ACETYLATION [LARGE SCALE ANALYSIS] AT ALA-2, CLEAVAGE OF INITIATOR METHIONINE [LARGE SCALE ANALYSIS], IDENTIFICATION BY MASS SPECTROMETRY [LARGE SCALE ANALYSIS]
ACETYLATION [LARGE SCALE ANALYSIS] AT ALA-2, CLEAVAGE OF INITIATOR METHIONINE [LARGE SCALE ANALYSIS], IDENTIFICATION BY MASS SPECTROMETRY [LARGE SCALE ANALYSIS]
ACETYLATION [LARGE SCALE ANALYSIS] AT ALA-2, CLEAVAGE OF INITIATOR METHIONINE [LARGE SCALE ANALYSIS], IDENTIFICATION BY MASS SPECTROMETRY [LARGE SCALE ANALYSIS]
modifications of USP15 and USP4 by phosphorylation are important for the regulation of their localization required for cellular function in the spliceosome.
Study reports that USP15 affects cancer cell response to PARP inhibitors by regulating homologous recombination repair. USP15 is recruited to DNA double-strand breaks (DSBs) by MDC1. USP15 deubiquitinates BARD1 BRCT domain and promotes BARD1-HP1gamma interaction resulting in BRCA1/BARD1 retention at DSBs. Cancer-associated USP15 mutations with decreased USP15-BARD1 interaction increases PARP inhibitor sensitivity.
First example of isoform-specific deubiquitylase phospho-regulation and a novel role for USP15 in guarding genome integrity. USP15 is required for TOP2A accumulation and USP15 depletion leads to the formation of anaphase chromosome bridges., Phosphorylation
The dominant effect of prolonged USP15 depletion upon signal amplitude is due to a decrease in CRAF levels while allowing for the possibility that USP15 may also function to dampen MAPK signaling through direct stabilization of BRAP.
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