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Rakesh Kumar, Ph.D. 1984, All India Institute of Medical Sciences UT M. D. Anderson Cancer Center |
Research Interests: Chromatin and transcription controls, human EGF receptor family signaling, coregulators, breast cancer and metastasis, mammary gland development, and knockout and transgenic murine models
The overall goal of my laboratory is to understand the roles of chromatin modifiers play in the transcriptional controls of pathways important in the development, differentiation, proliferation, and tumorigenesis of mammary epithelial cells. A particular emphasis is on the modulation of the above events by growth factor and steroidal signaling. State-of-the-art approaches such as two-hybrid, molecular, genetic, chromatin, and bioinformatic methodologies are utilized to gain insight into these events. The current research projects include- (a) the roles of specific chromatin modifiers in the hormonal responsiveness of mammary epithelial and cancer cells; (b) characterization of transgenic and knock-out murine models of estrogen receptor coactivators and corepressors; (c) characterization of recently identified novel binding partners and chromatin targets of Pak1 and MTA; (d) characterization of EGFR family signaling components and steroid coregulators in epithelial-to-mesenchymal transition; (e) discovering novel functions of estrogen receptor-alpha and -beta, in breast and endometrial cells; (f) characterization of newly identified pathways responsive for hormonal sensitivity of reproductive tissues, and the molecular basis of tamoxifen resistance in breast cancer.
A tutorial in my laboratory will provide hands-on-experience combined with critical analytical reasoning in the areas of cell culture, signal transduction, chromatin assays, molecular biology, tumorogenesis, and mouse models.
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Barnes, C.J., Vadlamudi, R.K., Mishra, S.K., Jacobson, R.H., Li, F., and Kumar, R. (2003) Functional inactivation of a transcriptional corepressor by a signaling kinase. Nature Struc. Biol. 10: 662-628.
Kumar, R. (2003) Another tie that binds MTA family to breast cancer. Cell 113:142-143.
Kumar, R., Wang, R-W, Mazumdar, A., Talukder, A.H., Mandal, M., Yang, Z., Bagheri-Yarmand, R., Sahin, A., Hortobagyi, G., Adam, L., Barnes, C.J., and Vadlamudi, R.K. (2002) A Naturally occurring MTA1 variant sequesters estrogen receptor in the cytoplasm, Nature 418:654-657.
Vadlamudi, R.K., Feng, L., Adam, L., Nguyen, D., Ohta, Y., Stossel, T.H., and Kumar, R. (2002) Filamin is essential for p21-activated kinase 1-mediated actin cytoskeletal assembly. Nature Cell Biol. 4:681-690.
Wang, R.A., Mazumdar, A., Vadlamudi, R.K., and Kumar, R. (2002) P21-activated kinase phosphorylates and transactivates estrogen receptor-a and promotes hyperplasia in mammary epithelium. EMBO J. 21:5437-5447.
Program Affiliations:
Program in Cancer Biology