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TP63 encodes a member of the p53 family of transcription factors. Zusätzlich bieten wir Ihnen p63 Antikörper (87) und p63 Proteine (10) und viele weitere Produktgruppen zu diesem Protein an.
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Expression of TAp63, I (zeige RPE65 ELISA Kits)KKbeta and XBP1s is also increased (zeige TP53 ELISA Kits) in livers of obese patients with liver steatosis .
p63 (zeige RPE65 ELISA Kits) may act as either an oncogene (zeige RAB1A ELISA Kits) or a tumor suppressor gene in different scenarios: TA isoforms of p63 (zeige RPE65 ELISA Kits) 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)
Low TP63 expression is associated with neoplasms.
Studies suggest for dissecting tumor protein p63 (p63)-controlled mechanisms in normal and diseased epidermal development and for developing therapeutic options [Review].
In leukoplakia, increased expression of survivin reflects on the increased expression of ki-67 (zeige MKI67 ELISA Kits) and p63 (zeige RPE65 ELISA Kits).
Gene-gene interaction between MSX1 (zeige MSX1 ELISA Kits) 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 (zeige RPE65 ELISA Kits) 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 (zeige RPE65 ELISA Kits) in the cartilage tissues of osteoarthritis (OA) patients inhibited chondrocyte autophagy thereby contributing to the malignant progression of OA.
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
Down-regulation of p63 (zeige CKAP4 ELISA Kits) attenuates liver steatosis in p53 (zeige TP53 ELISA Kits) knockout mice and in diet-induced obese mice, whereas the activation of p63 (zeige CKAP4 ELISA Kits) induces lipid accumulation.
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.
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