anti-Tumor Protein P63 (TP63) Anticorps

Human Tumor Protein P63 (TP63) interaction partners

1. Data identified an enhancer region within the TP63/LEPREL1 locus containing genetic variants associated with bladder cancer risk.

2. The malignant lesions showed significantly lower values than the benign lesions in the percentage of p63+ clusters, the percentage of p63+ single cells in the clusters, and the number of p63+ single cells in the background.

3. Expression of TAp63, IKKbeta and XBP1s is also increased in livers of obese patients with liver steatosis .

4. p63 may act as either an oncogene or a tumor suppressor gene in different scenarios: TA isoforms of p63 gene are generally tumor-suppressive through repressing cell proliferation, survival and metastasis; DeltaN isoforms, however, may initiate tumorigenesis via promoting cell proliferation and survival. (Review)

5. Low TP63 expression is associated with neoplasms.

6. Studies suggest for dissecting tumor protein p63 (p63)-controlled mechanisms in normal and diseased epidermal development and for developing therapeutic options [Review].

7. In leukoplakia, increased expression of survivin reflects on the increased expression of ki-67 and p63.

8. Gene-gene interaction between MSX1 and TP63 may influence the risk of nonsyndromic cleft lip with or without cleft palate in Asian populations.

9. High N-terminally truncated isoform of p63 expression is associated with squamous cell carcinogenesis.

10. The rs35592567 polymorphism in TP63 affected the expression of TP63 by interfering with its interaction with miR-140, and could serve as an explanation for the increased risk of Gastric Cancer.

11. The data from this study showed that p63 was a tumor suppressor mainly through regulating PTEN in chondrosarcoma cells.

12. we first demonstrated that upregulation of P63 in the cartilage tissues of osteoarthritis (OA) patients inhibited chondrocyte autophagy thereby contributing to the malignant progression of OA.

13. high DeltaNp63beta expression up-regulates KLK6-PAR2 and down-regulates PAR1, inducing malignant transformation in oral epithelium with stimulating proliferation through ERK signal activation

14. multiple ankyloblepharon-ectodermal defects-cleft lip/palate syndrome-associated p63 mutations, but not those causative of other diseases, lead to thermodynamic protein destabilization, misfolding, and aggregation

15. LINC01503 is increased in squamous cell carcinoma (SCC) cells compared with non-tumor cells. TP63 bound to the super enhancer at the LINC01503 locus activates its transcription which promotes SCC cell proliferation, migration, invasion, and growth of xenograft tumors.

16. we provide evidence that S100A7 also inhibits YAP expression and activity through p65/NFkappaB-mediated repression of DeltaNp63, and S100A7 represses drug-induced apoptosis via inhibition of YAP.

17. DeltaNp63 promotes head and neck squamous cell carcinoma tumorigenesis via regulation of hyaluronic acid metabolism. p63 expression is a negative prognostic factor of HNSCC patient survival.

18. cases illustrate that: there is significant familial variability, including discordant major but concordant minor anomalies in the first ever reported set of molecularly confirmed monozygotic twins with pathogenic variants in TP63.

19. results reveal a critical role for KMT2D in the control of epithelial enhancers and p63 target gene expression.

20. Loss of Nrf2 inhibits deltaNp63 stem cell mobilization, a key event for reconstitution of radiation-injured lung, while promoting a myofibroblast phenotype that is central for fibrosis.

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

2. 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.

3. Low TP63 expression is associated with neoplasms.

4. 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.

5. 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.

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

7. 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.

8. 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.

9. 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.

10. 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.

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

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

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

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

15. 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.

16. 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.

17. increased DeltaNp63alpha protein levels facilitate oncogenic transformation in the epidermis as well as in the bile duct.

18. miR-20a-5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.

19. Taken together, these data show that p63 regulates the self-renewal and differentiation of oesophageal stem cells in humans and mice.

20. IL-6/P-STAT3 activation influences p63 isoform expression in healing wounds, which may contribute to wound-induced hair follicle neogenesis.

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.