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UCHL1 activates TP53. 17 / 23
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"It is possible that in cells with wild type p53, UCH-L1 promotes degradation p53, resulting in reduced p53 signaling and inhibition of cell death (XREF_FIG)."
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"Western blot showed that UCHL1 promoted p53 accumulation in breast tumor cells, along with the reduction of MDM2, while UCHL1 C90S did not increase p53 accumulation, but partly decreased the expression of MDM2 (XREF_FIG)."
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"Thus , in breast cancer models , UCHL1 can induce the levels of p53 and reduce mdm2 protein levels ."
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"Li et al. showed that UCHL1 promotes tumour suppressor p53 signaling and is silenced due to its promoter methylation in nasopharyngeal carcinoma [XREF_BIBR]."
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"In breast cancer, ectopic expression of UCHL1 is able to induce apoptosis by stabilizing p53."
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"The results indicated that probably the extrinsic (Fas, Fas-L, Trail, DR4 and DR5) and intrinsic (cytochrome C) apoptotic pathways, the activation of p53 (phospho-Mdm-2 and phospho-p53) and the Bcl-2 family members (pro apoptotic member Bax, anti-apoptotic members Bcl-2 and Bcl-xL) combined with each other, participating in the process of apoptosis induced by UCH-L1 in MCF7 cells."
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"Hypermethylation of RASSF1A may contribute as well by releasing the inhibition of JNK , whereas loss of UCHL1 expression may destabilize p53 and thus its downstream effector CDKN1A ( 243 , 244 ) ."
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"Interestingly, UCHL1 promotes p53 signaling in nasopharyngeal carcinoma 40 and PADI2 facilitates p53 degradation in breast cancer cells."
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"Contradictorily, UCHL1 has recently been shown to induce G0/G1 cell cycle arrest and apoptosis by stabilizing p53 and has also been shown to be frequently silenced in primary breast tumors, but not in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Further studies are needed to determine specifically how UCH-L1 modulates p53."
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"Furthermore, using catalytic mutant UCHL1 C90S as a control, the accumulation of p53 mediated by UCHL1 was observed, subsequently, p21, as key p53 downstream target genes and regulators of cell cycle G1/S checkpoint, as well as cleaved-caspase 3 and PARP, were obviously upregulated, accompanied by UCHL1 mediated p53 activation, but not in UCHL1 C90S expressing breast cancer cells."
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"Studies showed that UCHL1 could induce apoptosis by stabilizing p53 in breast and hepatocellular carcinoma XREF_BIBR, XREF_BIBR, and promote ovarian cancer cell apoptosis associated with Bcl-2 family proteins regulated caspase activation 37."
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"Western blots again indicated that UCHL1 overexpression in LNCaP cells induces accumulation of p53 whereas MDM2 protein is decreased compared to mock control cell line."
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"We further found that UCHL1 induced p53 accumulation and reduced MDM2 protein level, and subsequently upregulated the expression of p21, as well as cleavage of caspase3 and PARP, but not in catalytic mutant UCHL1 C90S expressed cells."
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"Interestingly , UCHL1 promotes p53 signaling in nasopharyngeal carcinoma 40 and PADI2 facilitates p53 degradation in breast cancer cells ."
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"The exact mechanism by which UCHL1 regulates tumor development remains uncertain, although recent data suggest that UCHL1 increases the half-life of p53 and p14 ARF, decreases the half-life of Mdm2, and activates the p53 signaling pathway XREF_BIBR, XREF_BIBR."
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"Subcellular localization study showed that UCHL1 increased cytoplasmic abundance of p53."
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