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COPS5 activates TP53. 30 / 34
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"Here, we show that phosphorylation at the threonine 155 residue is essential for Jab1 mediated p53 nuclear export."
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"Curcumin prevents Jab1 mediated p53 nuclear export."
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"We therefore used curcumin, a CSN associated kinase inhibitor, to test whether CSN dependent phosphorylation is involved in Jab1 mediated p53 regulation."
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"CSN5 and Jab1 is also thought to promote degradation of p53 tumor suppressor via phosphorylation by a CSN associated protein kinase [16]."
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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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"Interestingly, curcumin treatment significantly inhibited Jab1 mediated p53 cytoplasmic localization with only 16% of the cells displaying p53 in the cytoplasm (XREF_FIG, panels 13-16)."
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"To further confirm the effect of curcumin on Jab1 mediated p53 nuclear export, the nucleus and cytoplasm of cells were fractionated and analyzed by western blotting."
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"We next assessed the effects of curcumin on the Jab1 mediated p53 nuclear export in the U2OS osteoblastoma cell line harboring intact p53."
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"Cell fractionation analysis further supported our finding that ectopic Jab1 expression induced p53 accumulation in the cytoplasm, and this was reversed by curcumin treatment (XREF_FIG)."
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"We demonstrate here that ESD increases the nuclear localization of p53 by JAB1, and it is vitally important to find a new factor to regulate p53 and inhibit tumor growth.Here, we found that a novel factor esterase D (ESD) reduced the interaction between JAB1 and p53 to suppress cancer cell growth."
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"Phosphorylation of Thr 155 on p53 is required for Jab1 mediated p53 nuclear export."
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"When Jab1 was co-expressed with S149D and T150E, their nuclear export pattern was similar to wild-type p53, and was inhibited by curcumin, suggesting that S149 and T150 on p53 are dispensable for Jab1 mediated p53 translocation (XREF_FIG and XREF_SUPPLEMENTARY, panels 1-12 and 21-32)."
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"JAB1 induces p53 cytoplasmic localization and its subsequent degradation, which helps to maintain low levels of p53 under normal conditions XREF_BIBR, XREF_BIBR, XREF_BIBR."
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"Thus, we hypothesize that the increased BMP signaling activity in Jab1 cKO chondrocytes might also enhance p53 transcriptional activity, which leads to the activation of p53 downstream targets Puma, Bax, and cleaved caspase 3 (Figure 8)."
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"Jab1/CSN5 was found to compete with p53 to bind directly to the oxygen-dependent death domain of HIF-1α, leading to stabilization of HIF-1α by blocking hypoxia-dependent p53-mediated degradation ( Bem[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"30 CSN5 expression facilitates MDM2-mediated p53 ubiquitination and promotes p53 nuclear export."
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"Although CSN5 have been reported as a negative regulator of p53, 31 the mechanism by which CSN5 mediates p53-dependent tumorigenic process remains not well understood."
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"Significantly, inhibition of CSN associated kinase activity or knockdown of CSN5 impairs JFK promoted p53 degradation, enhances p53 dependent transcription, and promotes cell growth suppression, G (1) arrest, and apoptosis."
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"Similarly, knockdown of UCH37 and USP14 or b-AP15 treatment rescued p53 protein, induced by COPS5 overexpression, and enhanced the activity of transfected luciferase reporter plasmids for p53, Bax, and p21 expression and protein levels of p53 downstream target genes BAX and p21."
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"In this study, we found that activating ESD by FPD5 significantly inhibited the interaction between JAB1 and p53, which would reduce the effect of nuclear exportation of p53 by JAB1, which increased the nuclear localization of p53 and provided a good condition for p53 to regulate other genes’ expression in the nucleus."
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"The nuclear and cytoplasmic co-localization between COPS5 and p53 suggests a mechanism of COPS5 and p53 interaction and relocalization of p53 from the nucleus to the cytoplasm, and treatment of MG132, a potent proteasome inhibitor, significantly inhibited proteasome dependent protein degradation of p53 and enhanced its levels in cytoplasm, which indicated the degradation of p53 induced by COPS5."
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"Consistently, we found that p53 induced by curcumin or CSN5 RNAi was lack of obvious transcriptional activity."
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"Jab1 expression facilitates MDM2-mediated p53 ubiquitination and promotes p53 nuclear export [ 39 , 40 ]."
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"Moreover, Thr155 phosphorylation is necessary for p53 nuclear export mediated by Jun activation domain-binding protein 1 (JAB1) (Figure 4b)."
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"Among them, COPS5 was associated with p53 [ 23 ] and promoted tumor progression by degrading p53 [ 24 ]."
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"Correspondingly, Jab1/CSN5 facilitates MDM2-mediated p53 degradation and promotes p53 nuclear export."
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"The substitution of threonine 155 for valine (T155V) abrogated Jab1 mediated p53 nuclear export, indicating that phosphorylation at this site is essential for Jab1 mediated regulation of p53."
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"Notably, COPS5 promoted tumor progression by degrading p53 [ 24 ]."
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"Jab1 also promotes the nuclear export and cytoplasmic degradation of p53 in coordination with HDM2 [4,5]."
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"Jab1 induces the cytoplasmic localization and degradation of p53 in coordination with Hdm2."
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