Robert T. Abraham, Ph.D.

Robert Abraham's Research Focus

Dr. Abraham investigates a variety of intracellular signaling pathways related to cell-cycle control and cancer development. He has long-standing research interests in the biochemical events that trigger activation, anergy, and apoptosis in antigen-responsive T cells. In separate projects, Dr. Abraham’s group has cloned several members of a novel family of protein kinases, termed PI 3-kinase related kinases (PIKKs). They are intensively investigating the roles of these protein kinases in normal cell functions, including cell growth and signaling through DNA damage-induced cell cycle checkpoints. These research efforts are providing new insights into the pathogenesis of human diseases, particularly cancer, and are leading to the identification of novel targets for anticancer drug discovery.

Robert Abraham's Bio

Robert Abraham earned his Ph.D. in Pharmacology from the University of Pittsburgh in 1981. He trained as a postdoctoral fellow in pharmacology and immunology at the Mayo Clinic and Mayo Foundation in Rochester, Minnesota, where he was promoted to Assistant Professor in 1986 and Associate Professor in 1992. In 1997, Dr. Abraham joined the Department of Pharmacology and Cancer Biology at Duke University Medical Center, where, in 1999, he was appointed Glaxo-Wellcome Professor of Molecular Cancer Biology. Dr. Abraham was recruited to Sanford-Burnham Medical Research Institute in 2001 to found and direct the Institute's Signal Transduction Program. He served as Director of the Institute's NCI-Designated Cancer Center from 2002–2005, at which time he was recruited to Wyeth Laboratories to direct their cancer drug discovery program. Dr. Abraham maintains collaboration with Sanford-Burnham as an Adjunct Professor.

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Regulation of hypoxia-inducible factor 1alpha expression and function by the mammalian target of rapamycin.

Hudson CC, Liu M, Chiang GG, Otterness DM, Loomis DC, Kaper F, Giaccia AJ, Abraham RT

Mol Cell Biol 2002 Oct ;22(20):7004-14

Pleiotropic defects in TCR signaling in a Vav-1-null Jurkat T-cell line.

Cao Y, Janssen EM, Duncan AW, Altman A, Billadeau DD, Abraham RT

EMBO J 2002 Sep 16 ;21(18):4809-19

ATR/ATM-mediated phosphorylation of human Rad17 is required for genotoxic stress responses.

Bao S, Tibbetts RS, Brumbaugh KM, Fang Y, Richardson DA, Ali A, Chen SM, Abraham RT, Wang XF

Nature 2001 Jun 21 ;411(6840):969-74

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Divergent S phase checkpoint activation arising from prereplicative complex deficiency controls cell survival.

Lau E, Chiang GG, Abraham RT, Jiang W

Mol Biol Cell 2009 Sep ;20(17):3953-64

Targeting the mTOR signaling network in cancer.

Chiang GG, Abraham RT

Trends Mol Med 2007 Oct ;13(10):433-42

The phosphatidylinositol 3-kinase inhibitor, PX-866, is a potent inhibitor of cancer cell motility and growth in three-dimensional cultures.

Howes AL, Chiang GG, Lang ES, Ho CB, Powis G, Vuori K, Abraham RT

Mol Cancer Ther 2007 Sep ;6(9):2505-14

SKAP55 modulates T cell antigen receptor-induced activation of the Ras-Erk-AP1 pathway by binding RasGRP1.

Kosco KA, Cerignoli F, Williams S, Abraham RT, Mustelin T

Mol Immunol 2008 Jan ;45(2):510-22

The FRB domain of mTOR: NMR solution structure and inhibitor design.

Leone M, Crowell KJ, Chen J, Jung D, Chiang GG, Sareth S, Abraham RT, Pellecchia M

Biochemistry 2006 Aug 29 ;45(34):10294-302

The functional role of Cdc6 in S-G2/M in mammalian cells.

Lau E, Zhu C, Abraham RT, Jiang W

EMBO Rep 2006 Apr ;7(4):425-30

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