波士顿大学G蛋白研究博士后职位

日期:2015-01-05
We are looking for candidates with a recent Ph.D. to fill one or possibly two open postdoctoral positions. The ideal candidates should have a strong background in Cell Biology Molecular Biology and Biochemistry applied to Signal Transduction research

We are looking for candidates with a recent Ph.D. to fill one or possibly two open postdoctoral positions. The ideal candidates should have a strong background in Cell Biology, Molecular Biology and Biochemistry applied to Signal Transduction research. Preference will be given to candidates with solid first author publications to demonstrate experience.

The overall goal of our lab is to understand how dysregulation of trimeric G proteins underlies the molecular basis of disease. Trimeric G proteins are critical mediators of signal transduction activated by G protein couple receptors (GPCRs), and as such they are key pharmacological targets that play critical roles in physiology and disease. We have recently discovered a GPCR-independent mechanism of trimeric G protein activation that “rewires” this signaling pathway to regulate multiple cellular processes (cell migration, mitosis, autophagy, etc) and diseases (cancer metastasis, developmental defects).

We use a multidisciplinary approach that combines different experimental model systems (mammalian cells, yeast, proteins in vitro, Xenopus embryos), genetic screens, cell biology (microscopy, BRET), bioinformatics, molecular biology and high-throughput drug screens to gain further insights into the molecular basis of this mechanism in disease and its possible pharmacological targeting. We are currently funded by multiple grants from the NIH and private foundations.

The selected candidate(s) will join this dynamic environment to carry out projects devoted to the identification and characterization of novel non-GPCR G protein activators by using approaches described above.

Boston University School of Medicine is located in the heart of Boston, a city with an unparalleled scientific and cultural environment for young scientists.

Interested candidates should send a CV, including contact information for 3 letters of reference, and a short statement describing experience, goals and reasons for the interest in this position to:

Mikel Garcia-Marcos, PhD. Assistant Professor
mikel.garcia.marcos@gmail.com
http://www.bumc.bu.edu/biochemistry/people/faculty/mikel-garcia-marcos/

RELATED LITERATURE:

1. Garcia-Marcos, M., Ghosh, P., & Farquhar, M. G. (2014) GIV/Girdin transmits signals from multiple receptors by triggering trimeric G prtoein activation. J. Biol. Chem, in press. (REVIEW)
2. Ghosh, P., Garcia-Marcos, M., & Farquhar, M. G. (2011) GIV/Girdin is a rheostat that fine-tunes growth factor signals during tumor progression. Cell Adh Migr 5: 237-248. (REVIEW)
3. Garcia-Marcos, M., Ghosh, P., & Farquhar, M. G. (2009) GIV is a nonreceptor GEF for G alpha i with a unique motif that regulates Akt signaling. Proc Natl Acad Sci USA 106: 3178-3183.
4. Ghosh, P., et al. (2010) A G{alpha}i-GIV molecular complex binds epidermal growth factor receptor and determines whether cells migrate or proliferate. Mol Biol Cell 21: 2338-2354.
5. Garcia-Marcos, M., Ear, J., Farquhar, M. G., & Ghosh, P. (2011) A GDI (AGS3) and a GEF (GIV) regulate autophagy by balancing G protein activity and growth factor signals. Mol Biol Cell 22: 673-686.
6. Garcia-Marcos, M., et al. (2012) Functional characterization of the guanine nucleotide exchange factor (GEF) motif of GIV protein reveals a threshold effect in signaling. Proc Natl Acad Sci USA
7. Garcia-Marcos, M., et al. (2011) Expression of GIV/Girdin, a metastasis-related protein, predicts patient survival in colon cancer. Faseb J 25: 590-599….

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