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Data show that codon usage bias (CUB) was moderate in P73 gene and the percentage of mean C was the highest followed by G. The gene variants were GC rich. The GC-ending codons showed increasing usage with increasing GC3 while AT-ending codons showed the opposite with increasing GC3 bias. ATA and AGA were absent among the synonymous codons in P73 gene. Both mutation pressure and natural selection might influence the CUB.
NQO1 is a FAD-dependent, two-domain multifunctional stress protein acting as a Phase II enzyme, activating cancer pro-drugs and stabilizing p53 and p73a oncosuppressors.tructural protein:protein interaction studies reveal that the cancer-associated polymorphism does not abolish the interaction with p73alpha, indicating that oncosuppressor destabilization largely mirrors the low intracellular stability of p.P187S.
Tumor protein p73 (TAp73) and kallmann syndrome 1 sequence protein (KAI1) expression levels are positively correlated in colorectal cancer.
the present study verified a novel molecular link between miRNA663b and TP73, and indicated that miRNA663b may be a critical therapeutic target in breast cancer.
role of p73 in autophagy induction under nitrosative stress in K562 cells
DeltaNp73 was abundantly expressed in the atopic dermatitis epidermis and increased the release of TSLP via NF-kappaB activation.
PRIMA-1 could cause the demethylation of TP73, through DNMT1 depletion, to subsequently enhance the unfolded protein response
Data found that P73 G4C14-to-A4T14 polymorphism was significantly associated with non-small cell lung cancer risk in Chinese population.
In p53-deficient breast cancers, compensatory mechanism of NFkB repression by p63 and p73 during genotoxic stress could lead to complex effects that would influence all aspects of tumor progression.
DeltaNp73 had no leukemic transformation capacity by itself and apparently did not cooperate with the PML/RARA fusion protein to induce a leukemic phenotype in a murine BM transplantation model.
In colorectal tumor cells RPL26 regulates p73 expression via two distinct mechanisms: protein stability and mRNA translation.
Data show that a dominant-negative effect is widely spread within the p53/p63/p73 family as all p53 loss-of-function hotspot mutants and several of the isoforms of p53 and p73 tested exhibit a dominant-negative potential.
p73 supports mitochondria respiration in medulloblastoma via regulation of glutamine metabolism
Study suggests that the cleavage of p73 on specific sites may release its pro-apoptotic function and contribute to cell death in breast cancer.
the transactivation inhibitory (TI) domains within the alpha-isoform-specific C termini of p63 and p73 are essential for binding to p53R175H.
High TP73 expression is associated with glioblastoma cell invasion.
In the present study, we provide evidence that the tumor suppressor gene p73 is highly susceptible to Mn-induced neurotoxicity in the nigrostriatal system.
HECW2 is an ubiquitin ligase that stabilises p73, a crucial mediator of neurodevelopment and neurogenesis. This study implicates pathogenic genetic variants in HECW2 as potential causes of neurodevelopmental disorders in humans.
Imbalance of the apoptosis pathway, with dysregulation of p73 and TRAIL, seems to play a role in the oncogenesis of odontogenic tumors
High TP73 expression is associated with Metastasis of Hepatocellular Carcinoma.
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)
p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming.
P73 role in differentiating stem cells.RASSF1A promotes a YAP-p73 transcriptional programme that enables differentiation.
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.
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.
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.
both p53 and p73 are critical in apoptosis induced by DNA damage and differentiation.
New function of p73, independent of p53, in the neurogenic architecture of the SVZ of rodent brain.
these results therefore highlight an unanticipated role for p53 family proteins in a regulatory network that integrates essential Wnt-Tcf and nodal-Smad inputs.
TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of Motile multiciliated cell progenitors.
p73 drives multiciliogenesis, both through transcriptional activation of a master ciliogenesis transcription factor FoxJ1 and through regulation of multiple genes central to ciliogenesis.
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.
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.
In vivo inhibition of both p63 and p73 in combination accelerates tumor regression and increases survival of p53-deficient mice.
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.
MDM2 mediates p73 ubiquitination
p73 is required for endothelial cell differentiation, migration and the formation of vascular networks regulating VEGF and TGFbeta signaling
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.
Ribosomal proteins L11 and L5 activate TAp73 by overcoming MDM2 inhibition.
the p73 status has to be considered when studying the regulatory role of p53 protein in gliomagenesis [review]
cDNA and amino acid sequences; characterization of expression pattern during fish development as well as in some adult tissues
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.
transformation related protein 73
, tumor protein p73
, tumor protein p73-like
, p53-like transcription factor
, p53-related protein