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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.
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p53R245W tumors are the most aggressive and exhibit metastases to lung and liver.
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L3MBTL2 plays a protective role in kidney injury, in part by inhibiting the DNA damage-p53-apoptosis pathway.
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results indicate that miR-148b-3p contributes to the regulation of hypoxia/reoxygenation-induced cardiomyocyte apoptosis in vitro through targeting SIRT7 and modulating p53-mediated pro-apoptotic signaling
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Data provide evidence that p53 enhances NOXA-induced apoptosis when autophagy is inhibited.
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The p53 is critical in activation of T lymphocytes not only by regulating proliferation and apoptosis but also because of its effective function in the pathogenesis of septic complications.
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133p53 promotes tumour invasion via IL-6 by activation of the JAK-STAT and RhoA-ROCK pathways.
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Results show an association of PD with p53 and active caspase-3 overexpression and beta-adrenergic receptor underexpression in the heart, potentially promoting the cardiac autonomic dysfunction frequently observed in PD.
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These results show that ischemic preconditioning increased neuronal MDM2 protein levels, which prevented ischemia-induced p53 stabilization and neuronal death.
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In studies of lymphomagenesis, mutant TRP53 drives tumorigenesis primarily through dominant-negative effects, which modulates wild-type TRP53 function in a manner advantageous for neoplastic transformation.
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p53 deteriorated cardiac functions and cardiac hypertrophy, apoptosis, and fibrosis by partially inhibition of HIF1alpha and VEGF.
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p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in unilateral urethral obstruction.
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Knockdown of the Sprr2b gene or inhibition of SPRR2B phosphorylation attenuates USP7/MDM2 binding and p53 degradation, leading to fibroblasts cell cycle arrest.
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MDMX is an important regulator of p53 DNA binding, which complements the role of MDM2 in regulating p53 level.
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the disruption of Mdm2/p53 interaction affects the early-embryonic otic progenitor cells and their descendants.
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Deletion of NF1 leads to mutant oligodendrocyte precursor cell (OPC) expansion through increased proliferation and decreased differentiation, the deletion of p53 impairs OPC senescence. Signaling analysis showed that, while PI3K and MEK pathways go through stepwise over-activation, mTOR signaling remains at the basal level in pre-transforming mutant OPCs but is abruptly up-regulated in tumor OPCs.
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findings uncover a new function of p53 in the regulation of Akt signaling and reveal how p53, ASS1, and Akt are interrelated to each other.
