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TP63 encodes a member of the p53 family of transcription factors. 再加上，我们可以发p63 试剂盒 (31) 和 p63 蛋白 (10)和数多这个蛋白质的别的产品。
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Human Polyclonal p63 Primary Antibody for WB - ABIN657886
Miki, Kubo, Takahashi, Yoon, Kim, Lee, Zo, Lee, Hosono, Morizono, Tsunoda, Kamatani, Chayama, Takahashi, Inazawa, Nakamura, Daigo: Variation in TP63 is associated with lung adenocarcinoma susceptibility in Japanese and Korean populations. in Nature genetics 2010
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In leukoplakia, increased expression of survivin reflects on the increased expression of ki-67 (显示 MKI67 抗体) and p63 (显示 RPE65 抗体).
Gene-gene interaction between MSX1 (显示 MSX1 抗体) 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 (显示 RPE65 抗体) expression is associated with squamous cell carcinogenesis.
The rs35592567 polymorphism in TP63 affected the expression of TP63 by interfering with its interaction with miR (显示 MLXIP 抗体)-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 (显示 RPE65 抗体) 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 (显示 KLK1 抗体)-PAR2 (显示 F2RL1 抗体) and down-regulates PAR1 (显示 MARK2 抗体), inducing malignant transformation in oral epithelium with stimulating proliferation through ERK (显示 EPHB2 抗体) signal activation
multiple ankyloblepharon-ectodermal defects-cleft lip/palate syndrome-associated p63 (显示 RPE65 抗体) mutations, but not those causative of other diseases, lead to thermodynamic protein destabilization, misfolding, and aggregation
LINC01503 is increased in squamous cell carcinoma (SCC (显示 CYP11A1 抗体)) cells compared with non-tumor cells. TP63 bound to the super enhancer at the LINC01503 locus activates its transcription which promotes SCC (显示 CYP11A1 抗体) cell proliferation, migration, invasion, and growth of xenograft tumors.
we provide evidence that S100A7 (显示 S100A7 抗体) also inhibits YAP (显示 YAP1 抗体) expression and activity through p65 (显示 GORASP1 抗体)/NFkappaB (显示 NFKB1 抗体)-mediated repression of DeltaNp63, and S100A7 (显示 S100A7 抗体) represses drug-induced apoptosis via inhibition of YAP (显示 YAP1 抗体).
p63 expression was significantly lower in the chronic laminitic hoof than in that of control horses
they unravel essential roles of TAp63 and p53 (显示 TP53 抗体) to promote both keratinocyte proliferation and their terminal differentiation by promoting Notch (显示 NOTCH1 抗体) signalling and caspase 3 (显示 CASP3 抗体) activity.
the p63 transcription factor is upregulated to initiate this apoptotic pathway and directly activates puma (显示 BBC3 抗体) 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 (显示 RPS19 抗体)-deficient phenotype is mediated by dysregulation of deltaNp63 and p53 (显示 TP53 抗体) and results in hematopoietic and developmental abnormalities resembling Diamond-Blackfan anemia
The results indicate that ZIP10 (显示 SLC39A10 抗体) plays important roles in epidermal development via, at least in part, the ZIP10 (显示 SLC39A10 抗体)-zinc-p63 (显示 CKAP4 抗体) 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 (显示 IDH2 抗体) in protection against UVB-induced skin damage and a new connection between IDH2 (显示 IDH2 抗体) 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 (显示 IL31 抗体) and IL-33 (显示 IL33 抗体) are key players in the signaling pathways.
cells expressing both p63 (显示 CKAP4 抗体) and p73 (显示 ARHGAP24 抗体) 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 (显示 TP53 抗体) p63 (p63 (显示 CKAP4 抗体)) 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 (显示 HSP70 抗体) expression via E2F1 transcription factor (显示 E2F1 抗体) 1 (显示 HNF1A 抗体), promoting Wasf3/Wave3 (显示 WASF3 抗体)/MMP9 (显示 MMP9 抗体) signaling and bladder cancer invasion
these results therefore highlight an unanticipated role for p53 (显示 TP53 抗体) family proteins in a regulatory network that integrates essential Wnt (显示 WNT2 抗体)-Tcf (显示 HNF4A 抗体) and nodal-Smad (显示 SMAD1 抗体) inputs.
the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 (显示 TP53 抗体) 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 (显示 TGFB3 抗体)-induced down-regulation of p63 (显示 CKAP4 抗体) 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 (显示 BMP4 抗体).
The role of p63 as a negative Wnt (显示 WNT2 抗体)-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