Sanford-Burnham Science Blog
Sanford-Burnham researchers identified a potential drug target to prevent the hardening of arteries...
The U.S. Defense Advanced Research Projects Agency (DARPA) has awarded $6 million to a team of...
Sanford-Burnham researchers discover that several children born with rare diseases called Congenital...
Sanford-Burnham researchers identify microRNAs as the missing link between the two defining features...
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Today, April 8, 2013, at 11 a.m. ET, thousands of patient and research advocates, survivors, researchers, clinicians, business leaders, and members of the general public will gather on the steps of the Carnegie Library in Washington, D.C., to Rally for Medical Research. The event, organized by the American Association for Cancer Research, calls on our nation’s policymakers to prioritize medical research funding. This is a unified call for sustained investment in the National Institutes of Health (NIH), an investment to improve health, spur progress, inspire hope, and save lives.
How can you participate?
Giuseppina Claps received her JMNMF award at a special recognition ceremony. She is pictured here with her mentor Ze'ev Ronai (left) and Robert Rickert (right), associate dean of the Sanford-Burnham Graduate School of Biomedical Sciences.
Congratulations to Giuseppina Claps, a student in the Sanford-Burnham Graduate School of Biomedical Sciences, on receiving one of ten nationally competitive 2013 Research Scholar Awards from the Joanna M. Nicolay Melanoma Foundation (JMNMF)! These $10,000 grants support exceptional graduate student research in melanoma.
Malene Hansen, Ph.D., assistant professor in our Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research and native of Denmark, gave a faculty promotion seminar last week. It was her chance to show off her science and service to a committee that will evaluate her for promotion to associate professor. Check out her lab members in attendance. They’re showing their support with Danish flag scarves! Best of luck to Hansen and her team.
#RallyMedRes
What: Rally for Medical Research
When: April 8, 2013, 11 a.m – 12:15 p.m. ET
Where: Carnegie Library, Washington, D.C. and webcast live at www.rallyformedicalresearch.org
On Twitter at #RallyMedRes
Left: In fat tissue from a lean mouse, neutrophil elastase and a1-antitrypsin levels are balanced. Right: In fat tissue from an obese mouse, they are imbalanced—neutrophil elastase levels are high (dark staining) and a1-antitrypsin levels are low.
Imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver in mice and humans—providing a new therapeutic target for these health conditions
Many recent studies have suggested that obesity is associated with chronic inflammation in fat tissues. In a new study, researchers discovered that an imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. This enzyme is produced by white blood cells called neutrophils, which play an important role in the body’s immune defense against bacteria.
The Florida Translational Research Program provides Florida-based scientists with access to Sanford-Burnham's drug-discovery technology and expertise.
We announced today the selection of the first five research organizations that will participate in the Florida Translational Research Program (FTRP) to advance drug discovery in the state. The projects focus on cancer, diabetes, and obesity, and are led by scientists from the University of Central Florida, the University of Florida, the University of Miami, Scripps Florida, and a team of our own Lake Nona scientists. The Florida Department of Health and Sanford-Burnham established the FTRP as a competitive grant program that provides funding for collaborative drug discovery projects. The overall goal of the program is to translate research discoveries made in Florida laboratories into the medicines of tomorrow.
Prostate cancer cells expressing a mutant form of c-Myc that cannot be altered by PKCzeta (left) are more aggressive and more invasive than prostate cancer cells in which PKCzeta is able to keep tabs on c-Myc (right).
The enzyme PKCζ acts as a tumor suppressor by keeping the pro-tumor c-Myc gene in check, in both mice and humans.
Researchers have identified how an enzyme called PKCζ suppresses prostate tumor formation. The finding, which also describes a molecular chain of events that controls cell growth and metastasis, could lead to novel ways to control disease progression.
Michael Jackson, Ph.D., vice president of drug discovery and development in Sanford-Burnham's Conrad Prebys Center for Chemical Genomics (photo by Mark Dastrup)
On April 4, the San Diego chapter of Oxbridge Biotech Roundtable (OBR) will present a free event, Personalized Medicine: Road to New Opportunities.
Drug development scientist Rita Lim-Wilby, Ph.D. will lead a panel discussion on this fascinating and quickly evolving topic. The panel includes Michael Jackson, Ph.D., Sanford-Burnham’s vice president of drug discovery and development, Rob Bookstein, M.D., of Illumina, James Christensen, Ph.D., of Pfizer, Ashley Van Zeeland, Ph.D., M.B.A., of Cyber Genomics, and Paul Billings, M.D., Ph.D., of Life Technologies.
What: Personalized Medicine: Road to New Opportunities
When: Thursday, April 4, 2013, 5:15 p.m. PT
Where: W.M. Keck Foundation Amphitheater, The Scripps Research Institute
10550 N. Torrey Pines Rd, La Jolla, CA 92037
Registration: http://www.oxbridgebiotech.com/events/personalizedmedicine
Scientific research isn’t always easy to explain—or to understand. Whichever side of the conversation you’re on, you might feel a communication gap. The California Institute for Regenerative Medicine (CIRM) , the state’s stem cell agency, recently set out to bridge that gap with a #SciencePitch Challenge. Their goal was to encourage stem cell researchers to develop their “elevator pitch” — the short overview of their work that they’d give if a fellow elevator passenger asked them what they do and they only had a short ride in which to explain it. In the process, the participants are also demonstrating the importance of stem cell research and generating excitement about their work.
Left to Right: Rep. Darrell Issa; Dr. Kristiina Vuori, Sanford-Burnham president and interim CEO; Greg Lucier, Life Technologies CEO (Photo by Augustine Agado, Life Technologies)
San Diego is a hub for life science research. According to San Diego Regional EDC, the region is home to more than 600 life science companies and 80 research institutes, which employ more than 42,000 people. Much of this industry is located in California’s 49th Congressional District, represented by Congressman Darrell Issa, chairman of the House Oversight and Government Reform Committee. Last Friday, Rep. Issa sat down with many of San Diego’s life science leaders.
Neurons from a normal mouse (left) are longer and fuller than neurons from a mouse lacking SNX27 (right).
Researchers discover that the extra chromosome inherited in Down syndrome impairs learning and memory because it leads to low levels of SNX27 protein in the brain.
What is it about the extra chromosome inherited in Down syndrome—chromosome 21—that alters brain and body development? Researchers have new evidence that points to a protein called sorting nexin 27, or SNX27. SNX27 production is inhibited by a molecule encoded on chromosome 21. The study, published March 24 in Nature Medicine, shows that SNX27 is reduced in human Down syndrome brains. The extra copy of chromosome 21 means a person with Down syndrome produces less SNX27 protein, which in turn disrupts brain function. What’s more, the researchers showed that restoring SNX27 in Down syndrome mice improves cognitive function and behavior.
Beaker by the numbers:
Sanford-Burnham’s Beaker blog is 3 years old today!
On March 24, 2010, we published the very first blog post
Since then, we’ve published 538 posts - an average of one post every 2 days
19 regular and guest bloggers have contributed to Beaker
329,059 people have visited the site
Skeletal myospheres ("mini muscles") generated by adding MyoD and BAF60C to embryonic stem cells
To make “mini muscles” from stem cells, you need the protein BAF60C.
Pier Lorenzo Puri, Ph.D., and his team study what makes a muscle cell just that—a muscle cell. They’re especially interested in applying that information to regenerate new muscle for people with muscular dystrophy.
Last year, the team discovered that two proteins called MyoD and BAF60C work together to mark the DNA of precursor cells, setting them on a course to become muscle cells. When the MyoD/BAF60c complex receives the right signals, it unwinds the cell’s genome and begins the process of producing muscle-specific proteins. This chain of events eventually triggers these precursor cells—those that hang out in our normal muscle tissue—to mature into new muscle cells.
