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UCHL1 activates TP53. 22 / 28
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"UCH-L1 prolongs the half-life of p53 and p14ARF proteins through its deubiquitinase activity and shortens the half-life of MDM2 proteins through ubiquitination, resulting in the inhibition of NPC cell proliferation (67)."
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"When the expression level of UCH-L1 increases, UCH-L1 further activates and stabilizes p53 signaling by inhibiting the degradation of p53, leading to cell cycle arrest at G0/G1 and apoptosis (Fig. 4) (26)."
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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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"Further UCHL1 mediated p53 stabilization might be contributing to muscle cell apoptosis."
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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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"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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"Further studies are needed to determine specifically how UCH-L1 modulates p53."
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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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"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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"Subcellular localization study showed that UCHL1 increased cytoplasmic abundance of p53."
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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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"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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"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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"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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"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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"In nasopharyngeal carcinoma, UCHL1 could remove ubiquitin from p53 and p14 (ARF) and add ubiquitin molecules to MDM2 in order to stabilize p53 and enhance p53 signaling, suppressing tumor progression [15]."
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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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"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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"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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"UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and 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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"In breast cancer, ectopic expression of UCHL1 is able to induce apoptosis by stabilizing p53."
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