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TP63 encodes a member of the p53 family of transcription factors. De plus, nous expédions p63 Anticorps (87) et p63 Protéines (10) et beaucoup plus de produits pour cette protéine.
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In leukoplakia, increased expression of survivin reflects on the increased expression of ki-67 (Montrer MKI67 Kits ELISA) and p63 (Montrer RPE65 Kits ELISA).
Gene-gene interaction between MSX1 (Montrer MSX1 Kits ELISA) and TP63 may influence the risk of nonsyndromic cleft lip with or without cleft palate in Asian populations.
High N-terminally truncated isoform of p63 (Montrer RPE65 Kits ELISA) expression is associated with squamous cell carcinogenesis.
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.
The data from this study showed that p63 was a tumor suppressor mainly through regulating PTEN in chondrosarcoma cells.
we first demonstrated that upregulation of P63 (Montrer RPE65 Kits ELISA) in the cartilage tissues of osteoarthritis (OA) patients inhibited chondrocyte autophagy thereby contributing to the malignant progression of OA.
high DeltaNp63beta expression up-regulates KLK6 (Montrer KLK1 Kits ELISA)-PAR2 (Montrer F2RL1 Kits ELISA) and down-regulates PAR1, inducing malignant transformation in oral epithelium with stimulating proliferation through ERK (Montrer EPHB2 Kits ELISA) signal activation
multiple ankyloblepharon-ectodermal defects-cleft lip/palate syndrome-associated p63 (Montrer RPE65 Kits ELISA) mutations, but not those causative of other diseases, lead to thermodynamic protein destabilization, misfolding, and aggregation
LINC01503 is increased in squamous cell carcinoma (SCC (Montrer CYP11A1 Kits ELISA)) cells compared with non-tumor cells. TP63 bound to the super enhancer at the LINC01503 locus activates its transcription which promotes SCC (Montrer CYP11A1 Kits ELISA) cell proliferation, migration, invasion, and growth of xenograft tumors.
we provide evidence that S100A7 (Montrer S100A7 Kits ELISA) also inhibits YAP (Montrer YAP1 Kits ELISA) expression and activity through p65/NFkappaB (Montrer NFKB1 Kits ELISA)-mediated repression of DeltaNp63, and S100A7 (Montrer S100A7 Kits ELISA) represses drug-induced apoptosis via inhibition of YAP (Montrer YAP1 Kits ELISA).
p63 expression was significantly lower in the chronic laminitic hoof than in that of control horses
they unravel essential roles of TAp63 and p53 (Montrer TP53 Kits ELISA) to promote both keratinocyte proliferation and their terminal differentiation by promoting Notch (Montrer NOTCH1 Kits ELISA) signalling and caspase 3 (Montrer CASP3 Kits ELISA) activity.
the p63 transcription factor is upregulated to initiate this apoptotic pathway and directly activates puma (Montrer BBC3 Kits ELISA) 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 (Montrer RPS19 Kits ELISA)-deficient phenotype is mediated by dysregulation of deltaNp63 and p53 (Montrer TP53 Kits ELISA) 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 (Montrer CKAP4 Kits ELISA) 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 (Montrer IDH2 Kits ELISA) in protection against UVB-induced skin damage and a new connection between IDH2 (Montrer IDH2 Kits ELISA) 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 (Montrer IL31 Kits ELISA) and IL-33 (Montrer IL33 Kits ELISA) 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 (Montrer TP53 Kits ELISA) p63 (p63 (Montrer CKAP4 Kits ELISA)) 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 (Montrer TP53 Kits ELISA) family proteins in a regulatory network that integrates essential Wnt (Montrer WNT2 Kits ELISA)-Tcf (Montrer HNF4A Kits ELISA) and nodal-Smad (Montrer SMAD1 Kits ELISA) inputs.
the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 (Montrer TP53 Kits ELISA) 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 (Montrer TGFB3 Kits ELISA)-induced down-regulation of p63 (Montrer CKAP4 Kits ELISA) 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 (Montrer BMP4 Kits ELISA).
The role of p63 as a negative Wnt (Montrer WNT2 Kits ELISA)-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