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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 (275) and Tumor Protein p73 Proteins (5) and many more products for this protein.
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p73 (show ARHGAP24 ELISA Kits) drives multiciliogenesis, both through transcriptional activation of a master ciliogenesis transcription factor FoxJ1 (show FOXJ1 ELISA Kits) and through regulation of multiple genes central to ciliogenesis.
The p73 (show ARHGAP24 ELISA Kits) acts as a critical regulator of multiciliogenesis in its capacity as a sequence-specific transcription factor, through genomic binding and regulation of genes.
Data show that the Mdm4 (show MDM4 ELISA Kits)-p73 (show ARHGAP24 ELISA Kits) axis cannot override the dominant role of p53 (show TP53 ELISA Kits) in development and tumorigenesis and that Mdm4 (show MDM4 ELISA Kits) and p73 (show ARHGAP24 ELISA Kits) interaction during development and tumorigenesis suggests new insight into the role of p53 (show TP53 ELISA Kits) family members.
In vivo inhibition of both p63 (show CKAP4 ELISA Kits) and p73 (show ARHGAP24 ELISA Kits) in combination accelerates tumor regression and increases survival of p53 (show TP53 ELISA Kits)-deficient mice.
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]
Expression of XAF1 (show XAF1 ELISA Kits) and TAp73 was also upregulated in casticin-treated T24 cells.
A p73-dependent mechanism for curcumin-induced apoptosis involves the mitochondria-mediated pathway.
caveolin-1 (show CAV1 ELISA Kits) represents one of the genes whose expression is strongly activated by Np73beta in non-small lung cancer cells
Study shows that AR modulates the expression of both p21 (show CDKN1A ELISA Kits) and p73 via directly binding to the promoters, indicating that p73 and p21 (show CDKN1A ELISA Kits) are the downstream target genes of AR in triple-negative breast cancer cells.
P73 is capable of inducing apoptosis by co-ordinately activating several BH3-only (show BBC3 ELISA Kits) proteins, such as Bik (show BIK ELISA Kits).
knockdown of p73 also decreases NAMPT (show NAMPT ELISA Kits) inhibition-induced autophagy and cell death, whereas overexpression of p73 alone enhances these effects.
data suggest that PCBP2 (show PCBP2 ELISA Kits) regulates p73 expression via mRNA stability and p73-dependent biological function in ROS (show ROS1 ELISA Kits) production and cellular senescence.
our study demonstrates a novel mechanism of PLK2 (show PLK2 ELISA Kits) in promoting tumor progression, whereby it directly binds to enriched TAp73, catalyzes Ser48 phosphorylation of TAp73, and inhibits TAp73 transcriptional activity
Meta-analysis results suggest that the p73 G4C14-A4T14 polymorphism is associated with an increased risk of cervical squamous cell carcinoma.
Similar to TAp73, DNp73 is stabilized by hypoxia in a HIF-1a-dependent manner, which otherwise is degraded by Siah1.
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