p63 (D9L7L) XP® Rabbit mAb (BSA and Azide Free) #64471
- WB
- IHC
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 75 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This product is the carrier-free version of product #39692. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN, or CUT&Tag assays. If you require a carrier-free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Supplied in 1X PBS, BSA and Azide Free.
For standard formulation of this product see product #39692.
Storage
Specificity / Sensitivity
p63 (D9L7L) XP® Rabbit mAb (BSA and Azide Free) 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).
Limited Uses
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