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p63 (D9L7L) XP® Rabbit mAb #39692

Filter:
  • WB
  • IP
  • IHC
  • IF
Western Blotting Image 1: p63 (D9L7L) XP® Rabbit mAb
Western blot analysis of extracts from various cell lines cells using p63 (D9L7L) XP® Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).

To Purchase # 39692

Supporting Data

REACTIVITY H
SENSITIVITY Endogenous
MW (kDa) 75
Source/Isotype Rabbit IgG
Application Key:
  • WB-Western Blotting 
  • IP-Immunoprecipitation 
  • IHC-Immunohistochemistry 
  • IF-Immunofluorescence 
Species Cross-Reactivity Key:
  • H-Human 
  • Related Products

Product Information

Product Usage Information

Application Dilution
Western Blotting 1:1000
Immunoprecipitation 1:50
Immunohistochemistry (Paraffin) 1:450 - 1:1800
Immunofluorescence (Immunocytochemistry) 1:400 - 1:1600

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

For a carrier-free (BSA and azide free) version of this product see product #64471.

Protocol

Specificity / Sensitivity

p63 (D9L7L) XP® Rabbit mAb recognizes endogenous levels of total p63. Based on the sequence of the immunogenic peptide, this antibody is expected to recognize both full length (TA) p63 as well as DeltaN p63 isoforms that contain exon 4, such as alpha, beta, and gamma. This antibody will not detect DeltaNp73L (Q9H3D4-10/NM_001329146.1).

Species Reactivity:

Human

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asn118 of human p63 protein.

Background

The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head, and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy terminus yields the α, β, and γ isoforms (3,4).
For Research Use Only. Not For Use In Diagnostic Procedures.
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