Anti-TP63 monoclonal antibody, clone 5F6

Name: Anti-TP63 monoclonal antibody, clone 5F6
SKU: DCABH-13807
Rating: 5 (1 reviews)

Mouse anti-Human TP63 monoclonal antibody for WB, IHC-P, ELISA

Write a review

COA

SDS

Datasheet

Summary

Specifications

Clone

5F6

Species Reactivity

Human; Monkey; Mouse; Rat

Immunogen

A synthetic peptide corresponding to human TP63.

Conjugate

Unconjugated

Applications

Application Notes

ELISA (1:10000); WB (1:500-1:2000); Immunohistochemistry (1:200-1:1000) & The optimal working dilution should be determined by the end user.

Target

Alternative Names

TP63; tumor protein p63; TP53CP, TP53L, TP73L, tumor protein p53 competing protein , tumor protein p53 like , tumor protein p73 like; tumor protein 63; EEC3; KET; NBP; OFC8; p51; p53CP; p63; p73H; p73L; SHFM4; CUSP; transformation-related protein 63; tumo

Entrez Gene ID

8626

UniProt ID

Q9H3D4

Product Background

Antigen Description

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.

Pathway

Apoptosis, organism-specific biosystem; Direct p53 effectors, organism-specific biosystem; TP53 network, organism-specific biosystem;

Citations

Have you cited DCABH-13807 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

The regulation of hydroxysteroid 17 beta-dehydrogenase type 1 and 2 gene expression in breast cancer cell lines by estradiol, dihydrotestosterone, microRNAs, and genes related to breast cancer

ONCOTARGET

Authors: Hilborn, Erik; Stal, Olle; Alexeyenko, Andrey; Jansson, Agneta

Abstract

Aim. To investigate the influence of estrogen, androgen, microRNAs, and genes implicated in breast cancer on the expression of HSD17B1 and HSD17B2. Materials. Breast cancer cell lines ZR-75-1, MCF7, T47D, SK-BR-3, and the immortalized epithelial cell line MCF10A were used. Cells were treated either with estradiol or dihydrotestosterone for 6, 24, 48 hours, or 7 days or treated with miRNAs or siRNAs predicted to influence HSD17B expression Results and discussion. Estradiol treatment decreased HSD17B1 expression and had a time-dependent effect on HSD17B2 expression. This effect was lost in estrogen receptor-alpha down-regulated or negative cell lines. Dihydrotestosterone treatment increased HSD17B2 expression, with limited effect on HSD17B1 expression. No effect was seen in cells without AR or in combination with the AR inhibitor hydroxyflutamide. The miRNA-17 up-regulated HSD17B1, while miRNA-210 and miRNA-7-5p had up- and down-regulatory effect and miRNA-1304-3p reduced HSD17B1 expression. The miRNA-204-5p, 498, 205-3p and 579-3p reduced HSD17B2 expression. Downregulation of CX3CL1, EPHB6, and TP63 increased HSD17B1 and HSD17B2 expression, while GREB1 downregulation suppressed HSD17B1 and promoted HSD17B2 expression. Conclusion. We show that HSD17B1 and HSD17B2 are controlled by estradiol, dihydrotestosterone, and miRNAs, as well as modulated by several breast cancer-related genes, which could have future clinical applications.

Ectrodactyly, ectodermal dysplasia, cleft lip, and palate (EEC syndrome) with Tetralogy of Fallot: a very rare combination

FRONTIERS IN PEDIATRICS

Authors: Sharma, Deepak; Kumar, Chetan; Bhalerao, Sanjay; Pandita, Aakash; Shastri, Sweta; Sharma, Pradeep

Abstract

Ectrodactyly, ectodermal dysplasia, and cleft lip/palate syndrome (EEC) syndrome is a rare genetic disorder with an incidence of around 1 in 90,000 in population. It is known with various names including split hand-split foot-ectodermal dysplasia-cleft syndrome or split hand, cleft hand, or lobster claw hand/foot. We report first case of EEC with associated heart disease (Tetralogy of Fallot) who was diagnosed as EEC on the basis of clinical features and EEC was confirmed with genetic analysis.