Key features and details
- Mouse monoclonal [4E5] to p63
- Suitable for: Flow Cyt, WB, ELISA, IHC-P
- Reacts with: Mouse, Rat, Human
- Isotype: IgG1
Product nameAnti-p63 antibody [4E5]
See all p63 primary antibodies
DescriptionMouse monoclonal [4E5] to p63
Tested applicationsSuitable for: Flow Cyt, WB, ELISA, IHC-Pmore details
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide of Human p63.
- A431, HeLa, Jurkat, THP1, NIH 3T3, COS7 and PC12 cell lysates. Ovarian cancer and lung cancer tissue.
This product was changed from ascites to supernatant. Lot no’s high than GR118984-25 are from Tissue Culture Supernatant
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Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferPreservative: 0.05% Sodium azide
Concentration information loading...
PurityProtein G purified
Purification notesPurified from tissue culture supernatant.
Our Abpromise guarantee covers the use of ab110038 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody.
|WB||1/500 - 1/2000. Detects a band of approximately 51 kDa (predicted molecular weight: 77 kDa).|
|IHC-P||1/200 - 1/1000.|
FunctionActs 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. 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.
Tissue specificityWidely 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.
Involvement in diseaseDefects in TP63 are the cause of acro-dermato-ungual-lacrimal-tooth syndrome (ADULT syndrome) [MIM:103285]; a form of ectodermal dysplasia. Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. 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 differs significantly from EEC3 syndrome by the absence of facial clefting.
Defects in TP63 are the cause of ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) [MIM:106260]. AEC is 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.
Defects in TP63 are the cause of ectrodactyly-ectodermal dysplasia-cleft lip/palate syndrome type 3 (EEC3) [MIM:604292]. EEC3 is an autosomal dominant syndrome characterized by ectrodactyly of hands and feet, ectodermal dysplasia and facial clefting.
Defects in TP63 are the cause of split-hand/foot malformation type 4 (SHFM4) [MIM:605289]. Split-hand/split-foot malformation is 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. There is restricted overlap between the mutational spectra of EEC3 and SHFM4.
Defects in TP63 are the cause of limb-mammary syndrome (LMS) [MIM:603543]. LMS is characterized by ectrodactyly, cleft palate and mammary-gland abnormalities.
Note=Defects in TP63 are a cause of cervical, colon, head and neck, lung and ovarian cancers.
Defects in TP63 are a cause of ectodermal dysplasia Rapp-Hodgkin type (EDRH) [MIM:129400]; also called Rapp-Hodgkin syndrome or anhidrotic ectodermal dysplasia with cleft lip/palate. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. EDRH is 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.
Defects in TP63 are the cause of non-syndromic orofacial cleft type 8 (OFC8) [MIM:129400]. Non-syndromic orofacial cleft is a common 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.
Sequence similaritiesBelongs to the p53 family.
Contains 1 SAM (sterile alpha motif) domain.
DomainThe transactivation inhibitory domain (TID) can interact with, and inhibit the activity of the N-terminal transcriptional activation domain of TA*-type isoforms.
modificationsMay be sumoylated.
Ubiquitinated. Polyubiquitination involves WWP1 and leads to proteasomal degradation of this protein.
- Information by UniProt
- AIS antibody
- Amplified in squamous cell carcinoma antibody
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Overlay histogram showing A431 cells stained with ab110038 (red line). The cells were fixed with 80% methanol (5 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab110038, 1/100 dilution) for 30 min at 22ºC. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22ºC. Isotype control antibody (black line) was mouse IgG1 [ICIGG1] (ab91353, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed. This antibody gave a positive signal in A431 cells fixed with 4% paraformaldehyde (10 min)/permeabilized with 0.1% PBS-Tween for 20 min used under the same conditions.
ab110038 at 1/200 dilution staining p63 in paraffin-embedded ovarian cancer tissue by Immunohistochemistry. Detection utilised DAB staining.
All lanes : Anti-p63 antibody [4E5] (ab110038) at 1/500 dilution
Lane 1 : A431 cell lysate.
Lane 2 : HeLa cell lysate.
Lane 3 : Jurkat cell lysate.
Lane 4 : THP1 cell lysate.
Lane 5 : NIH 3T3 cell lysate.
Lane 6 : COS-7 (African green monkey kidney fibroblast-like cell line) cell lysate.
Lane 7 : PC12 cell lysate.
Predicted band size: 77 kDa
Observed band size: 51 kDa why is the actual band size different from the predicted?
ab110038 should be used at a proposed dilution of 1/10000 for ELISA.
ab110038 at 1/200 dilution staining p63 in paraffin-embedded lung cancer tissue by Immunohistochemistry. Detection utilised DAB staining.
ab110038 has been referenced in 2 publications.
- Chen R et al. CD147 deficiency in T cells prevents thymic involution by inhibiting the EMT process in TECs in the presence of TGFß. Cell Mol Immunol N/A:N/A (2020). PubMed: 31900457
- Pérez-Mancera PA et al. The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma. Nature 486:266-70 (2012). WB . PubMed: 22699621