Tumor Protein P63 (TP63) ELISA Kits

Human Tumor Protein P63 (TP63) Interaktionspartner

1. we observed that the genetic variant rs10937405 of TP63 gene is associated with an increased risk of NSCLC in north Indian population.

2. These findings identify a disease mechanism whereby mutant p63 rewires the enhancer landscape and affects epidermal cell identity.

3. results were related to endogenous p63-p300 complex formation and Wnt/beta-catenin-responsive gene regulation by p63 in squamous cell carcinoma lines

4. DeltaNup63 loss is associated with adverse outcome of NMIBC.

5. Ablation of DeltaNp63 alpha leads to cell cycle arrest and growth retardation, due to, in part, upregulation of p38 MAPK phosphorylation and activation.

6. Overexpression of DeltaNp63gamma modulates cell invasion by inducing targetable SRC-Slug-evoked epithelial-to-mesenchymal transition in head and neck squamous cell carcinoma , which can be reversed by inhibitors of the SRC signaling.

7. p38alpha destabilizes p63 to limit epidermal stem cell frequency and tumorigenic potential

8. The data illuminate a novel axis regulating cell senescence: DeltaNp63alpha stimulates transcription of E3 ligase HERC3, which mediates ubiquitination of c-Myc modulator MM1 and targets it to proteasomal degradation; subsequently, c-Myc is derepressed by DeltaNp63alpha, thereby cell senescence is modulated by this axis.

9. CKAP4 has a role in esophageal cancer cell proliferation through p63 dependent DKK3 expression

10. We identified rare damaging variants in four genes known to be mutated in syndromic lip and/or cleft palate (syCL/P) : TP63 (one family), TBX1 (one family), LRP6 (one family) and GRHL3 (two families), and clinical reassessment confirmed the isolated nature of their lip and/or cleft palate (CL/P).

11. These results showed tumor-suppressive roles of DeltaNp63beta and miR-205 by inhibiting epithelial-to-mesenchymal transition (EMT) thorough modulating ZEB1 and ZEB2 expression in oral squamous cell carcinoma

12. we found that human lung epithelial (HuL) cells, derived from normal, peripheral lung tissue, in monolayer, mostly express both the N-terminally truncated isoform of p63 (Np63), a marker for airway basal cells, and thyroid transcription factor-1 (TTF-1), a marker for alveolar epithelial cells, even though these two molecules are usually expressed in a mutually exclusive way.

13. These findings identify a unique crosstalk between DeltaNp63+ TNBC cells and MDSCs that promotes tumor progression and metastasis, which could be exploited in future combined immunotherapy/chemotherapy strategies for TNBC patients.

14. Study comparing p63/p40 expression with myoepithelial markers in minor salivary gland tumors revealed that p63 expression is almost comparable with VIM in detecting myoepithelial cells, an immunolabeling pattern not followed by p40, and consequently, caution has to be taken during the interpretation of salivary gland tumor exhibiting an p63/p40 phenotype in order to avoid a misdiagnosis.

15. Study reports that DNA methylation profiles may vary even among chronic lymphocytic leukemia (CLL) patients with similar somatic hypermutation status and highlight p63 as a novel pro-survival factor in CLL.

16. 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.

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

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

19. 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.

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

Horse (Equine) Tumor Protein P63 (TP63) Interaktionspartner

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

Zebrafish Tumor Protein P63 (TP63) Interaktionspartner

1. During early zebrafish embryonic development, p63 binds to enhancers associated to neural plate-expressing genes, where it limits Sox3 binding and neural gene expression. p63 binds enhancers associated to epidermis-expressing genes when they are in a non-accessible chromatin state, leading to its opening and epidermal gene expression.

2. 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.

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

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

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

6. 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) Interaktionspartner

1. Studied role of transformation related protein 63 (p63) inactivation thru gene silencing in reprogramming of cardiac cells; found downregulation of p63 facilitates cell reprogramming of cardiac fiibroblasts to cardiomyocytes.

2. 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.

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

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

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

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

7. 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.

8. Low TP63 expression is associated with neoplasms.

9. 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.

10. 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.

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

12. 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.

13. 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.

14. 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.

15. 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.

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

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

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

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

20. 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.

Xenopus laevis Tumor Protein P63 (TP63) Interaktionspartner

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.