IndraLab
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"Despite the fact that both zebrafish UEV genes can functionally replace the yeast MMS2 DNA-damage tolerance function, they exhibited differences in DNA-damage response in zebrafish embryos : ablation of DrMms2, but not DrUev1, enhances both spontaneous and DNA-damage induced expression of p53 effectors p21 and mdm2."
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"Given the opposing responses of MDM2 and p53 elicited by HB-EGF (Fig. 3A), the enhanced association of p53 and MDM2 by HB-EGF stimulation (Fig. 3B) supported the hypothesis that MDM2 may negatively regulate p53 expression, possibly by stimulating direct binding of MDM2 to p53 following HB-EGF treatment [33]–[35]."
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"Mdm2 promotes the ubiquitination and degradation of the tumor suppressor protein p53.The 3E10-3G5 bsAb achieved cellular penetration and inhibited Mdm2 directed p53 ubiquitination to increase p53 levels and promote apoptosis in MC-7 human ovarian cancer cells and several human melanoma cancer cells [XREF_BIBR, XREF_BIBR]."
isi
"This study aimed to detect the protein expression of the DNA damage repair protein P53 and its upstream and downstream regulators, CHK1, GADD45A, and MDM2, in oral squamous cell carcinoma (OSCC), in order to analyse the association between the expression of these proteins and overall survival, and to assess their prognostic implications for OSCC patients."
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"Wt-ING1 stabilized both ubiquitinated and non ubiquitinated forms of p53 (XREF_FIG, lane 2), while MDM2 only increased levels of p53 monoubiquitinated on several residues (XREF_FIG, top panel, lane 5), but failed to promote accumulation of non ubiquitinated p53 (XREF_FIG, third panel, lane 5)."
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"While MDM2 KD also causes an increase in p53 levels in the MCF7-Six1 cells as compared with the Six1 cells with non targeting siRNA, the levels of p53, and its target p21, remain lower in the Six1 overexpressing cells than in the Ctrl cells, with or without MDM2 KD (XREF_FIG, lanes 2 and 4)."
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"Lentivirus-mediated shRNA knockdown of SHCBP1 in prostate cancer cell lines diminished cell growth, migration, and invasion dramatically both in vitro and in vivo, accompanied by an enhanced expression of large tumor suppressor 1 (LATS1) and tumor protein P53 (TP53) and inhibition of MDM2 proto-oncogene (MDM2), which suggested that SHCBP1 may promote proliferation and invasion in vitro via the LATS1-MDM2-TP53 pathway."
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"XREF_BIBR p53 expression was substantially increased after butein treatment (XREF_FIG and XREF_FIG), owing to the fact that p53 can bind to the specific response elements of MDM2 promoter region (the autoregulatory feedback loop), and thus the increase of p53 would enhance MDM2 transcription."
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"Our array CGH experiments showed predominant loss of the Cdkn2a locus in control tumors, whereas loss of Cdkn2a and amplification of Mdm2 were mainly found in Aurora-A tumors, suggesting that modulation of p53 levels by Mdm2 activity that allow some tumor suppressor function may be important for development of highly malignant tumors observed in Aurora-AGS mice."
isi
"On the other hand, the induction of p53 by either gamma-irradiation, by inhibiting the expression of MDM2 by treatment with its pharmacological inhibitor Nutlin-3, or through the conditional expression of its cellular inhibitor p14/p19ARFall result in a decrease in the expression of RUNX2 at the protein level."
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"RPS27a knockdown increased the expression of MDM2 and p53 (Fig. 4E; comparison of lane 3 with lane 2 in lower panels), MDM2 ubiquitinated p53, whereas RPS27a knockdown inhibited this ubiquitination that led to p53 accumulation (Fig. 4E; comparison of lane 3 with lane 2 in upper panel)."
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"This suggestion is supported by our finding that treatment of mice with the USP7 inhibitor P5091 effectively eliminated SnCs and reduced the expression of SASP factors caused by DOX.In conclusion, we reveal that USP7 is a novel senolytic target, and USP7 inhibition can selectively kill some SnCs with p53 downregulation in vitro and clear SnCs induced by chemotherapy in mice in part by destabilizing MDM2 to increase p53 expression."
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"P53 can be degraded by MDM2 via polyubiquitination and proteasome dependent pathways, however, p53 can also enhance MDM2 transcription through p53 specific response elements in the promoter region of MDM2, thus forming an autoregulatory feedback loop to control the balance of p53 and MDM2 in vivo [XREF_BIBR, XREF_BIBR]."
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"TIGAR can be induced by Nutlin-3, an antagonist of Mdm2 that increases p53 levels (185), radiotherapy (183, 186), glutamine (29), chemotherapy (187), UV light (187), TNFα, and radiotherapy mimetics (188) or by the Akt signaling pathway in response to the metabolic stress caused by PFKFB3 knockdown (189)."
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"Consistently, only coexpression of the antigen related TCRalpha p53-chain led to multimer binding (MFI 16.1) while none of the TCRalpha-chains of varying competitive strengths, even TCRalpha MDM2, owing to their species origin or TCR subfamily affiliation were able to reconstitute tetramer binding (MFIs 2.6) : Although the ' strong ' species related Mu TCRalpha MDM2 led to marked Vbeta3 expression of scTCR p53 in accordance with XREF_SUPPLEMENTARY for Jurkat-76, no tetramer staining was observed."
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"By direct binding, JNK also targets p53 for ubiquitin mediated degradation involving Mdm2-p53 degradation pathway Therefore, inactivation of JNK by anti-sense JNK1 or SP600125 would decrease the amount of JNK-p53 and/or Mdm2 and p53 complex to increase the steady state level of p53 by preventing p53 degradation in non stressed cells."