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Data suggest to reduce the risk of multiple primary cancers (MPCs) in germline tumor protein p53 (TP53) mutation carriers, radiotherapy should be avoided whenever possible, surgical treatment prioritised, and non-genotoxic treatments considered.
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findings reveal that the CHD4/NuRD complex regulates neural differentiation of ESCs by down-regulating p53.
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results suggest that p53 may block oncogenic transformation by decreasing BCL6 stability via caspase-1 up-regulation, whereas aberrant BCL6 expression inactivates transactivation of p53 target genes, either by inhibiting p53 acetylation by p300 or repressing TP53 gene transcription. These findings have implications for B cell development and lymphomagenesis.
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zinc deficiency disrupts neural tube closure through decreased p53 ubiquitylation.
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The effect of p53 on the capacity of cardiogenic transdifferentiation is evaluated using p53 wild-type (p53(+/+)), p53 heterozygous mutant (p53(+/-)), and p53 homozygous mutant (p53(-/-)) embryonic fibroblasts (MEFs). The effect of an important reprogramming factor Oct4 on cardiac transdifferentiation was also evaluated in the allelic series of p53 MEFs.
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Mechanical cues control mutant p53 stability through a mevalonate-RhoA axis.
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expression of multiple genes implicated in cell cycle control is altered in TFEB/TFE3 DKOs, revealing a previously unrecognized role of TFEB and TFE3 in the regulation of cell cycle checkpoints in response to stress.
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HBV-upregulated lnc-HUR1 promotes cell proliferation and tumorigenesis by interacting with p53 to block downstream gene transcription.
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p53 negatively regulates ischemia-induced angiogenesis and arteriogenesis. Inhibition of p53 increases ischemia-induced arteriogenesis and limb perfusion and thus represents a potential therapeutic strategy for arterial occlusive disease.
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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.
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Distinct events induced by spinal motor neuron deficiency converge on p53 to trigger selective death of vulnerable spinal muscular atrophy motor neurons.
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To uncover the molecular changes induced by the concurrent targeting of E-cadherin, p53, and Smad4 loss.
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TP53 haploinsufficiency completely rescues emergency granulopoiesis in FANCC(-/-) mice.
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P53 promotes retinoid acid-induced smooth muscle cell differentiation by targeting myocardin.
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A tight control of p53 levels in myoblasts regulates the balance between differentiation and return to quiescence.
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we found an unanticipated effect of p53 loss in mouse and human G1-checkpoint-deficient cells: reduction of DNA damage. We show that abrogation of the G1/S-checkpoint allowed cells to enter S-phase under growth-restricting conditions at the expense of severe replication stress manifesting as decelerated DNA replication, reduced origin firing and accumulation of DNA double-strand breaks
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indicating a general perturbation of the p53, miR-34a and SIRT1 pathway in Huntington's disease
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Using Fanca(-/-) HSCs expressing the separation-of-function mutant p53(515C) transgene, which selectively impairs the p53 function in apoptosis but keeps its cell-cycle checkpoint activities intact, we show that the p53 cell-cycle function is specifically required for the regulation of Fanca(-/-) HSC proliferation.
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lipid profiles are significantly altered by the lack of p53 in muscle tissues.
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p53 becomes activated in BM endothelial cells upon hematopoietic stresses such as irradiation and chemotherapeutic treatments. The conditional activation of p53 induces the expression of p53 target genes specifically in vascular endothelial cells, resulting in the dilation and collapse of vascular endothelial cells, reductions in perivascular mesenchymal stromal cells, and depletion of HSCs.
