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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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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.
Lack of embryonic brain development was found in p63 (show CKAP4 Antibodies)-knockout mice.
Data show that the transcription factor protein (show SSRP1 Antibodies) 63 (p63 (show CKAP4 Antibodies)) is a master regulator of the transition from the reserve to the active stem cell pool in the epithelium.
Pvrl1 (show PVRL1 Antibodies) is a bona fide target gene of the transcription factor p63 (show CKAP4 Antibodies), whereas Pvrl4 (show PVRL4 Antibodies) regulation is linked to epidermal differentiation and is under Irf6 (show IRF6 Antibodies)
Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells.
Some miRs control p63 (show CKAP4 Antibodies) expression, and p63 (show CKAP4 Antibodies) regulates the miR (show MLXIP Antibodies) expression profile in the epidermis. p63 (show CKAP4 Antibodies) controls miR (show MLXIP Antibodies) expression at different levels.
p63 (show CKAP4 Antibodies) antagonizes p53 (show TP53 Antibodies) to promote cellular survival, whereas p73 (show ARHGAP24 Antibodies) regulates self-renewal and p53 (show TP53 Antibodies)-mediated apoptosis versus senescence.
These studies highlight the importance of p63 (show CKAP4 Antibodies) in maintaining the self-renewal potential of mammary cancer stem cells via a positive modulation of the Hh signaling pathway.
A study evaluating the expression of P63 (show CKAP4 Antibodies) among basal cell subpopulations of the murine prostate epithelium is reported.
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