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TP73 encodes a member of the p53 family of transcription factors involved in cellular responses to stress and development. Additionally we are shipping Tumor Protein p73 Antibodies (205) and Tumor Protein p73 Proteins (5) and many more products for this protein.
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Results indicate that p73 (show ARHGAP24 ELISA Kits) 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.
MDM2 (show MDM2 ELISA Kits) mediates p73 (show ARHGAP24 ELISA Kits) ubiquitination
p73 (show ARHGAP24 ELISA Kits) is required for endothelial cell differentiation, migration and the formation of vascular networks regulating VEGF (show VEGFA ELISA Kits) and TGFbeta (show TGFB1 ELISA Kits) signaling
Although mouse TIGAR (show C12orf5 ELISA Kits) expression is clearly induced in the intestines of mice following DNA-damaging stress of ionizing radiation, that was not dependent on p53 (show TP53 ELISA Kits) or TAp73.
Ribosomal proteins L11 (show RPL11 ELISA Kits) and L5 activate TAp73 by overcoming MDM2 (show MDM2 ELISA Kits) inhibition.
the p73 (show ARHGAP24 ELISA Kits) status has to be considered when studying the regulatory role of p53 (show TP53 ELISA Kits) protein in gliomagenesis [review]
Suggest that TAp73 promotes anabolism to counteract cellular senescence rather than to support proliferation.
p63 (show CKAP4 ELISA Kits) antagonizes p53 (show TP53 ELISA Kits) to promote cellular survival, whereas p73 (show ARHGAP24 ELISA Kits) regulates self-renewal and p53 (show TP53 ELISA Kits)-mediated apoptosis versus senescence.
Inhibition of TAp73 results in an accumulation of HIF-1alpha (show HIF1A ELISA Kits) and up-regulation of HIF-1alpha (show HIF1A ELISA Kits) target genes.
The transcription factor TAp73 opposes HIF-1 (show HIF1A ELISA Kits) activity through a nontranscriptional mechanism, thus affecting tumor angiogenesis.
Similar to TAp73, DNp73 is stabilized by hypoxia in a HIF-1a-dependent manner, which otherwise is degraded by Siah1.
Data indicate tumor suppressors TP73, RASSF1A (show RASSF1 ELISA Kits), MLH1 (show MLH1 ELISA Kits) and BRCA1 as possible biomarkers to distinguish Pleomorphic invasive lobular cancer (pleomorphic ILC (show CCL27 ELISA Kits)} from classic ILC (show CCL27 ELISA Kits) and infiltrative ductal cancer (IDC (show LMNA ELISA Kits)).
This review establishes the possibility that p73 is indeed capable of both promoting and inhibiting angiogenesis, depending on the cellular context. [review]
Mechanistic investigations indicated that DNp73 acted by attenuating expression of miR (show MLXIP ELISA Kits)-885-5p, a direct regulator of the IGF1 (show IGF1 ELISA Kits) receptor (IGF1R (show IGF1R ELISA Kits)) responsible for stemness marker expression.
Tyrosine-99 phosphorylation determines the regulation of tumor suppressor p73.
MDM2 (show MDM2 ELISA Kits) mediates p73 ubiquitination
Mdm2 (show MDM2 ELISA Kits) overexpression and p73 loss cooperate in genomic instability and tumor development, indicating that the oncogenic function of Mdm2 (show MDM2 ELISA Kits) is a combined effect of inhibiting p53 (show TP53 ELISA Kits) and p73 functions
Authors demonstrate that IGFBP3 (show IGFBP3 ELISA Kits) is a direct TAp73alpha (the p73 isoform that contains the trans-activation domain) target gene and activates the expression of IGFBP3 (show IGFBP3 ELISA Kits) in actively proliferating cells.
TAp73 suppresses BNIP3 (show BNIP3 ELISA Kits) expression, directly binding its gene promoter.
Positive association between RPRM and p73 expression suggest that other members of the p53 gene family may participate in the regulation of RPRM expression.
This gene encodes a member of the p53 family of transcription factors involved in cellular responses to stress and development. It maps to a region on chromosome 1p36 that is frequently deleted in neuroblastoma and other tumors, and thought to contain multiple tumor suppressor genes. The demonstration that this gene is monoallelically expressed (likely from the maternal allele), supports the notion that it is a candidate gene for neuroblastoma. Many transcript variants resulting from alternative splicing and/or use of alternate promoters have been found for this gene, but the biological validity and the full-length nature of some variants have not been determined.
tumor protein p73
, tumor protein p73-like
, p53-like transcription factor
, p53-related protein
, transformation related protein 73