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TP63 encodes a member of the p53 family of transcription factors. Additionally we are shipping p63 Kits (31) and p63 Proteins (7) and many more products for this protein.
Showing 10 out of 77 products:
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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Human Monoclonal p63 Primary Antibody for IHC, WB - ABIN2673817
Zhang, Wei, Dang, Xie, Zhong, Ma, Chen: Primary urinary bladder adenosquamous carcinoma complicated with lower limb deep venous thromboses: a case report. in International journal of clinical and experimental pathology 2015
that both major p63 (show RPE65 Antibodies) protein isoforms are expressed in triple-negative breast cancers with different tumour characteristics, indicating distinct functional activities of p63 (show RPE65 Antibodies) variants in breast cancer
Wnt5a (show WNT5A Antibodies)-Ror2 (show ROR2 Antibodies) signaling enhanced tongue SCC (show CYP11A1 Antibodies) cell aggressiveness and promoted production of MMP-2 (show MMP2 Antibodies) following DeltaNp63beta-mediated EMT (show ITK Antibodies)
p63 (show RPE65 Antibodies)-DBD is capable of binding to anti-apoptotic BclxL (show BCL2L1 Antibodies) via its DNA binding interface, a feature that has only been shown for p53 (show TP53 Antibodies) so far.
The data indicate that EPCR (show PROCR Antibodies) can regulate p63 (show RPE65 Antibodies), is associated with highly proliferative keratinocytes, and is a potential human epidermal stem cell marker.
miR (show MLXIP Antibodies)-124 regulates p63 (show RPE65 Antibodies) via iASPP (show PPP1R13L Antibodies), while p63 (show RPE65 Antibodies) targets miR (show MLXIP Antibodies)-155 via the modulation of STAT1 (show STAT1 Antibodies) expression in colorectal cancer.
The number of p63 (show RPE65 Antibodies)(+) cells is significantly higher in both hyperplastic (1.53-fold, P < 0.0001) and squamous metaplastic (2.02-fold, P < 0.0001) epithelium from nasal polyps than from healthy controls
In p53 (show TP53 Antibodies)-deficient breast cancers, compensatory mechanism of NFkB repression by p63 (show RPE65 Antibodies) and p73 (show TP73 Antibodies) during genotoxic stress could lead to complex effects that would influence all aspects of tumor progression.
findings illustrate that DeltaNp63alpha can inhibit the levels of LIF (show LIF Antibodies) mRNA by direct transcription regulation and decrease LIF (show LIF Antibodies) mRNA stability by suppressing the expression of Lnc-LIF (show LIF Antibodies)-AS. An inverse interaction of LIF (show LIF Antibodies) and DeltaNp63alpha expression was as well validated in clinical samples of cervical cancer, and high level of LIF (show LIF Antibodies) in cervical cancers was related with poor patient survival.
Negative staining for CK5 (show KRT5 Antibodies)/6 and p63 (show RPE65 Antibodies) can be helpful to distinguish Well-differentiated neuroendocrine tumors (WDNETs) from cutaneous adnexal neoplasms. It is important to consider WDNETs in the differential diagnosis of cutaneous adnexal neoplasms as low-grade tumors may be the first sign of aggressive metastatic disease
EGFR (show EGFR Antibodies) pathway gene expression analysis indicated that DeltaNp63 alters EGFR (show EGFR Antibodies)-regulated genes involved in cell adhesion, migration, and angiogenesis. Addition of EGF (show EGF Antibodies) or neutralizing EGFR (show EGFR Antibodies) antibodies demonstrated that EGFR (show EGFR Antibodies) activation is responsible for DeltaNp63-mediated loss of cellular adhesion
p63 expression was significantly lower in the chronic laminitic hoof than in that of control horses
they unravel essential roles of TAp63 and p53 (show TP53 Antibodies) to promote both keratinocyte proliferation and their terminal differentiation by promoting Notch (show NOTCH1 Antibodies) signalling and caspase 3 (show CASP3 Antibodies) activity.
the p63 transcription factor is upregulated to initiate this apoptotic pathway and directly activates puma (show BBC3 Antibodies) 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 (show RPS19 Antibodies)-deficient phenotype is mediated by dysregulation of deltaNp63 and p53 (show TP53 Antibodies) and results in hematopoietic and developmental abnormalities resembling Diamond-Blackfan anemia
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 (show IL31 Antibodies) and IL-33 (show IL33 Antibodies) are key players in the signaling pathways.
cells expressing both p63 (show CKAP4 Antibodies) and p73 (show ARHGAP24 Antibodies) 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 (show TP53 Antibodies) p63 (p63 (show CKAP4 Antibodies)) 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 (show HSP70 Antibodies) expression via E2F1 transcription factor (show E2F1 Antibodies) 1 (show HNF1A Antibodies), promoting Wasf3/Wave3 (show WASF3 Antibodies)/MMP9 (show MMP9 Antibodies) signaling and bladder cancer invasion
these results therefore highlight an unanticipated role for p53 (show TP53 Antibodies) family proteins in a regulatory network that integrates essential Wnt (show WNT2 Antibodies)-Tcf (show HNF4A Antibodies) and nodal-Smad (show SMAD1 Antibodies) inputs.
the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 (show TP53 Antibodies) 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 (show TGFB3 Antibodies)-induced down-regulation of p63 (show CKAP4 Antibodies) 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.
miR-20a-5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.
Taken together, these data show that p63 (show CKAP4 Antibodies) regulates the self-renewal and differentiation of oesophageal stem cells in humans and mice.
IL-6 (show IL6 Antibodies)/P-STAT3 (show STAT3 Antibodies) activation influences p63 (show CKAP4 Antibodies) isoform expression in healing wounds, which may contribute to wound-induced hair follicle neogenesis.
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 (show BMP4 Antibodies).
The role of p63 as a negative Wnt (show WNT2 Antibodies)-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