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TRP63 encodes tumor protein p63, a member of the p53 family of transcription factors involved in cellular responses to stress and development.
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Data suggest that this the selective targeting of genes by tumor suppressor protein (show TP53 Antibodies) p63 (p63 (show CKAP4 Antibodies)) correlates with subtle, but measurable transcriptional differences in mouse and human keratinocytes that converges on major metabolic processes, which often exhibit species-specific trends.
p63alpha protein up-regulates heat shock protein 70 (show HSP70 Antibodies) expression via E2F1 transcription factor (show E2F1 Antibodies) 1 (show HNF1A Antibodies), promoting Wasf3/Wave3 (show WASF3 Antibodies)/MMP9 (show MMP9 Antibodies) signaling and bladder cancer invasion
these results therefore highlight an unanticipated role for p53 (show TP53 Antibodies) family proteins in a regulatory network that integrates essential Wnt (show WNT2 Antibodies)-Tcf (show HNF4A Antibodies) and nodal-Smad (show SMAD1 Antibodies) inputs.
the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 (show TP53 Antibodies) 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.
TGFb3 (show TGFB3 Antibodies)-induced down-regulation of p63 (show CKAP4 Antibodies) 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.
miR (show MLXIP Antibodies)-20a-5p contributes to hepatic glycogen (show GYS1 Antibodies) synthesis through targeting p63 (show CKAP4 Antibodies) to regulate p53 (show TP53 Antibodies) and PTEN (show PTEN Antibodies) expression.
Taken together, these data show that p63 (show CKAP4 Antibodies) regulates the self-renewal and differentiation of oesophageal stem cells in humans and mice.
IL-6 (show IL6 Antibodies)/P-STAT3 (show STAT3 Antibodies) activation influences p63 (show CKAP4 Antibodies) isoform expression in healing wounds, which may contribute to wound-induced hair follicle neogenesis.
In vivo inhibition of both p63 (show CKAP4 Antibodies) and p73 (show ARHGAP24 Antibodies) in combination accelerates tumor regression and increases survival of p53 (show TP53 Antibodies)-deficient mice.
p63 (show CKAP4 Antibodies) expression could be detected as early as E8.5 in mouse embryos preceding epidermal commitment.
This gene encodes tumor protein p63, a member of the p53 family of transcription factors involved in cellular responses to stress and development. The family members include tumor proteins p53, p63, and p73, which have high sequence similarity to one another. This similarity allows p63 and p73 to transactivate p53-responsive genes causing cell cycle arrest and apoptosis. The family members can interact with each other in many ways, including direct and indirect protein interactions. This results in mutual regulation of target gene promoters. Tumor protein p63 -/- mice have several developmental defects which include the lack of limbs and other tissues, such as teeth and mammary glands, which develop as a result of interactions between mesenchyme and epithelium. Both alternative splicing and the use of alternative promoters result in multiple transcript variants encoding different protein isoforms.
transformation-related protein 63
, tumor protein 63