Mikhail V. Blagosklonny

Inhibitors of transcription, proteasome inhibitors, and DNA-damaging drugs differentially affect feedback of p53 degradation.

T. Fojo, M. Blagosklonny, W. An, 1998, Experimental cell research.

Wild-type p53 is not sufficient for serum starvation-induced apoptosis in cancer cells but accelerates apoptosis in sensitive cells.

W. El-Deiry, K. Somasundaram, G. Wu, 1997, International journal of oncology.

Depletion of p185erbB2, Raf-1 and mutant p53 proteins by geldanamycin derivatives correlates with antiproliferative activity

L. Neckers, M. Blagosklonny, W. An, 1997, Cancer Chemotherapy and Pharmacology.

bcl-2 protein downregulation is not required for differentiation of multidrug resistant HL60 leukemia cells.

A. Fojo, L. Neckers, M. Blagosklonny, 1996, Leukemia research.

The Hsp90 inhibitor geldanamycin selectively sensitizes Bcr-Abl-expressing leukemia cells to cytotoxic chemotherapy

T. Fojo, K. Bhalla, J. Trepel, 2001, Leukemia.

Nickel-induced transformation shifts the balance between HIF-1 and p53 transcription factors.

M. Blagosklonny, W. An, G. Melillo, 1999, Carcinogenesis.

Mutant conformation of p53 translated in vitro or in vivo requires functional HSP90.

L. Neckers, J. Toretsky, M. Blagosklonny, 1996, Proceedings of the National Academy of Sciences of the United States of America.

Raf-1/bcl-2 phosphorylation: a step from microtubule damage to cell death.

T. Fojo, L. Neckers, W. El-Deiry, 1997, Cancer research.

Geldanamycin selectively destabilizes and conformationally alters mutated p53.

L. Neckers, J. Toretsky, M. Blagosklonny, 1995, Oncogene.