're excited about this program because of the quality of the projects, but also because it broadens the community of scientists supported by HHMI," said HHMI President and CU Distinguished Professor Tom Cech. "It incorporates people outside of the HHMI investigator program in solving important problems, and lets us do something really new."

A four-person research team led by HHMI Investigator Douglas Rees, which includes CU-Boulder faculty members Michael Stowell and Hang (Hubert) Yin and the California Institute of Technology's Rob Phillips, will be developing novel methods for analyzing the three-dimensional structures of membrane proteins. Located within the cell membranes, membrane proteins act as "gatekeepers" to control the two-way flow of nutrients, hormones and signaling molecules that regulate the permeability of the membranes and help cells stay healthy.

Rees and his team will build on earlier studies by Stowell of CU-Boulder's molecular, cellular and developmental biology department and his work on the structure of proteins found in neural synapses. Stowell has been targeting cell membrane lipids and their ability under some conditions to spontaneously assemble into "supramolecular" clusters in a laboratory dish.

More about this story from CU News Center

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