M M Nau - JoVE Visualize

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The EMBO Journal|April 1, 1992

p53: a transdominant regulator of transcription whose function is ablated by mutations occurring in human cancerT Unger, M M Nau, S Segal, et al.

Gynecologic Oncology|May 24, 2001

Synergistic induction of apoptosis by the combination of trail and chemotherapy in chemoresistant ovarian cancer cellsM Cuello, S A Ettenberg, M M Nau, et al.

Cancer Research|June 1, 1985

Characterization of variant subclasses of cell lines derived from small cell lung cancer having distinctive biochemical, morphological, and growth propertiesA F Gazdar, D N Carney, M M Nau, et al.

Cancer Research|July 1, 1986

Additive and differential biological activity of alpha-interferon A, difluoromethylornithine, and their combination on established human lung cancer cell linesG Bepler, D N Carney, M M Nau, et al.

Cancer Research|February 11, 1999

Chemotherapy augments TRAIL-induced apoptosis in breast cell linesM M Keane, S A Ettenberg, M M Nau, et al.

Proceedings of the National Academy of Sciences of the United States of America|October 1, 1980

Immunoglobulin V/J recombination is accompanied by deletion of joining site and variable region segmentsJ G Seidman, M M Nau, B Norman, et al.

Nature|November 10, 1983

Amplification and expression of the c-myc oncogene in human lung cancer cell linesC D Little, M M Nau, D N Carney, et al.

International Journal of Oncology|March 17, 2001

Physical interaction between p53 and primary response gene Egr-1J Liu, L Grogan, M M Nau, et al.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research|September 22, 2000

Molecular heterogeneity and function of EWS-WT1 fusion transcripts in desmoplastic small round cell tumorsJ Liu, M M Nau, J C Yeh, et al.

Molecular Cell Biology Research Communications : MCBRC|November 5, 1999

cbl-b inhibits EGF-receptor-induced apoptosis by enhancing ubiquitination and degradation of activated receptorsS A Ettenberg, Y R Rubinstein, P Banerjee, et al.

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Showing results (1-10 of 37) with videos related to

Sort By:

Pageof 4

The EMBO Journal|April 1, 1992

p53: a transdominant regulator of transcription whose function is ablated by mutations occurring in human cancerT Unger, M M Nau, S Segal, et al.

Gynecologic Oncology|May 24, 2001

Synergistic induction of apoptosis by the combination of trail and chemotherapy in chemoresistant ovarian cancer cellsM Cuello, S A Ettenberg, M M Nau, et al.

Cancer Research|June 1, 1985

Characterization of variant subclasses of cell lines derived from small cell lung cancer having distinctive biochemical, morphological, and growth propertiesA F Gazdar, D N Carney, M M Nau, et al.

Cancer Research|July 1, 1986

Additive and differential biological activity of alpha-interferon A, difluoromethylornithine, and their combination on established human lung cancer cell linesG Bepler, D N Carney, M M Nau, et al.

Cancer Research|February 11, 1999

Chemotherapy augments TRAIL-induced apoptosis in breast cell linesM M Keane, S A Ettenberg, M M Nau, et al.

Proceedings of the National Academy of Sciences of the United States of America|October 1, 1980

Immunoglobulin V/J recombination is accompanied by deletion of joining site and variable region segmentsJ G Seidman, M M Nau, B Norman, et al.

Nature|November 10, 1983

Amplification and expression of the c-myc oncogene in human lung cancer cell linesC D Little, M M Nau, D N Carney, et al.

International Journal of Oncology|March 17, 2001

Physical interaction between p53 and primary response gene Egr-1J Liu, L Grogan, M M Nau, et al.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research|September 22, 2000

Molecular heterogeneity and function of EWS-WT1 fusion transcripts in desmoplastic small round cell tumorsJ Liu, M M Nau, J C Yeh, et al.

Molecular Cell Biology Research Communications : MCBRC|November 5, 1999

cbl-b inhibits EGF-receptor-induced apoptosis by enhancing ubiquitination and degradation of activated receptorsS A Ettenberg, Y R Rubinstein, P Banerjee, et al.

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