- ADJUNCT ASSOCIATE PROFESSOR Developmental and Regenerative Biology
- ADJUNCT ASSOCIATE PROFESSOR Oncological Sciences
2002 - 2007
The Leukemia and Lymphoma Society
2001 - 2002
Charlotte-Geyer Foundation Award
1999 - 2001
Basil O'Connor Research Award
March of Dimes
Dean's Research Incentive Award
1995 - 1996
Fondation pour la Recherch Medicale
1993 - 1995
1987 - 1992
University Grants Commission, India
Sun H, Li L, Vercherat C, Gulbagci NT, Taneja R, Li J, Chung TK, Chin TH, Acharjee S. Stra13 regulates satellite cell activation by antagonizing Notch signaling. J Cell Biol 2007; 177(4): 647-657.
Thin TH, Li L, Taneja R, Sun H, Chung TK. Stra13 is induced by genotoxic stress and regulates ionizing-radiation-induced apoptosis. EMBO Rep 2007; 8: 401-407.
Kupumbati TS, Cattoretti G, Mira Y Lopez R, Farias EF, Taneja R, Marzan C. Dominant negative retinoic acid receptor initiates tumor formation in mice. Mol Cancer 2006; 5: 12.
Amzi S, Taneja R, Ozog A. Sharp-1/DEC2 inhibits skeletal muscle differentiation through repression of myogenic transcription factors. J Biol Chem 2004; 279(50): 52643-52652.
Grechez-Cassiau A, Panda S, Lacoche S, Teboul M, Delaunay F, Laudet V, Hogenesch JB, Taneja R, Azmi S. The transcriptional repressor STRA13 regulates a subset of peripheral circadian outputs. J Biol Chem 2004; 279: 1141-1150.
Azmi S, Taneja R, Ozog A, Sun H. mSharp-1/DEC2, a basic helix-loop-helix protein functions as a transcriptional repressor of E box activity and Stra13 expression. J Biol Chem 2003; 278: 20098-20109.
Taneja R, Azmi S. Embryonic expression of mSharp-1/mDEC2, which encodes a basic helix-loop-helix transcription factor. Mech Dev 2002; 114: 181-185.
Sun H, Lu B, Taneja R, Flavell RA, Li RQ. Defective T cell activation and autoimmune disorder in Stra13-deficient mice. Nat Immunol 2001; 2: 1047-1047.
Taneja R, Dhar M. Cross-regulatory interaction between Stra13 and USF results in functional antagonism. Oncogene 2001; 20(34): 4750-4756.
Taneja R, Sun H. Stra13 expression is associated with growth arrest and represses transcription through histone deacetylase (HDAC)-dependent and HDAC-independent mechanisms. Proc Natl Acad Sci U S A 2000; 97(8): 4058-4063.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr.Taneja is not currently required to report Industry relationships.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
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