Thomas Buschmann
Icahn School of Medicine at Mount Sinai
13 Papers
397 Citations
Thomas Buschmann is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Phosphorylation & Kinase. The author has an hindex of 11, co-authored 13 publications.
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Papers
JNK targets p53 ubiquitination and degradation in nonstressed cells
Serge Y. Fuchs,Victor Adler,Thomas Buschmann,Zhimin Yin,Xiangwei Wu,Stephen N. Jones,Ze'ev Ronai +6 more
TL;DR: Data indicate that JNK is an Mdm2-independent regulator of p53 stability in nonstressed cells.
Mdm2 association with p53 targets its ubiquitination
TL;DR: The mechanism by which Mdm2 regulates p53 degradation is elucidated, and in vitro and in vivo ubiquitination assays demonstrate that MDM2 association with p53 targets p53 ubiquitinations.
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Distinct pattern of p53 phosphorylation in human tumors
Toshinari Minamoto,Thomas Buschmann,Hasem Habelhah,Ekaterina Matusevich,Hidetoshi Tahara,Anne Lise Boerresen-Dale,Curtis C. Harris,David Sidransky,Ze'ev Ronai +8 more
TL;DR: Comparison of the pattern of p53 phosphorylation and acetylation in tumor-derived cell lines, tumor samples, and non-neoplastic cells suggests that analysis of two of the more abundant phosphorylated or acetylations on p53 is sufficient to detect 72% of tumor- derived p53 proteins.
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Amino-terminal-derived JNK fragment alters expression and activity of c-Jun, ATF2, and p53 and increases H2O2-induced cell death.
TL;DR: The ability to alter the activity of ATF2, c-Jun, and p53 and the degree of stress-induced cell death by a JNK-derived fragment identifies new means to elucidate the nature of JNK regulation and to change the cellular response to stress.
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Stabilization and activation of p53 by the coactivator protein TAFII31.
Thomas Buschmann,Yahong Lin,Nadia Aithmitti,Serge Y. Fuchs,Hua Lu,Lois Resnick-Silverman,James J. Manfredi,Ze'ev Ronai,Xiangwei Wu +8 more
TL;DR: The results suggest that direct interaction of TAFII31 and p53 not only mediates p53 transcriptional activation but also protects p53 from mdm2-mediated degradation, thereby resulting in activation of p53 functions.
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