Mouse Anti-TP63 Recombinant Antibody (CBYJT-4282) (CBMAB-T3758-YJ)

Mouse

Human

CBYJT-4282

IgG1

ELISA, WB

Human

IgG1

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

PBS, pH 7.4

Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

TP63 Gene(Protein Coding) Tumor Protein P63

TP63 is a member of the p53 family of transcription factors. The functional domains of p53 family proteins include an N-terminal transactivation domain, a central DNA-binding domain and an oligomerization domain. These isoforms function during skin development and maintenance, adult stem/progenitor cell regulation, heart development and premature aging. Some isoforms have been found to protect the germline by eliminating oocytes or testicular germ cells that have suffered DNA damage. Mutations in TP63 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.

Tumor Protein P63; Chronic Ulcerative Stomatitis Protein; Keratinocyte Transcription Factor KET; Tumor Protein P53-Competing Protein; Transformation-Related Protein 63; Tumor Protein P73-Like; TP73L; P73H; P73L; P40; P63; P51; KET; Amplified In Squamous Cell Carcinoma; Tumor Protein P53-Like

Acts as a sequence specific DNA binding transcriptional activator or repressor. The isoforms contain a varying set of transactivation and auto-regulating transactivation inhibiting domains thus showing an isoform specific activity. Isoform 2 activates RIPK4 transcription. May be required in conjunction with TP73/p73 for initiation of p53/TP53 dependent apoptosis in response to genotoxic insults and the presence of activated oncogenes. Involved in Notch signaling by probably inducing JAG1 and JAG2. Plays a role in the regulation of epithelial morphogenesis. The ratio of DeltaN-type and TA*-type isoforms may govern the maintenance of epithelial stem cell compartments and regulate the initiation of epithelial stratification from the undifferentiated embryonal ectoderm. Required for limb formation from the apical ectodermal ridge. Activates transcription of the p21 promoter.

Biological Process apoptotic process Source:ProtInc1 Publication
Biological Process cellular response to DNA damage stimulus Source:UniProtKB
Biological Process cellular senescence Source:Ensembl
Biological Process chromatin remodeling Source:Ensembl
Biological Process cloacal septation Source:Ensembl
Biological Process cranial skeletal system development Source:Ensembl
Biological Process ectoderm and mesoderm interaction Source:Ensembl
Biological Process embryonic forelimb morphogenesis Source:Ensembl
Biological Process embryonic hindlimb morphogenesis Source:Ensembl
Biological Process epidermal cell division Source:Ensembl
Biological Process epithelial cell development Source:Ensembl
Biological Process establishment of planar polarity Source:Ensembl
Biological Process establishment of skin barrier Source:UniProtKB
Biological Process female genitalia morphogenesis Source:Ensembl
Biological Process hair follicle morphogenesis Source:Ensembl
Biological Process intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source:Ensembl
Biological Process keratinocyte differentiation Source:Ensembl
Biological Process keratinocyte proliferation Source:Ensembl
Biological Process multicellular organism aging Source:Ensembl
Biological Process negative regulation of cellular senescence Source:UniProtKB
Biological Process negative regulation of DNA-templated transcription Source:UniProtKB1 Publication
Biological Process negative regulation of intracellular estrogen receptor signaling pathway Source:Ensembl
Biological Process negative regulation of keratinocyte differentiation Source:Ensembl
Biological Process negative regulation of mesoderm development Source:Ensembl
Biological Process negative regulation of transcription by RNA polymerase II Source:Ensembl
Biological Process neuron apoptotic process Source:Ensembl
Biological Process Notch signaling pathway Source:UniProtKB-KW
Biological Process odontogenesis of dentin-containing tooth Source:Ensembl
Biological Process polarized epithelial cell differentiation Source:Ensembl
Biological Process positive regulation of apoptotic signaling pathway Source:Ensembl
Biological Process positive regulation of cell cycle G1/S phase transition Source:UniProtKB
Biological Process positive regulation of DNA-templated transcription Source:UniProtKB2 Publications
Biological Process positive regulation of fibroblast apoptotic process Source:UniProtKB1 Publication
Biological Process positive regulation of keratinocyte proliferation Source:Ensembl
Biological Process positive regulation of Notch signaling pathway Source:UniProtKB1 Publication
Biological Process positive regulation of osteoblast differentiation Source:BHF-UCL1 Publication
Biological Process positive regulation of somatic stem cell population maintenance Source:Ensembl
Biological Process positive regulation of stem cell proliferation Source:Ensembl
Biological Process positive regulation of transcription by RNA polymerase II Source:BHF-UCL1 Publication
Biological Process post-anal tail morphogenesis Source:Ensembl
Biological Process prostatic bud formation Source:Ensembl
Biological Process protein tetramerization Source:InterPro
Biological Process proximal/distal pattern formation Source:Ensembl
Biological Process regulation of cysteine-type endopeptidase activity involved in apoptotic process Source:Ensembl
Biological Process regulation of epidermal cell division Source:UniProtKB
Biological Process regulation of transcription by RNA polymerase II Source:GO_Central1 Publication
Biological Process skeletal system development Source:Ensembl
Biological Process skin morphogenesis Source:Ensembl
Biological Process spermatogenesis Source:Ensembl
Biological Process squamous basal epithelial stem cell differentiation involved in prostate gland acinus development Source:Ensembl
Biological Process stem cell proliferation Source:Ensembl
Biological Process sympathetic nervous system development Source:Ensembl
Biological Process transcription by RNA polymerase II Source:Ensembl

Nucleus

Acro-dermato-ungual-lacrimal-tooth syndrome (ADULT syndrome):
A form of ectodermal dysplasia. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. ADULT syndrome involves ectrodactyly, syndactyly, finger- and toenail dysplasia, hypoplastic breasts and nipples, intensive freckling, lacrimal duct atresia, frontal alopecia, primary hypodontia and loss of permanent teeth. ADULT syndrome differs significantly from EEC3 syndrome by the absence of facial clefting. Inheritance is autosomal dominant.
Ankyloblepharon-ectodermal defects-cleft lip/palate (AEC):
An autosomal dominant condition characterized by congenital ectodermal dysplasia with coarse, wiry, sparse hair, dystrophic nails, slight hypohidrosis, scalp infections, ankyloblepharon filiform adnatum, maxillary hypoplasia, hypodontia and cleft lip/palate.
Ectrodactyly, ectodermal dysplasia, and cleft lip/palate syndrome 3 (EEC3):
A form of ectodermal dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. It is an autosomal dominant syndrome characterized by ectrodactyly of hands and feet, ectodermal dysplasia and facial clefting.
Split-hand/foot malformation 4 (SHFM4):
A limb malformation involving the central rays of the autopod and presenting with syndactyly, median clefts of the hands and feet, and aplasia and/or hypoplasia of the phalanges, metacarpals, and metatarsals. Some patients have been found to have intellectual disability, ectodermal and craniofacial findings, and orofacial clefting.
Limb-mammary syndrome (LMS):
Characterized by ectrodactyly, cleft palate and mammary-gland abnormalities.
Rapp-Hodgkin syndrome (RHS):
A form of ectodermal dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. Characterized by the combination of anhidrotic ectodermal dysplasia, cleft lip, and cleft palate. The clinical syndrome is comprised of a characteristic facies (narrow nose and small mouth), wiry, slow-growing, and uncombable hair, sparse eyelashes and eyebrows, obstructed lacrimal puncta/epiphora, bilateral stenosis of external auditory canals, microsomia, hypodontia, cone-shaped incisors, enamel hypoplasia, dystrophic nails, and cleft lip/cleft palate. RHS inheritance is autosomal dominant.
Orofacial cleft 8 (OFC8):
A birth defect consisting of cleft lips with or without cleft palate. Cleft lips are associated with cleft palate in two-third of cases. A cleft lip can occur on one or both sides and range in severity from a simple notch in the upper lip to a complete opening in the lip extending into the floor of the nostril and involving the upper gum.

May be sumoylated.
Ubiquitinated. Polyubiquitination involves WWP1 and leads to proteasomal degradation of this protein.