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Five things learned at Sanford-Burnham’s annual postdoc & grad student symposium in La Jolla

by Heather Buschman, Ph.D. on November 14, 2012 at 6:11 am | 0 Comments
Symposium attendees await the announcement of Best Talk and Best Poster awards (Photo by Karolina Kucharova)

Symposium attendees await the announcement of Best Talk and Best Poster awards (Photo by Karolina Kucharova)

Each year, the Sanford-Burnham Science Network, our organization of postdoctoral researchers and graduate students, holds a symposium for young scientists to practice presenting their work and gain valuable feedback from their peers and our faculty members. This year, the La Jolla group’s event was held at the Sanford Consortium for Regenerative Medicine.

Here are five random things we learned last week at the 11th annual symposium:

1. 80 percent of a cell’s energy is spent on making proteins. That makes the limitless ability of cancer cells to proliferate without much access to oxygen or nutrients all that more amazing.
—Robert Schneider, Ph.D., keynote speaker from New York University, who spoke about his work translating control of protein synthesis to breast cancer therapy

2. There are five things that contribute to longevity in many different species: 1) reduced insulin signaling, 2) reduced caloric intake, 3) reduced TOR signaling, 4) reduced mitochondrial respiration, and 4) germline removal. And a cellular process called autophagy seems to be the common factor in each of these. (A note on that last longevity factor: C. elegans worms live longer when their gonads are removed. Likewise, genealogical records for Korean eunuchs—castrated males—show they lived significantly longer than the average Korean. Who knew?)
—Louis Lapierre, Ph.D., Hansen lab, who studies how a certain transcription factor regulates autophagy and longevity in C. elegans, a valuable model for aging studies

3. One underlying problem in inflammatory bowel disease (IBD) may be a breakdown in the unfolded protein response, meaning that intestinal cells can’t respond properly when their proteins are folded incorrectly and the cells begin to die.
—Stewart Cao, Ph.D., Kaufman lab, who studies the role of a particular enzyme in the unfolded protein response and the development of IBD

4. Resident muscle stem cells keep muscles healthy. They differentiate (becoming new muscle cells) and fuse with existing muscle tissue or they self-renew (making more stem cells) and sit quietly until needed in the future.
—Matthew Tierney, graduate student in the Sacco lab, who studies the regenerative potential of fetal-derived muscle stem cells

5. Sweet taste receptors tell your pancreas how much insulin to release, thus helping to regulate your blood sugar levels. But this process seems to malfunction in type 2 diabetes.
—George Kyriazis, Ph.D., Pratley lab, who studies sweet taste receptors and how they contribute to type 2 diabetes

Congratulations to the winners!
Best talk: Stewart Cao, Ph.D., Kaufman lab
Best poster: Melanie Hoefer, Ph.D., Kaul lab

Interested in applying to graduate school or conducting your postdoctoral training at Sanford-Burnham? Visit sanfordburnham.org/training.

Tags: aging, Alessandra Sacco, autophagy, cancer, diabetes, education, IBD, iniflammatory bowel disease, La Jolla, longevity, Malene Hansen, Marcus Kaul, muscle stem cells, postdocs, Randal Kaufman, Richard Pratley, SBSN, Stem Cells, type 2 diabetes, unfolded protein response, UPR

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