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TP63 encodes a member of the p53 family of transcription factors.
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DeltaNp63 promotes head and neck squamous cell carcinoma tumorigenesis via regulation of hyaluronic acid metabolism. p63 (zeige RPE65 ELISA Kits) expression is a negative prognostic factor of HNSCC patient survival.
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.
results reveal a critical role for KMT2D (zeige MLL2 ELISA Kits) in the control of epithelial enhancers and p63 (zeige RPE65 ELISA Kits) target gene expression.
Loss of Nrf2 (zeige GABPA ELISA Kits) inhibits deltaNp63 stem cell mobilization, a key event for reconstitution of radiation-injured lung, while promoting a myofibroblast phenotype that is central for fibrosis.
PKC-delta (zeige PKCd ELISA Kits) played as a protective role in squamous cell carcinomas partly by down-regulating p63 (zeige RPE65 ELISA Kits), leading to the suppression of squamous cell carcinomas cell proliferation
Immunocytochemical staining using cocktail antibody targeting p63 (zeige RPE65 ELISA Kits)/CK14 (zeige KRT14 ELISA Kits) was useful for the differential diagnosis of FA and DCIS in FNAC of the breast.
Authors conclude that TP63 mutations are frequent in cutaneous melanoma, support UV etiology, but their role in melanomagenesis is unclear.
that both major p63 (zeige RPE65 ELISA Kits) protein isoforms are expressed in triple-negative breast cancers with different tumour characteristics, indicating distinct functional activities of p63 (zeige RPE65 ELISA Kits) variants in breast cancer
Wnt5a (zeige WNT5A ELISA Kits)-Ror2 (zeige ROR2 ELISA Kits) signaling enhanced tongue SCC (zeige CYP11A1 ELISA Kits) cell aggressiveness and promoted production of MMP-2 (zeige MMP2 ELISA Kits) following DeltaNp63beta-mediated EMT (zeige ITK ELISA Kits)
p63 (zeige RPE65 ELISA Kits)-DBD is capable of binding to anti-apoptotic BclxL (zeige BCL2L1 ELISA Kits) via its DNA binding interface, a feature that has only been shown for p53 (zeige TP53 ELISA Kits) so far.
p63 expression was significantly lower in the chronic laminitic hoof than in that of control horses
they unravel essential roles of TAp63 and p53 (zeige TP53 ELISA Kits) to promote both keratinocyte proliferation and their terminal differentiation by promoting Notch (zeige NOTCH1 ELISA Kits) signalling and caspase 3 (zeige CASP3 ELISA Kits) activity.
the p63 transcription factor is upregulated to initiate this apoptotic pathway and directly activates puma (zeige BBC3 ELISA Kits) transcription in response to ER stress.
Early zebrafish embryos express a dominant-negative form of p63 (DeltaNp63), which accumulates in the nucleus just as epidermal growth begins. (p63)
DeltaNp63 expression blocks neural development and promotes nonneural development, even in the absence of Bmp signaling. (DeltaNp63)
rps19 (zeige RPS19 ELISA Kits)-deficient phenotype is mediated by dysregulation of deltaNp63 and p53 (zeige TP53 ELISA Kits) and results in hematopoietic and developmental abnormalities resembling Diamond-Blackfan anemia
The results indicate that ZIP10 plays important roles in epidermal development via, at least in part, the ZIP10-zinc-p63 (zeige CKAP4 ELISA Kits) signaling axis, thereby highlighting the physiological significance of zinc regulation in the maintenance of skin epidermis.
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.
present study, we provided a role for IDH2 (zeige IDH2 ELISA Kits) in protection against UVB-induced skin damage and a new connection between IDH2 (zeige IDH2 ELISA Kits) and DeltaNp63.
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 (zeige IL31 ELISA Kits) and IL-33 (zeige IL33 ELISA Kits) are key players in the signaling pathways.
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.
Data suggest that this the selective targeting of genes by tumor suppressor protein (zeige TP53 ELISA Kits) p63 (p63 (zeige CKAP4 ELISA Kits)) correlates with subtle, but measurable transcriptional differences in mouse and human keratinocytes that converges on major metabolic processes, which often exhibit species-specific trends.
p63alpha protein up-regulates heat shock protein 70 expression via E2F1 transcription factor 1, promoting Wasf3/Wave3/MMP9 signaling and bladder cancer invasion
these results therefore highlight an unanticipated role for p53 (zeige TP53 ELISA Kits) family proteins in a regulatory network that integrates essential Wnt (zeige WNT2 ELISA Kits)-Tcf (zeige HNF4A ELISA Kits) and nodal-Smad (zeige SMAD1 ELISA Kits) inputs.
the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 (zeige TP53 ELISA Kits) 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.
TGFb3 (zeige TGFB3 ELISA Kits)-induced down-regulation of p63 (zeige CKAP4 ELISA Kits) 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.
Data indicate that pluripotency genes sox2, p63 and oct60 are upregulated early during the process of lens regeneration.
The results suggest that DeltaNp63 is an essential gene in early epidermal specification under the control of BMP4 (zeige BMP4 ELISA Kits).
The role of p63 as a negative Wnt (zeige WNT2 ELISA Kits)-regulator thus matches with the frequently observed downregulation of p63 during tumor progression, when cancer cells adopt a more mesenchymal, invasive phenotype.
This gene encodes a member of the p53 family of transcription factors. An animal model, p63 -/- mice, has been useful in defining the role this protein plays in the development and maintenance of stratified epithelial tissues. p63 -/- mice have several developmental defects which include the lack of limbs and other tissues, such as teeth and mammary glands, which develop as a result of interactions between mesenchyme and epithelium. Mutations in this gene are associated with ectodermal dysplasia, and cleft lip/palate syndrome 3 (EEC3)\; split-hand/foot malformation 4 (SHFM4)\; ankyloblepharon-ectodermal defects-cleft lip/palate\; ADULT syndrome (acro-dermato-ungual-lacrimal-tooth)\; limb-mammary syndrome\; Rap-Hodgkin syndrome (RHS)\; and orofacial cleft 8. Both alternative splicing and the use of alternative promoters results in multiple transcript variants encoding different proteins. Many transcripts encoding different proteins have been reported but the biological validity and the full-length nature of these variants have not been determined.
, amplified in squamous cell carcinoma
, chronic ulcerative stomatitis protein
, keratinocyte transcription factor KET
, transformation-related protein 63
, tumor protein 63
, tumor protein p53-competing protein
, tumor protein p63 deltaN isoform delta
, tumor protein p63
, transformation related protein 63
, tumor protein 63 kDa
, tumor protein 63-like