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MDM2 increases the amount of TP53. 137 / 155
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"Under physiological conditions, p53 expression is inhibited by MDM2 dependent proteasomal degradation while its expression is increased in response to stress including hypoxia."

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"Meanwhile, p53 enhances MDM2 transcription, forming an auto-regulatory feedback loop."

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"In A549 cells, Cr (VI) causes the dissociation of p53 from mdm2, which leads to elevated p53 levels and p53 activation [XREF_BIBR]."

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"P53 could regulate MDM2 transcription through a feedback mechanism, which would give rise to an oscillated expression pattern of both proteins."

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"Under normal condition, p53 is expressed at low amount due to its continuous degradation by its negative regulator MDM2."

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"The levels of MDM2 and p53 are tightly regulated, as they act in a negative feedback loop where p53 induces MDM2 transcription in response to genotoxic stress, whereas MDM2 binds, inhibits and directs p53 for proteasomal degradation by ubiquitinylation [XREF_BIBR - XREF_BIBR]."

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"It may be of particular interest to investigate how MDM2 mediated regulation of HUWE1 protein stability contributes to the steady-state p53 levels as well as p53 activation in response to cellular stress."

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"Down-regulation of MDM2 allowed elevated expression and acetylation of p53, which increased p21 levels, leading to decreased cell cycle progression and promoted p53 mediated apoptosis."

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"miR-25, miR-32, miR-661 and miR-339-5p target MDM2 to up-regulate p53 protein levels and function [XREF_BIBR - XREF_BIBR]."

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"Together, IR induced modifications of p53 and Mdm2 stabilize p53 and enhance transcription of p53 regulated proteins."

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"Specifically, P53 binds the promoter region of MDM2 and activates MDM2 transcription, whereas the expressed MDM2 blocks P53 transcription through the interaction of the P53 transactivation domain and promotes P53 proteasome dependent degradation."

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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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"Previous work has shown that p53 * hDM2 antagonists stabilize p53 levels and induce expression of the p53 target genes hDM2 and p21."

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"In unstressed cells, Mdm2 mediated ubiquitination maintains a low basal level of p53."

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"As expected, HDM2 depletion increased p53 levels when compared to transfection with non targeting siRNA (XREF_FIG), but it also surprisingly upregulated LZAP levels, suggesting that HDM2 may work as E3 ubiquitin ligase degrading LZAP."

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"Thus, the physiological consequence of Hausp loss is destabilization of Mdm2, which leads to increased p53 levels and activity."

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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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"We, therefore, focused our study on RPS27L silencing and found that p53 reduction, upon RPS27L silencing, was MDM2 dependent, since simultaneous silencing RPS27L and MDM2 restored the p53 level (XREF_FIG, lanes 3 vs. 4)."

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"Control of p53 expression by MDM2 is lost in tumors harboring mutant p53, resulting in p53 hyperstabilization and accumulation [XREF_BIBR]."

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"In this study, we found that miR-1827 binds to the 3 '-UTR of MDM2 to down-regulate MDM2 levels, which in turn enhances p53 levels and function."

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"However, p53 enhances Mdm2 transcription, thus forming an autoregulatory feedback loop."

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"The knock-out of HAX-1 leads to the inactivity of the Ak1t and MDM2 axis, which leads to increased levels of p53, and finally generates cell cycle arrest and results in the apoptosis of glioblastoma cells."

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"Under normal circumstances, both p53 and MYCN induce MDM2, but upon MDM2 inhibition MYCN mediated transcription of p53 allows p53 to accumulate and increases activity."

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"A452 increases wild-type p53 levels by destabilizing MDM2 and decreases mutant p53 by inducing MDM2 [39]."
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"Most recently, He et al. demonstrated that ubiquitin specific peptidase 7 (USP7) inhibitor P5091 accelerated MDM2 ubiquitination and degradation, which in turn increased intracellular p53 expression and cleared senescent cells by activating cellular apoptosis."

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"Depletion of HDM2 and TRIM24 by siRNA in untreated hESCs increased p53 protein levels (XREF_SUPPLEMENTARY), increased p21 RNA and protein, and decreased OCT4 and NANOG expression (XREF_SUPPLEMENTARY)."

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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]."

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"Since MDM2 is a direct transcriptional target of p53, the down-regulation of MDM2 by miR-339-5p could increase p53 protein levels and in turn transcriptionally induce MDM2, which could partially compromise the inhibitory effect of miR-339-5p on MDM2."

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"Transfection of ARF plasmid decreased MDM2 protein expression, which in turn increased p53 protein expression."

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"In contrast, combined inhibition of CDK4/6 and MDM2 led to diminished RNA Polymerase II recruitment and thus decreased transcription of p53 target genes."

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"In addition, MDM2 mediated p53 degradation causes low p53 levels in the absence of p19Arf, thus preventing cell cycle arrest and apoptosis [XREF_BIBR]."

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"Conversely, p53 can activate Mdm2 transcription, thereby forming a negative feedback loop that curtails p53 activity."

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"On the other hand, ERBB4 ICD promotes ubiquitination and degradation of Hdm2 oncogene, which in turn increases the levels of tumor suppressor p53."

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"Of note, except for dysfunction of NF-κB, dysregulation of Mdm2 results in increasing p53 expression in response to NM treatment combined with 5 Gy ionizing radiation (IR) in pancreatic cancer (23)."

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"In addition, PRMT5 is required for p53 expression and induction of p53 targets MDM2 and p21 upon DNA damage."

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"Knockdown of mdm2 by siRNA did not increase the p53 protein level in the absence or presence of etoposide."

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"In this study, we found that miR-339-5p directly represses MDM2 expression, which in turn increases p53 protein levels and enhances p53 functions in regulating apoptosis and senescence in colorectal cancer cells in response to stress."

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"MK0457, a small molecule pan-Aurora kinase inhibitor, activates p53; Nutlin-3, a small molecule antagonist of MDM2, increases p53 levels to induce p53 mediated apoptosis."

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"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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"P53 activates Mdm-2 transcription through binding to its promoter and up-regulates Mdm-2 expression."

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"Furthermore, the down-regulation of MDM2 by miR-1827 in turn increased p53 protein levels in these cells."

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"However, this situation is further complicated by the observation that p53 can stimulate MDM2 transcription."

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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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"If Mdm2-P is attracted to the complex, then it can be protected against degradation and, in fact, Mdm2-P can stimulate p53 expression."

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"We speculated that MDM2 may promote podocyte MC by mediating p53 expression."

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"The NF2 shRNA knockdown resulted in the upregulation of p53 and MDM2 in MESO257 (XREF_FIG), indicating that NF2 regulates the interaction of MDM2 and p53, and that upregulation of p53 expression by MDM2 inhibition (nutlin-3) is NF2 dependent."

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"We thus hypothesize that a significantly high level of p53 was caused by a combination of absents of MDM2 in parallel with p53 microvesicles storage."

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"Conversely, knockdown of DJ-1 upregulated p53 expression by disrupting the interaction between p53 and MDM2 and inhibiting CRC cell proliferation, revealing the pro-oncogenic mechanism of DJ-1 in CRC."

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"Mouse double minute (MDM) 2 single nucleotide polymorphism (SNP) 309G allele in the second promoter of MDM2 enhances vitreous induced expression of Mdm2 and degradation of the tumor suppressor protein p53."

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"We showed that although downregulation of MDM2 by triptolide remarkably increased p53 expression in these wt-p53 and MDM2-ovrexpressing ALL cells, there was no corresponding increase in expression of p21 or cell-cycle arrest in G1 phase."

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"P53 expression was remarkably enhanced by MDM2 depletion, and the additional knockdown of UNC119A did not affect p53 expression."

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"The up-regulation of PTEN inhibited Akt and MDM2, which enhanced the level of p53, thereby inducing G (2)/M arrest and apoptosis."

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"The up-regulation of PTEN inhibits AKT and MDM2, which enhance the level of p53, thereby inducing G2/M arrest and apoptosis [XREF_BIBR]."

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"We found that, while CagA inhibits p53, downregulation of HDM2 increases p53 protein levels in CagA transfected cells, further supporting data that degradation of p53 by H. pylori is mediated by CagA and HDM2."

"Hdm2 binds p53 to inhibit its transactivation function and shuttles p53 from the nucleus to the cytoplasm to facilitate its degradation Hdm2 is also an E3 ubiquitin ligase that targets p53 for the ubiquitin-dependent 26S proteosome in the cytoplasm"

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"Several reports have focused on the p53 mediated apoptotic pathway, upon endogenous p53 protein re-expression by the small-molecule MDM2 antagonists (Nutlins) and target genes which may be involved in p53 dependent apoptosis in MM cells which have been identified."

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"Additionally, antisense HDM2 oligonucleotides increase both p53 levels and activity by reducing HDM2 protein levels."

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"Overexpression of MDM2, most notably in haematological cancers, leads to low levels of P53 [95]."

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"Upon cellular stress, p53 becomes resistant to MDM2 and, in a feedback loop, up-regulates mdm2 transcription."

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"Mdm2 inhibits p53 mediated cell cycle arrest and apoptotic functions, 55,62 and overexpression of Mdm2 can reduce the amount of endogenous p53."

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"22 Cleavage of Mdm2 increases protein levels of p53, elevates expression of p53 target genes including the cyclin dependent kinase inhibitor p21, and induces cell cycle arrest."

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"The Mdm2 protein represses transcriptional activation of p53 while simultaneously lowering p53 protein levels through ubiquitin mediated degradation."

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"Similarly, Mdm2 siRNA also caused a dose dependent increase in p53 protein levels (XREF_FIG, bottom, lanes 1, 7, and 8) and reduced p53 degradation under anoikis conditions (XREF_FIG, bottom, lanes 5, 9, and 10)."

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"Inhibition of Mdm2 cleavage would be predicted to result in increased total Mdm2 and decreased p53 levels."

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"It is notable that basal levels of p53 and p21 were increased by MDM2 siRNA, but this is to be expected since MDM2 knock-down is known to stabilize and activate p53."

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"Induction of p53 by NO is preceded by a rapid decrease in Mdm2 protein, which may enable to elevate p53 levels early after exposure to NO [XREF_BIBR]."

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"P53, on the other hand, induces MDM2 transcription in response to genotoxic stress [XREF_BIBR - XREF_BIBR]."

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"Importantly, loss of KLF6 leads to reduced trans-repression of mdm2, thereby promoting loss of p53 through its accelerated degradation."

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"Indeed, LY294002, proteasome inhibitors, inhibitors of P53-MDM2 interaction (nutlin3a and RITA), and depletion of MDM2 rescued P53 levels in infected cells."

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"However, p53 also activates MDM2 transcription leading to a feedback loop mechanism [XREF_BIBR, XREF_BIBR]."

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"We have therefore examined whether an MDM2 antagonist; Nutlin-3, might rescue and increase p53 expression and induce growth inhibition or apoptosis in RCC cells that retain wild-type p53."

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"Arf and Mdm2 mediated stabilization of p53 protein and the resulting mRNA expression of the p53 target genes were reported."

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"Downregulation of MDM2 increases TP53 protein expression and activates stress response during 5-FU treatment [XREF_BIBR]."

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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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"Furthermore, at least in the experimental system used in those particular studies, the NES of Hdm2 was found dispensable for the relocal ization of p53 to the cytoplasm, since Hdm2 lacking NES (Hdm2 a[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In fact, p53 activates MDM2 transcription, inducing negative feedback on its expression."

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"Interestingly, HIF-1α has been described to upregulate p53 levels by inhibiting Mdm2-mediated degradation, while HIF-2α has been reported to have a contrary effect over p53, by inhibiting this protein in an Mdm2-independent manner [81,84,85]."

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"Several reports have focused on the p53 mediated apoptotic pathway, upon endogenous p53 protein re-expression by the small-molecule MDM2 antagonists (Nutlins) and target genes wich may be involved in p53 dependent apoptosis in MM cells have been identified."

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"The sequestration of Mdm2 allows p53 levels to accumulate, leading to induction of target genes such as p21 Cip1 and 14-3-3sigma that promote cell cycle arrest [11]."

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"Nuclear p53 induces mdm2 transcription, while MDM2 antagonizes p53 by promoting multistep ubiquitination and proteasome dependent degradation of p53 XREF_BIBR, XREF_BIBR."

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"Conversely, p53 enhances mdm2 transcription through its interaction with a pair of tandem p53 binding sites in P2 intronic promoter of the mdm2 gene."

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"Our results implied that oridonin might increase p53 expression by down-regulating Mdm2 expression.The important transcription factor p53 has multiple functions (34)."

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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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"In addition, MDM2 binds to p53 transactivation domain and suppress p53-mediated transcription (Schuler and Green, 2005; Schuler et al., 2003)."

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"The ubiquitin ligase Mdm2, which targets p53 for degradation [43], promotes HSC survival by blunting the expression of p53 in response to stress [44]."

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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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"Nutlin-3 treatment reactivated p53 function in E/R expressing leukemic cell lines, leading to cell cycle arrest, enhanced apoptosis, and increased expression of p53 direct targets p21, MDM2, and the pro apoptotic BAX and PUMA."

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"Consequently, 17AAG increased the gene expression of the classic p53 targets MDM2, p21 and p53 upregulated modulator of apoptosis (PUMA), validating p53 activation (XREF_FIG)."

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"In turn, p53 activates Mdm2 transcription and down-regulates the level of nuclear Mdm2 by inhibiting Mdm2 nuclear translocation through inactivation of the kinase Akt."

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"MDM2 interacts with lincRNA-p21 to promote the expression level of p53 [69]."

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"P53 upregulates MDM2 transcription to establish a negative feedback loop."

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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."

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"This is also not so surprising because CK2 is known to be a robust enzyme with a broad pH and salt range.From these and other data we hypothesize : (1) cisplatin-treatment leads to severe changes of t[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"We confirmed this effect in prostate cancer cells, in which Mdm2 siRNA induced higher levels of nuclear p53 while transient over-expression of Mdm2 reduced these levels (XREF_SUPPLEMENTARY), mimicking the 280 effect on p53."

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"Through binding to the multiple sites at the 3 '-UTR of MDM2 mRNA, miR-1827 negatively regulates MDM2, which in turn induces p53 protein levels and activates p53 transcriptional activity and p53 mediated stress responses, including apoptosis and senescence."

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"In addition, upregulation of PTEN represses the expression levels of AKT kinase and the activity of murine double minute 2 (MDM2), which enhances the levels of TP53, leading to the induction of cell-cycle arrest or apoptosis."

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"Interestingly, p53 enhances MDM2 transcription through p53 specific response elements in the promoter region of MDM2, thus forming an auto-regulatory feedback loop, which is critical to control the balance of p53 and MDM2 (XREF_FIG)."

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"It is concluded that MDM2 specific antisense oligonucletides can inhibit the expression of MDM2, induce the expression of P53 and increase the apoptosis of leukemia cells after chemotherapy."

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"The expression of JWA, Cullin1, p53, XRCC1, CHIP, FAK, MMP-2, MDM2 and p21 was determined on the microarray by immunohistochemistry."

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"Nutlin-3 upregulated expression of several p53 dependent targets including Bax, PUMA, Noxa, p21, and Hdm2 itself (XREF_TABLE), and induced caspase-3 cleavage (XREF_SUPPLEMENTARY)."

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"In conclusion, our findings demonstrate that MDM2 overexpression or amplification in wild-type p53 expressing ovarian tumor cells likely contribute to tumor cell immune evasion."

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"This interaction is tightly regulated, and destabilization of Mdm2 by the ubiquitin-specific-processing protease 7 (USP7) induces p53 expression and cell cycle arrest 36."

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"The MDM2 antagonist (R)-5a activates p53 and induces the expression of p53 dependent genes."

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"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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"P53 induces mdm2 gene transcription at the conclusion of DNA repair to re-engage cellular homeostasis thus creating an autoregulatory feedback loop between Mdm2 and p53."

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"The p53 protein level can be negatively modulated by MDM2 and MDMX, two E3 ubiquitin protein ligases that mediate p53 protein degradation through ubiquitin dependent proteolysis [XREF_BIBR]."

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"Efficient depletion of Mdm2 by siRNA restored the p53 levels, indicating that CDC7 suppression of p53 levels might directly or indirectly involve Mdm2."

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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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"In its turn, p53 stimulates Mdm2 transcription."

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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 promotes Mdm2 transcription creating an important negative feedback loop, where the balance between p53 and Mdm2 is essential for cell survival, as demonstrated by the embryonic lethality of mdm2 knockout in mice, although rescued by concomitant p53 knockout XREF_BIBR."

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"Mdm2, being a transcriptional target of p53, is upregulated and regulates p53 levels through its E3 ligase activity in ubiquitinating p53, mediating its degradation."

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"For example, efforts have been invested on targeting HDM2, the E3 ligase for tumor suppressor p53, aiming to elevate the protein level of p53."

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"XREF_BIBR, XREF_BIBR - XREF_BIBR MDM2 and p53 form a negative feedback loop, in which p53 activates MDM2 transcription and MDM2, in turn, inactivates p53 by targeting it for ubiquitination and proteasomal degradation."

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"The upregulation of PTEN represses AKT and MDM2 activity, which enhances the level of p53, thereby inducing G2/M arrest and apoptosis."

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"XREF_BIBR, XREF_BIBR Interestingly, p53 enhances MDM2 transcription by binding to p53 responsive elements located in the promoter region of MDM2, thereby forming an autoregulatory negative feedback loop, which is crucial to maintain the balance of p53 and MDM2."

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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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"In the present study, miR-188-3p overexpression reduced the expression of MDM2, which consequently upregulated the protein expression of p53."

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"24 In addition, it was shown that both Mdm2 and ARF-BP1 knockdown can further increase p53 levels in the presence of ARF suggesting both Mdm2 and ARF-BP1 are the links between ARF and p53."

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"In MYCN amplified neuroblastoma, MDM2 served to induce MYCN expression, which was found to increase p53 expression as well."

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"The smaller mdm2 protein, p76, increases the level of p53 by blocking the function of p90."

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"MEG3 down-regulates MDM2, which in turn up-regulates p53 expression level 100."

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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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"In all the cell lines MDM2 transcripts were modestly reduced by PD0332991, possibly reflecting the CDK4 inhibitor induced loss of p53 (XREF_SUPPLEMENTARY)."

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"In the physiological condition, Mdm2 mediated ubiquitination and proteasomal degradation control p53 levels."

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"Here we illustrate how the p53-Mdm2 protein protein and p53 mRNA-Mdm2 interactions affect Mdm2 mediated control of p53 expression using the Phe19Ala p53 mutant."

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"Interactions of the p53 and Mdm2 are a kind of autoregulatory feedback loop, because the activated p53 significantly increases the mdm2 gene transcription."

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"Hypoxia induced expression of the p53 target MDM2 that downregulates HIPK2, thus MDM2 inhibition by siRNA restored the HIPK2 and p53Ser46 response to drug."

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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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"P53 enhances MDM2 transcription through p53 specific response elements in the promoter region of MDM2, thus forming an autoregulatory feedback loop critical to controlling the balance of p53 and MDM2 [XREF_BIBR]."

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"The expression of MDM2, MDM4, p53 and p21 in myeloid neoplasms and the effect of MDM2/MDM4 dual inhibitor."

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"The MDM2 protein acts as a p53 antagonist and is linked to p53 in a feedback-loop where p53 enhances MDM2 transcription in response to genotoxic stress, whereas MDM2 binds to p53 and directs it for proteosomal degradation through ubiquitinylation [XREF_BIBR, XREF_BIBR]."

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"It is totally unexpected that the protein level of both MDM2 and p53 is downregulated by MDM2 degraders based on ligands derived from Ugi reactions."

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"We also observed that tripartite motif containing 25 formed a complex with p53 and mouse double minute 2 homolog (MDM2) in both human lung cancer tissues and in lung cancer cells and tripartite motif containing 25 silencing increased the expression of p53."

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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."

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"TDP521252, TDP665759, PXN727, PXN822 and isoindolinones are other compounds currently under pre-clinical development that target MDM2 to increase p53 levels by inhibiting the MDM2-p53 interaction [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."

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"PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21."