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TAp73 deficiency results in a pronounced reduction in tumorigenic potential, which can be rescued by forced PFKL expression.
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p73 exerts its functions in neuronal biology at least partially through the regulation of metabolic pathways.
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Data (including data from studies in knockout/transgenic mice) suggest Ppp2ca supports cortical neuronal growth and cognitive function via regulating p73/Gls2 signal transduction in neurons of hippocampus. Ppp2ca gene knock-out results in embryonic cortical atrophy with learning/memory deficits. (Ppp2ca = protein phosphatase 2a catalytic subunit alpha isoform; p73 = transformation related protein 73; Gls2 = glutaminase-2)
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p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming.
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P73 role in differentiating stem cells.RASSF1A promotes a YAP-p73 transcriptional programme that enables differentiation.
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Absence of TAp73 leads to activation of TGF-beta signaling through a Sma and Mad-related proteins-independent pathway, favoring oncogenic transforming growth factor-beta effects and epithelial-to-mesenchymal transition.
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Findings reinforce the role of TAp73 as tumor suppressor gene and indicate that the regulation of cellular metabolism by TAp73 contributes to its tumor suppressor function.
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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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both p53 and p73 are critical in apoptosis induced by DNA damage and differentiation.
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New function of p73, independent of p53, in the neurogenic architecture of the SVZ of rodent brain.
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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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TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of Motile multiciliated cell progenitors.
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p73 drives multiciliogenesis, both through transcriptional activation of a master ciliogenesis transcription factor FoxJ1 and through regulation of multiple genes central to ciliogenesis.
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The p73 acts as a critical regulator of multiciliogenesis in its capacity as a sequence-specific transcription factor, through genomic binding and regulation of genes.
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Data show that the Mdm4-p73 axis cannot override the dominant role of p53 in development and tumorigenesis and that Mdm4 and p73 interaction during development and tumorigenesis suggests new insight into the role of p53 family members.
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In vivo inhibition of both p63 and p73 in combination accelerates tumor regression and increases survival of p53-deficient mice.
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Results indicate that p73 regulates basal and starvation-induced fuel metabolism in the liver, a finding that is likely to be highly relevant for metabolism-associated disorders, such as diabetes and cancer.
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MDM2 mediates p73 ubiquitination
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p73 is required for endothelial cell differentiation, migration and the formation of vascular networks regulating VEGF and TGFbeta signaling
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Although mouse TIGAR expression is clearly induced in the intestines of mice following DNA-damaging stress of ionizing radiation, that was not dependent on p53 or TAp73.
