| p53 helps maintain DNA methylation homeostasis and clonal homogeneity, a function that may contribute to its tumor suppressor activity. | None |
| Arf (smArf) protein corrects p53-independent developmental defects of Arf tumor suppressor-deficient mice | None |
| study uncovered a novel candidate gene in the regulation of NK cell maturation, namely Trp53; using mice deficient for Trp53, confirm that this tumor suppressor regulates NK cell functional maturation | None |
| In myoblasts silenced for the expression of muscle regulatory transcription factor MyoD, tumor suppressor p53 binding to the PUMA promoter is diminished in response to culture in differentiation medium. | None |
| These results suggest that p53 mediates DDR and exerts its tumor suppressive role in part by regulating the expression of ACER2, which in turn regulates the bioactive sphingolipid lipids. | None |
| Authors show that loss of the tumor suppressor p53 increased MYC mRNA levels even in the absence of estrogen stimulation. However, in cells with wild-type p53, SRC acted to overcome p53-mediated inhibition of estrogen-stimulated cell cycle entry and progression. | None |
| Studies suggest that depending on the wild-type or mutant tumor suppressor gene TP53 (p53) context, microRNAs contribute substantially to suppress or exacerbate tumor development [Review]. | None |
| Infection of HIV-1 and subsequent HIV-1 reverse transcription are inhibited in HCT116 p53(+/+) cells in comparison to HCT116 p53(-/-) cells. Tumor suppressor gene p53 expression is upregulated in non-cycling cells. The restrictions of HIV by p53 is associated with the suppression of ribonucleotide reductase R2 subunit expression and phosphorylation of SAMHD1 protein. | None |
| In wild-type and p53 knockout HCT116 cells, pyruvate dehydrogenase (PDH) enzyme activity was monitored by acetyl-CoA formation, independent of competing cytosolic metabolism. The results confirmed the positive regulation of mitochondrial PDH activity by p53, a well-known tumor suppressor. | None |
| he early expansion of centrosome amplification correlated with and was dependent on loss of function of the tumor suppressor p53 both through loss of wild-type expression and hotspot mutations. Our work shows that centrosome amplification in human tumorigenesis can occur before transformation, being repressed by p53. | None |
| RXRalpha provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells. | None |
| We found that the impaired homeostatic synaptic downscaling in Fmr1 KO neurons is caused by loss-of-function dephosphorylation of an epilepsy-associated ubiquitin E3 ligase, neural precursor cell expressed developmentally down-regulated gene 4-2, Nedd4-2. Such dephosphorylation of Nedd4-2 is surprisingly caused by abnormally stable tumor suppressor p53 and subsequently destabilized kinase Akt. | None |
| Overexpression of TRAF3 in HPV(+) cell lines with decreased endogenous TRAF3 inhibited NF-kappaB2/RELB expression, nuclear localization, and NF-kappaB reporter activity, while increasing the expression of IFNA1 mRNA and protein and sensitizing cells to its growth inhibition. Overexpression of TRAF3 also enhanced TP53 and RB tumor suppressor proteins and decreased HPV E6 oncoprotein in HPV(+) cells | None |
| The tumor suppressor p53 (p53) mutant lacking the disordered C-terminal (CT) domain abolished Intersegmental transfer (IST), whereas the mutant lacking the structured core domain maintained IST, indicating the importance of the CT domain. | None |
| Fluctuations in the oscillatory pattern of the tumor suppressor p53 upon gamma radiation trigger a sharp switch between p21 and CDK2, leading to escape from arrest. | None |
| PIM2 is upregulated by strongly activated tumor suppressor protein p53. | None |
| Results showed that in invasive ductal carcinomas, p53 was mutated in 13% cases. Considering that Mieap is a downstream target of p53, this novel mechanism for mitochondrial quality control is a new function of the p53 tumor suppressor. | None |
| It has been proposed that a subset of p53 targets regulated by a long, non-coding RNA are required for effective tumor suppression. | None |
| the ability to regulate the stability and activity of the p53 tumour suppressor protein, shared by many of the TRIMs, represents the preeminent link between this protein family and chemoresistance. Indeed, they can modulate p53 degradation, localization and subset of transactivated target genes | None |
| The GTPase KRAS suppresses the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells. | None |