anti-Tumor Protein P63 (TP63) Antibodies

Human Tumor Protein P63 (TP63) interaction partners

1. Structure determination of the transactivation domains of p63 and p73 in complex with the p300 Taz2 domain further revealed that, in contrast to p53 and p73, p63 has a single transactivation domain.

2. a critical role for p63 in response to DNA damage in cervical cancer cells, is reported.

3. TCL1A interacts with TP63 and enhances the survival of Raji Burkitt lymphoma cell line.

4. Cullin3/KCTD5 downregulates the DNA-binding affinity of DeltaNp63alpha, impairing either its transactivity or its transinhibitory activity. Functionally, Cullin3/KCTD5 abates the proproliferation activity of DeltaNp63alpha. These findings suggest that KCTD5-based CRL3 may mediate monoubiquitination and is a novel regulator of DeltaNp63alpha.

5. Letter: loss of TP63/TRP63 directly facilitates cutaneous squamous cell carcinoma development and progression through activation of Wnt/beta-catenin signaling.

6. P63alpha inhibited cyclin D1 protein expression.

7. Exogenous p51A gene can increase its expression in A549 and NCI-H1299 cells, suppress cell growth and induce cell apoptosis. Moreover, it can also cooperate with chemotherapy and reduce the dose and side-effect. p51A gene can suppress tumours in spite of p53 status and p21 gene might be involved.

8. Case Report: TP63 mutation responsible for ankyloblepharon-ectodermal defects-cleft lip/palate-syndrome with choanal atresia and skin erosions.

9. Thus, epithelial barrier and ciliogenesis of nasal epithelium are regulated in a p63-negative manner in normal and upper airway diseases.

10. Letter/Case Report: heterozygous mutation in the SAM domain of the TP63 gene resulting in mild form of ectodermal dysplasia.

11. ATDC is required for TP63-induced bladder tumor invasion and metastasis.

12. Expression of p63 was not elevated in gestational trophoblastic disease

13. Study reinforces that p63 is a crucial gene for maintaining epithelial tissue integrity and support the deregulation of the cell-cell adhesion program, which plays a critical role in squamous cell carcinoma development.

14. Data indicate keratins K5/K14 and p53 homolog p63 as markers of breast epithelial stem cells.

15. The mutation was not previously described in the literature or databases and should be included into these as probably pathogenic. A multidisciplinary approach is necessary to care for a patient with Hay-Wells syndrome, such care however can provide good results.

16. Mechanistically, Delta133p53 binds to DeltaNp63 and utilizes its transactivation domain to upregulate GLUT1, GLUT4, and PGM expression driving glycolysis. While increased glycolysis provides cancer cells with anabolic metabolism critical for proliferation and survival, it can be harnessed for selective cancer cell killing.

17. Study investigates the biological significance of the Rbm38-p63 loop and finds that Rbm38 and p63 function as intergenic suppressors in aging and tumorigenesis.

18. ROCK-dependent phosphorylation of NUP62 regulates p63 nuclear transport and squamous cell carcinoma proliferation.

19. TP63 role in the squamous cancer progression.CCAT1 is a key target co-regulated by TP63 and SOX2 through a super-enhancer in squamous cancer cells.

20. lncRNA RP185F18.6 and DeltaNp63 may be considered unfavorable biomarkers, whereas GSDMD may be a favorable biomarker in colorectal cancer (CRC) ; these markers may prove valuable in the future diagnosis and prognosis of CRC.

Horse (Equine) Tumor Protein P63 (TP63) interaction partners

1. p63 expression was significantly lower in the chronic laminitic hoof than in that of control horses

Zebrafish Tumor Protein P63 (TP63) interaction partners

1. they unravel essential roles of TAp63 and p53 to promote both keratinocyte proliferation and their terminal differentiation by promoting Notch signalling and caspase 3 activity.

2. the p63 transcription factor is upregulated to initiate this apoptotic pathway and directly activates puma transcription in response to ER stress.

3. Early zebrafish embryos express a dominant-negative form of p63 (DeltaNp63), which accumulates in the nucleus just as epidermal growth begins. (p63)

4. DeltaNp63 expression blocks neural development and promotes nonneural development, even in the absence of Bmp signaling. (DeltaNp63)

5. rps19-deficient phenotype is mediated by dysregulation of deltaNp63 and p53 and results in hematopoietic and developmental abnormalities resembling Diamond-Blackfan anemia

Mouse (Murine) Tumor Protein P63 (TP63) interaction partners

1. GSK-3beta was essential for sustaining fetal oocyte survival and folliculogenesis via fine-tuning the cytoplasmic-nuclear translocation of beta-catenin, which in turn modulates timely TAp63 expression during meiotic prophase I in mice.

2. P63 mediates the apoptosis of male germ cells and regulates three stages of spermatogenesis transcriptionally.

3. Letter: loss of TP63/TRP63 directly facilitates cutaneous squamous cell carcinoma development and progression through activation of Wnt/beta-catenin signaling.

4. Altogether, these results demonstrate that CCDC3 modulates liver lipid metabolism by inhibiting liver de novo lipogenesis as a downstream player of the p63 network.

5. TAp63 in POMC neurons is one key molecular driver for the sexual dimorphism in energy homeostasis

6. Down-regulation of p63 attenuates liver steatosis in p53 knockout mice and in diet-induced obese mice, whereas the activation of p63 induces lipid accumulation.

7. Low TP63 expression is associated with neoplasms.

8. The results indicate that ZIP10 plays important roles in epidermal development via, at least in part, the ZIP10-zinc-p63 signaling axis, thereby highlighting the physiological significance of zinc regulation in the maintenance of skin epidermis.

9. Notch signaling maintains p63 levels and horizontal basal cell (HBC) dormancy, in contrast to its suppression of p63 expression in other tissues. Additionally, Notch1, but not Notch2, is required to maintain HBC dormancy after selective neuronal degeneration.

10. present study, we provided a role for IDH2 in protection against UVB-induced skin damage and a new connection between IDH2 and DeltaNp63.

11. Overexpression of DeltaNp63 in transgenic mouse epidermis results in a severe skin phenotype that shares many of the key clinical, histological and molecular features associated with Atopic dermatitis and IL-31 and IL-33 are key players in the signaling pathways.

12. 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.

13. Data suggest that this the selective targeting of genes by tumor suppressor protein p63 (p63) correlates with subtle, but measurable transcriptional differences in mouse and human keratinocytes that converges on major metabolic processes, which often exhibit species-specific trends.

14. Using a combination of biophysical methods as well as cell and ovary culture experiments the authors explain how TAp63alpha is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.

15. p63alpha protein up-regulates heat shock protein 70 expression via E2F1 transcription factor 1, promoting Wasf3/Wave3/MMP9 signaling and bladder cancer invasion

16. TAp63 suppresses mammary tumorigenesis through regulation of the Hippo pathway

17. controls limb development through transcriptional regulation of different target molecules with different roles in the apical ectodermal ridge

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

19. the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 and TAp63 are dispensable for arrest caused by sex body defects. These data affirm that recombination-dependent and sex body-deficient arrests occur via genetically separable mechanisms.

20. TGFb3-induced down-regulation of p63 in the medial edge epithelia of the palatal shelves is a pre-requisite for palatal fusion by facilitating periderm migration from, and reducing the proliferative potential of, the midline epithelial seam thereby preventing cleft palate.

Xenopus laevis Tumor Protein P63 (TP63) interaction partners

1. Data indicate that pluripotency genes sox2, p63 and oct60 are upregulated early during the process of lens regeneration.

2. The results suggest that DeltaNp63 is an essential gene in early epidermal specification under the control of BMP4.

3. The role of p63 as a negative Wnt-regulator thus matches with the frequently observed downregulation of p63 during tumor progression, when cancer cells adopt a more mesenchymal, invasive phenotype.