Mechanisms of Carcinogenesis Involving Wild-Type

Manfredi, James J.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Cancer Institute (NCI)
• Type: First Independent Research Support & Transition (FIRST) Awards (R29)
• Project #: 3R29CA069161-02S1
• Application #: 2761657
• Study Section: Chemical Pathology Study Section (CPA)
• Program Officer: Pelroy, Richard
• Project Start: 1996-04-01
• Project End: 2001-03-31
• Budget Start: 1998-01-01
• Budget End: 1998-03-31
• Support Year: 2
• Fiscal Year: 1998

Institution

• Name: Mount Sinai School of Medicine
• Department: Internal Medicine/Medicine
• Type: Schools of Medicine
• DUNS #: 114400633
• City: New York
• State: NY
• Country: United States
• Zip Code: 10029

Publications

Thornborrow, Edward C; Patel, Sejal; Mastropietro, Anthony E et al. (2002) A conserved intronic response element mediates direct p53-dependent transcriptional activation of both the human and murine bax genes. Oncogene 21:990-9

Buschmann, T; Lin, Y; Aithmitti, N et al. (2001) Stabilization and activation of p53 by the coactivator protein TAFII31. J Biol Chem 276:13852-7

Thornborrow, E C; Manfredi, J J (2001) The tumor suppressor protein p53 requires a cofactor to activate transcriptionally the human BAX promoter. J Biol Chem 276:15598-608

Thornborrow, E C; Manfredi, J J (1999) One mechanism for cell type-specific regulation of the bax promoter by the tumor suppressor p53 is dictated by the p53 response element. J Biol Chem 274:33747-56

Resnick-Silverman, L; St Clair, S; Maurer, M et al. (1998) Identification of a novel class of genomic DNA-binding sites suggests a mechanism for selectivity in target gene activation by the tumor suppressor protein p53. Genes Dev 12:2102-7

Tang, H Y; Zhao, K; Pizzolato, J F et al. (1998) Constitutive expression of the cyclin-dependent kinase inhibitor p21 is transcriptionally regulated by the tumor suppressor protein p53. J Biol Chem 273:29156-63