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TP63

GeneName

TP63

Summary

TP63, also known as p63, p40, or KET, is a 77kDa transcription factor that plays a vital role in the development and maintenance of epithelial tissues. It is predominantly expressed in the nucleus and is involved in various cellular processes, including chromatin binding and DNA damage response. TP63 is crucial for keratinocyte proliferation and differentiation, and it regulates apoptotic processes and cellular senescence. The protein is localised in several cellular compartments, including the chromatin, cytoplasm, and dendrites, and is implicated in the morphogenesis of various structures such as the epidermis and cranial skeletal system.

Importance

TP63 is relevant to: - Epithelial tissue development and homeostasis, influencing skin barrier establishment and keratinocyte function - Cancer research, particularly in squamous cell carcinomas, due to its role in regulating cell proliferation and apoptosis - Developmental biology, as it is involved in limb morphogenesis and organogenesis - Stem cell biology, given its positive regulation of stem cell proliferation and maintenance

Top Products

For researchers investigating TP63, we recommend two excellent primary antibodies that have garnered significant attention in the field. The first is the well-cited Anti-p63 antibody [4A4] (ab735), a monoclonal antibody that has been extensively used in immunohistochemistry (IHC) and boasts an impressive 195 citations, highlighting its reliability and trust within the research community. In addition, we offer the recombinant Anti-p63 antibody [EPR5701] (ab124762), which has also received considerable recognition with 187 citations. This versatile antibody is validated for multiple applications, including IHC, western blotting (WB), immunocytochemistry (ICC), and flow cytometry (FC). The recombinant nature of this product ensures batch-to-batch consistency, making it an excellent choice for researchers seeking dependable TP63 detection across various experimental setups. The Anti-p63 antibody ELISA Kit (ab124762), supported by 187 citations, is an excellent option for researchers looking to accurately measure TP63 levels in their samples.

Abcam Product Citation Summary

The data indicates that TP63 is extensively studied in various contexts, particularly in human tissues such as lung, gastric cancer, and mammary glands, as well as in mouse models. The applications of Abcam antibodies for TP63 include Western blotting, immunohistochemistry, and immunofluorescence, highlighting its relevance in cancer research, wound healing, and gene expression regulation during pregnancy.

Abcam Product Citation Table

ab124762
Human
IF
wound healing
27829065
ab124762
Human
IHC
idiopathic pulmonary fibrosis
27423691
ab124762
Rabbit
IHC-IF
limbal epithelial stem cells
29967694
ab124762
Human
WB
cell differentiation
31732694
ab124762
Human
WB
gastric cancer
32292506
ab124762
Rat
WB
corneal epithelial regeneration
33772031
ab124762
Mouse
WB
gene expression regulation during pregnancy
34336839
ab53039
Mouse
WB
squamous cell carcinoma transition
28387316
ab735
Mouse
IHC
P63 expression
29362488
ab735
Human
IHC
head and neck cancer
32293356
ab735
Human
WB
3D culture phenotypes
30332774
ab735
Human
WB
acinar morphogenesis
30332774
ab735
Human
IF
epidermal 3D organoids
32967725

Domain

The transactivation inhibitory domain (TID) can interact with, and inhibit the activity of the N-terminal transcriptional activation domain of TA*-type isoforms.

Function

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.

Involvement in disease

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.

None

The disease is caused by variants affecting the gene represented in this entry.

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.

None

The disease is caused by variants affecting the gene represented in this entry.

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.

None

The disease is caused by variants affecting the gene represented in this entry.

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.

None

The disease is caused by variants affecting the gene represented in this entry.

Limb-mammary syndrome

LMS

Characterized by ectrodactyly, cleft palate and mammary-gland abnormalities.

None

The disease is caused by variants affecting the gene represented in this entry.

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.

None

The disease is caused by variants affecting the gene represented in this entry.

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.

None

The disease is caused by variants affecting the gene represented in this entry.

Premature ovarian failure 21

POF21

A form of premature ovarian failure, an ovarian disorder defined as the cessation of ovarian function under the age of 40 years. It is characterized by oligomenorrhea or amenorrhea, in the presence of elevated levels of serum gonadotropins and low estradiol. POF21 inheritance is autosomal dominant.

None

The disease is caused by variants affecting the gene represented in this entry. Gain-of-function variants located in the transactivation inhibition domain are responsible for premature ovarian failure by inducing accelerated oocyte loss, as shown in mutant mice carrying the pathogenic variant p.Arg647Cys.

Post-translational modifications

May be sumoylated.

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

Sequence Similarities

Belongs to the p53 family.

Tissue Specificity

Widely expressed, notably in heart, kidney, placenta, prostate, skeletal muscle, testis and thymus, although the precise isoform varies according to tissue type. Progenitor cell layers of skin, breast, eye and prostate express high levels of DeltaN-type isoforms. Isoform 10 is predominantly expressed in skin squamous cell carcinomas, but not in normal skin tissues.

Cellular localization

Alternative names

KET, P63, P73H, P73L, TP73L, TP63, Tumor protein 63, p63, Chronic ulcerative stomatitis protein, Keratinocyte transcription factor KET, Transformation-related protein 63, Tumor protein p73-like, p40, p51, CUSP, p73L

swissprot:Q9H3D4 omim:603273 entrezGene:8626