Browse our anti-Tumor Protein p73 (TP73) Antibodies

Human Tumor Protein P73 (TP73) interaction partners

1. TP73 G4C14-A4T14 polymorphism causes an upgrade cancer risk, especially in Caucasian population. G4C14-A4T14 polymorphism might be a potential biomarker for judging the tumorigenesis of cervical cancer and colorectal cancer.

2. The transcriptional activity of p73 is regulated by acetylation of the lysine residues located in the C-terminal region.SIRT2-mediated inactivation of p73 is critical for the proliferation and tumorigenicity of glioblastoma cells.

3. TopBP1 transcriptional activity is regulated by AKT, and treatment with AKT inhibitors suppresses expression of E2F1 and p73 without interfering with ATR signaling.

4. TAp73 deficiency results in a pronounced reduction in tumorigenic potential, which can be rescued by forced PFKL expression.

5. cytoplasmic apoptotic function of p73 is mediated through a noncanonical mode of Bcl-XL recognition

6. TP73-AS1 overlaps with TP73 in a tail-to-tail configuration with an overlap length of 216 nt.

7. high levels of Np73 stabilize HIF-1alpha protein, allowing for it to accumulate and further potentiating its transcriptional activity and supporting tumor progression.

8. Knockdown of tumor protein p73 (TAp73) in tumor suppressor p53 (p53)-/- cells using CRISPR/Cas9 significantly prolonged the duration of resistance.

9. miR647 functions as a tumor promoter in Gastric Cancer by repressing TP73.

10. 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.

11. 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.

12. Tumor protein p73 (TAp73) and kallmann syndrome 1 sequence protein (KAI1) expression levels are positively correlated in colorectal cancer.

13. 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.

14. role of p73 in autophagy induction under nitrosative stress in K562 cells

15. DeltaNp73 was abundantly expressed in the atopic dermatitis epidermis and increased the release of TSLP via NF-kappaB activation.

16. PRIMA-1 could cause the demethylation of TP73, through DNMT1 depletion, to subsequently enhance the unfolded protein response

17. Data found that P73 G4C14-to-A4T14 polymorphism was significantly associated with non-small cell lung cancer risk in Chinese population.

18. 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.

19. 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.

20. In colorectal tumor cells RPL26 regulates p73 expression via two distinct mechanisms: protein stability and mRNA translation.

Mouse (Murine) Tumor Protein P73 (TP73) interaction partners

1. Results suggest that the loss of tumor suppressor protein p73 (p73) during the embryonic period is critical for hydrocephalus development.

2. Current understanding indicates that various products from TP73 genes, originated by alternative gene promoter usage and differential splicing, might differentially participate in complex networks that regulate cell growth, differentiation and death. TAp73alpha is found as the exclusive, or major, expressed isoform in most of the biological system analyzed. [review]

3. TAp73 deficiency results in a pronounced reduction in tumorigenic potential, which can be rescued by forced PFKL expression.

4. p73 exerts its functions in neuronal biology at least partially through the regulation of metabolic pathways.

5. 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)

6. p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming.

7. P73 role in differentiating stem cells.RASSF1A promotes a YAP-p73 transcriptional programme that enables differentiation.

8. 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.

9. 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.

10. 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.

11. both p53 and p73 are critical in apoptosis induced by DNA damage and differentiation.

12. New function of p73, independent of p53, in the neurogenic architecture of the SVZ of rodent brain.

13. these results therefore highlight an unanticipated role for p53 family proteins in a regulatory network that integrates essential Wnt-Tcf and nodal-Smad inputs.

14. TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of Motile multiciliated cell progenitors.

15. p73 drives multiciliogenesis, both through transcriptional activation of a master ciliogenesis transcription factor FoxJ1 and through regulation of multiple genes central to ciliogenesis.

16. 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.

17. 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.

18. In vivo inhibition of both p63 and p73 in combination accelerates tumor regression and increases survival of p53-deficient mice.

19. 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.

20. MDM2 mediates p73 ubiquitination

Zebrafish Tumor Protein P73 (TP73) interaction partners

1. cDNA and amino acid sequences; characterization of expression pattern during fish development as well as in some adult tissues