IndraLab

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COPS5 inhibits TP53. 23 / 24
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"124 Inhibition of CSN‐related kinase activity or knockdown of CSN5 inhibits SCF(JFK) degradation of p53, enhances p53‐dependent transcription, and leads to cell growth inhibition, cell G1 phase arrest and apoptosis."
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"As Jab1 can promote the degradation of p27 [XREF_BIBR] and p53 [XREF_BIBR], we further explored the effect of T83 on these two proteins."
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"Jab1, a co-activator of AP-1 transcription factor and the fifth subunit of the COP9 signalosome, mediates degradation of the tumor suppressor p53 and p27 (Kip1) and functions as a tumor promoter in different types of human cancer."
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"Asrij and OCIAD1 suppresses CSN5 mediated p53 degradation and maintains mouse hematopoietic stem cell quiescence."
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"JAB1 can promote the nuclear output of p53 and assist MDM2, an E3 ubiquitin ligase, to promote the degradation of p53 in the cytoplasm [22]."
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"CSN5 can sequester p53 at the cytoplasm by either directly binding to promote the protein into the ubiquitin-proteasome-mediated protein degradation, or by linking the protein to the COP9 complex [XREF_BIBR, XREF_BIBR]."
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"As CSN5 is also known to promote the degradation of several proteins, e.g. p53, IkappaBalpha, or p27 [24,25,37], we asked if CSN5 might also affect the degradation of SIAH-1."
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"How Jab1 regulates Rad51 protein and mRNA expression is not completely understood, but it is clear that Jab1 affects the major regulator of Rad51, p53, which was detected in high levels in Jab1 -/- embryos, Jab1 deficient MEFs, and Jab1 knockdown U2OS cells in our study; furthermore, these results have been supported by several other studies that found that JAB1 contributes to the stability of Mdm2 and accelerates p53 degradation and that p53 negatively regulates Rad51 at the transcriptional level through a p53 response element."
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"JAB1 (C-Jun activation domain binding protein-1) promotes the degradation of the tumor suppressor, p53, and the cyclin dependent kinase inhibitor, p27."
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"Jab1 is also involved in ubiquitination and degradation of tumor-inhibiting factors including P53 and Smad4/7 [ 36 , 37 ]."
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"JAB1 also promotes the degradation of the tumor suppressor, p53, and the cyclin dependent kinase inhibitor, p27."
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"Consistently, ectopic over-expression of a V5 tagged CSN5 (CSN5-V5), thereby overcoming cellular CSN5 depletion by curcumin, was able to significantly but not completely repress p53 induction by 15 and 30 muM curcumin treatment in HepG2 cells."
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"CSN5 can also promote cell proliferation and inhibit apoptosis by accelerating the nuclear export of p53 and inducing its degradation in a MDM2-mediated manner [38]."
35870903
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"Also, COPS5 alters cytoplasmic localizations of TP53 and induces the degradation of TP53 (Li et al., 2013)."
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"Significantly, we further show that CSN5 antagonizes the transcriptional activity of p53."
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"However, when CSN5 siRNA was co-transfected with a p53 specific siRNA, thereby blocking CSN5 siRNA induced p53 accumulation, also diminished the inducible p62 degradation and autophagosome formation in HepG2 cells."
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"These results imply that Jab1 can suppress the transcriptional activity of p53, independently of subcellular localization of p53, and possibly via direct binding."
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"Jab1 and CSN5 was found to compete with p53 to bind directly to the oxygen dependent death domain of HIF-1alpha, leading to stabilization of HIF-1alpha by blocking hypoxia dependent p53 mediated degradation [XREF_BIBR]."
20955608
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"Inhibition or knockdown of COP9 or CSN5 impairs FBXO42 promoted p53 degradation resulting in enhanced p53 dependent transcription, growth suppression, cell cycle arrest and apoptosis [XREF_BIBR]."
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"Moreover, Jab1/CSN5 overexpression leads to the stabilization of MDM2 and antagonizes the transcriptional activity of p53 in human cancer ."
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"Depletion of CSN5 induces senescence in p53-null fibroblasts XREF_BIBR, but knockout of the CSN5 gene upregulates p53 expression XREF_BIBR, indicating that CSN5 occurs upstream of both p53 dependent and -independent senescence pathways (XREF_FIG) and that interaction between CSN5 and CDK2 may take part in the p53 independent pathway."
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"Jab1/COPS5 mediates p53 degradation, while Asrij/OCIAD1 inhibits this process and suppresses the proliferative capacity of murine hematopoietic stem cells [37]."
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"Jab1 and CSN5 knockdown also impaired proliferation and enhanced apoptosis in these cells regardless of the genotype of the tumor suppressor p53 [XREF_BIBR]."
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