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Altogether, these results demonstrate that CCDC3 modulates liver lipid metabolism by inhibiting liver de novo lipogenesis as a downstream player of the p63 network.
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TAp63 in POMC neurons is one key molecular driver for the sexual dimorphism in energy homeostasis
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Down-regulation of p63 attenuates liver steatosis in p53 knockout mice and in diet-induced obese mice, whereas the activation of p63 induces lipid accumulation.
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Low TP63 expression is associated with neoplasms.
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The results indicate that ZIP10 plays important roles in epidermal development via, at least in part, the ZIP10-zinc-p63 signaling axis, thereby highlighting the physiological significance of zinc regulation in the maintenance of skin epidermis.
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Notch signaling maintains p63 levels and horizontal basal cell (HBC) dormancy, in contrast to its suppression of p63 expression in other tissues. Additionally, Notch1, but not Notch2, is required to maintain HBC dormancy after selective neuronal degeneration.
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present study, we provided a role for IDH2 in protection against UVB-induced skin damage and a new connection between IDH2 and DeltaNp63.
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Overexpression of DeltaNp63 in transgenic mouse epidermis results in a severe skin phenotype that shares many of the key clinical, histological and molecular features associated with Atopic dermatitis and IL-31 and IL-33 are key players in the signaling pathways.
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cells expressing both p63 and p73 exist in mouse epidermis and hair follicle and that hetero-tetramer complexes can be detected by immunoprecipitation in differentiating keratinocytes.
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Data suggest that this the selective targeting of genes by tumor suppressor protein p63 (p63) correlates with subtle, but measurable transcriptional differences in mouse and human keratinocytes that converges on major metabolic processes, which often exhibit species-specific trends.
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Using a combination of biophysical methods as well as cell and ovary culture experiments the authors explain how TAp63alpha is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.
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p63alpha protein up-regulates heat shock protein 70 expression via E2F1 transcription factor 1, promoting Wasf3/Wave3/MMP9 signaling and bladder cancer invasion
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TAp63 suppresses mammary tumorigenesis through regulation of the Hippo pathway
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controls limb development through transcriptional regulation of different target molecules with different roles in the apical ectodermal ridge
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these results therefore highlight an unanticipated role for p53 family proteins in a regulatory network that integrates essential Wnt-Tcf and nodal-Smad inputs.
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the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 and TAp63 are dispensable for arrest caused by sex body defects. These data affirm that recombination-dependent and sex body-deficient arrests occur via genetically separable mechanisms.
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TGFb3-induced down-regulation of p63 in the medial edge epithelia of the palatal shelves is a pre-requisite for palatal fusion by facilitating periderm migration from, and reducing the proliferative potential of, the midline epithelial seam thereby preventing cleft palate.
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increased DeltaNp63alpha protein levels facilitate oncogenic transformation in the epidermis as well as in the bile duct.
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miR-20a-5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.
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Taken together, these data show that p63 regulates the self-renewal and differentiation of oesophageal stem cells in humans and mice.
