p63 Antibody [C10M16] | Primary Antibodies

Application: Reactivity: Human

Lane 1: HaCAT, Lane 2: ME-180

Usage Information

Dilution
WB1:1000 IP1:50 IHC1:450 - 1:1800 IF1:450 - 1:1800

Application
WB, IP, IHC, IF

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
75 kDa

Positive Control	Human intraductal and infiltrating carcinoma of the breast; Human prostate carcinoma; ME-180 cells; HaCaT cells; NHEK cells
Negative Control	MCF7 cells

Datasheet & SDS

Biological Description

Specificity
p63 Antibody [C10M16] detects endogenous levels of total p63 protein.

Clone
C10M16

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

Background
p63 (TP63) is a transcription factor from the p53 family, essential for epithelial development and stratification, and is expressed as two main isoforms, TAp63, which contains an N-terminal transactivation domain, and ΔNp63, a truncated variant predominant in basal keratinocytes—produced via alternative promoters and splicing (α/β/γ). p63 features an N-terminal TA domain (present in TAp63 only) for mediator recruitment, a proline-rich region (PRR) with PXXP motifs for SH3 interactions, a core DNA-binding domain (DBD, ~residues 190–300) with an immunoglobulin-like fold and specialized loops and helices for sequence-specific DNA recognition (with unique tolerance for half-site spacers), an oligomerization domain (four-helix bundle forming a tetramer of dimers), a sterile alpha motif (SAM, for protein-protein interactions except in γ isoforms), and a transinhibition domain (TID) regulating activity. TAp63α induces cell cycle arrest and apoptosis via p53-like targets (PUMA, NOXA, P21) during genotoxic stress through ATM/Chk2-mediated phosphorylation that relieves autoinhibition, and enforces epidermal progenitor maintenance by repressing epidermal differentiation complex (EDC) enhancers while activating KLF4 and SOX2. ΔNp63α, on the other hand, sustains basal keratinocyte self-renewal by repressing miR-205/124 and TGF-β/SMAD signaling, while YAP/TEAD coactivation and SAM-mediated recruitment of ETS2/EP300 amplify EDC shutdown and super-enhancer formation, thereby blocking terminal differentiation. p63 tetramers scan DNA through 1D sliding and 3D hopping, with cooperative binding enabled by unique half-site spacing preferences. Mutations in the DBD (e.g., R311H) or SAM domain disrupt DNA affinity and oligomer stability, resulting in ectodermal dysplasia syndromes (EEC, ADULT) with limb and skin defects. ΔNp63 overexpression drives squamous cell carcinoma progression (lung, head and neck) through metabolic reprogramming (GLUT1, PKM2) and immune evasion (PD-L2), whereas TAp63 acts as a tumor suppressor in UV-induced skin cancers.

Background

p63 (TP63) is a transcription factor from the p53 family, essential for epithelial development and stratification, and is expressed as two main isoforms, TAp63, which contains an N-terminal transactivation domain, and ΔNp63, a truncated variant predominant in basal keratinocytes—produced via alternative promoters and splicing (α/β/γ). p63 features an N-terminal TA domain (present in TAp63 only) for mediator recruitment, a proline-rich region (PRR) with PXXP motifs for SH3 interactions, a core DNA-binding domain (DBD, ~residues 190–300) with an immunoglobulin-like fold and specialized loops and helices for sequence-specific DNA recognition (with unique tolerance for half-site spacers), an oligomerization domain (four-helix bundle forming a tetramer of dimers), a sterile alpha motif (SAM, for protein-protein interactions except in γ isoforms), and a transinhibition domain (TID) regulating activity. TAp63α induces cell cycle arrest and apoptosis via p53-like targets (PUMA, NOXA, P21) during genotoxic stress through ATM/Chk2-mediated phosphorylation that relieves autoinhibition, and enforces epidermal progenitor maintenance by repressing epidermal differentiation complex (EDC) enhancers while activating KLF4 and SOX2. ΔNp63α, on the other hand, sustains basal keratinocyte self-renewal by repressing miR-205/124 and TGF-β/SMAD signaling, while YAP/TEAD coactivation and SAM-mediated recruitment of ETS2/EP300 amplify EDC shutdown and super-enhancer formation, thereby blocking terminal differentiation. p63 tetramers scan DNA through 1D sliding and 3D hopping, with cooperative binding enabled by unique half-site spacing preferences. Mutations in the DBD (e.g., R311H) or SAM domain disrupt DNA affinity and oligomer stability, resulting in ectodermal dysplasia syndromes (EEC, ADULT) with limb and skin defects. ΔNp63 overexpression drives squamous cell carcinoma progression (lung, head and neck) through metabolic reprogramming (GLUT1, PKM2) and immune evasion (PD-L2), whereas TAp63 acts as a tumor suppressor in UV-induced skin cancers.

References
https://pubmed.ncbi.nlm.nih.gov/39791744/ https://pubmed.ncbi.nlm.nih.gov/21464285/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%