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Member,
JCCC Gene Regulation Program Area
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ACCESS Affinity Group:
ACCESS Affinity - Gene Regulation
Awards and Honors:
University of California, Los Angeles
1992 UCLA Alumni Association Distinguished Scholars Award
1993 UCLA College of Letters & Science Scholar Award
1994 Harvard National Scholarship
1994 The Arthur Furst Award, UCLA
1995 Lucy Wortham James Student Research Award, Harvard Medical School
1996 Howard Hughes Medical Institute Research Fellowship
1997 Howard Hughes Medical Institute Continued Fellowship Support
1999 James Tolbert Shipely Prize, Harvard Medical School
2001 Howard Hughes Medical Institute Postdoctoral Research Fellowship for Physicians
2003 UCLA Chancellor's Award for Postdoctoral Fellows
2006 Howard Hughes Medical Institute Early Career Award
2007 Beckman Young Investigator Award
Member of the MSTP Admissions Committee
Research Interest:
Siavash K. Kurdistani is an Assistant Professor in the Department of Biological Chemistry with Joint appointment in the Department of Pathology and Laboratory Medicine. He is also a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. His research focuses on the role of epigenetic processes in biology and medicine. His lab investigates the roles of histone modifications in cellular transformation and differentiation and includes a translational research component to assess the clinical utility of histone modifications in cancer diagnosis and prognosis.
Studies of histone modifications in cancer have been, by and large, focused on gene-specific differences in occurrences of various modifications. However, his group has revealed that cell-to-cell differences in total or global levels of histone modifications is a previously unappreciated but prevalent phenomenon in cancer (Seligson et al. Nature 2005). This novel cellular epigenetic heterogeneity is, remarkably, predictive of clinical outcome in multiple cancers. Such global alterations in histone modifications are also caused by DNA tumor virus oncoproteins such as the adenovirus e1a, suggesting that processes resulting in global epigenetic reprogramming are linked to oncogenic transformation (Horwitz et al. and Ferrari et al. Science 2008). However, the general knowledge about the mechanisms that control the global epigenetic landscape of a cell in normal biology or cancer remains rudimentary. His laboratory intends to decipher the mechanisms that regulate the global levels of histone modifications and how these regulatory mechanisms contribute to viral and non-viral mediated carcinogenesis.
Cancer development and progression are associated with reversal of a differentiated cell to increasingly more de-differentiated states. In fact, “cellular division without differentiation” is a hallmark of cancer. This phenomenon has cellular and molecular similarities to how embryonic stem cells maintain an undifferentiated, self-renewal state. The Kurdistani group is also expending significant effort in understanding the similarities and differences in epigenetic requirements for maintenance of a de-differentiated state in cancer and embryonic stem cells.
Biography:
Siavash Kurdistani is an Assistant Professor in the Department of Biological Chemistry. He earned his B.S. in Biochemistry from UCLA and M.D. from Harvard Medical School.
Publications:
Ferrari Roberto, Pellegrini Matteo, Horwitz Gregory A, Xie Wei, Berk Arnold J, Kurdistani Siavash K Epigenetic reprogramming by adenovirus e1a..
Science (New York, N.Y.).
2008; 321(5892):
1086-8.
Horwitz Gregory A, Zhang Kangling, McBrian Matthew A, Grunstein Michael, Kurdistani Siavash K, Berk Arnold J Adenovirus small e1a alters global patterns of histone modification..
Science (New York, N.Y.).
2008; 321(5892):
1084-5.
Peng Weimin, Togawa Cynthia, Zhang Kangling, Kurdistani Siavash K Regulators of cellular levels of histone acetylation in Saccharomyces
cerevisiae..
Genetics.
2008; 179(1):
277-89.
Pham Hung, Ferrari Roberto, Cokus Shawn J, Kurdistani Siavash K, Pellegrini Matteo Modeling the regulatory network of histone acetylation in
Saccharomyces cerevisiae..
Molecular systems biology.
2007; 3(1):
153.
Seligson DB, Horvath S, Shi T, Yu H, Tze S, Grunstein M, Kurdistani SK Global histone modification patterns predict risk of prostate cancer recurrence..
Nature. .
2005; 435(7046):
1262-6.
Robyr D, Kurdistani SK, Grunstein M Analysis of genome-wide histone acetylation state and enzyme binding using DNA microarrays..
Methods in enzymology. .
2004; 376:
289-304.
Kim KT, Ongusaha PP, Hong YK, Kurdistani SK, Nakamura M, Lu KP, Lee SW Function of Drg1/Rit42 in p53-dependent mitotic spindle checkpoint..
The Journal of biological chemistry. .
2004; 279(37):
38597-602.
Kurdistani SK, Tavazoie S, Grunstein M Mapping global histone acetylation patterns to gene expression..
Cell. .
2004; 117(6):
721-33.
Kurdistani SK, Grunstein M Histone acetylation and deacetylation in yeast.
Nat Rev Mol Cell Biol.
2003; 4(4):
276-84.
Kurdistani SK, Grunstein M In vivo protein-protein and protein-DNA crosslinking for genomewide binding microarray..
Methods (San Diego, Calif.) .
2003; 31(1):
90-5.
Kurdistani SK, Robyr D, Tavazoie S, Grunstein M Genome-wide binding map of the histone deacetylase Rpd3 in yeast..
Nature genetics. .
2002; 31(3):
248-54.
Robyr D, Suka Y, Xenarios I, Kurdistani SK, Wang A, Suka N, Grunstein M Microarray deacetylation maps determine genome-wide functions for yeast histone deacetylases..
Cell. .
2002; 109(4):
437-46.
Wang A, Kurdistani SK, Grunstein M Requirement of Hos2 histone deacetylase for gene activity in yeast..
Science. .
2002; 298(5597):
1412-4.
Reimer CL, Borras AM, Kurdistani SK, Garreau JR, Chung M, Aaronson SA, Lee SW Altered regulation of cyclin G in human breast cancer and its specific localization at replication foci in response to DNA damage in p53+/+ cells..
The Journal of biological chemistry. .
1999; 274(16):
11022-9.
Kurdistani SK, Arizti P, Reimer CL, Sugrue MM, Aaronson SA, Lee SW Inhibition of tumor cell growth by RTP/rit42 and its responsiveness to p53 and DNA damage..
Cancer research. .
1998; 58(19):
4439-44.
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