CDKN2A/p14ARF Antibody [A5L13] | Primary Antibodies

Application: Reactivity: Human

Lane 1: PC-3, Lane 2: Hela

Usage Information

Dilution
WB1:1000 IP1:80 IF1:250 FCM1:120

Application
WB, IP, IF, FCM

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 Observed MW
14 kDa 14 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
CDKN2A/p14ARF Antibody [A5L13] detects endogenous levels of total CDKN2A/p14ARF protein.

Clone
A5L13

Synonym(s)
CDKN2; MLM; CDKN2A; Tumor suppressor ARF; Alternative reading frame; Cyclin‑dependent kinase inhibitor 2A; p14ARF; ARF

Background
CDKN2A/p14ARF, encoded by the INK4a/ARF locus, functions as a pivotal tumor suppressor protein that diverges from its p16INK4a sibling through alternative reading frame usage, primarily stabilizing p53 to enforce cell cycle checkpoints and apoptosis. It features a compact structure with two α-helical domains that mediate high-affinity binding to MDM2, sequestering this E3 ligase in the nucleolus to prevent p53 ubiquitination and degradation, thereby amplifying p53-dependent transcription of p21 and BAX while licensing DNA damage-induced G1 arrest and caspase activation. This nucleolar detention of MDM2 integrates p14ARF into the ARF-MDM2-p53 signaling axis, where hyperproliferative signals like oncogenic MYC or RAS trigger ARF induction via E2F1 derepression, creating a surveillance mechanism that couples aberrant mitogenic drive to p53 restoration; concurrently, p14ARF binds E2F1 to directly blunt its transactivation of S-phase genes and interacts with TOP1 to enhance rRNA synthesis while promoting NPM1 polyubiquitination for ribosome biogenesis control. p14ARF inhibits cyclin B1-CDK1 complexes for G2/M blockade and represses BCL6 transcriptional activity, ensuring robust antiproliferative barriers in epithelial and hematopoietic contexts. This position p14ARF as a guardian of tissue homeostasis during development and regeneration, ideal for researchers probing oncogene-induced senescence in co-culture assays or dissecting nucleolar stress responses with isoform-specific knockdowns. Inactivation via homozygous deletion or methylation unleashes MDM2 hyperactivity in cancers like melanoma, pancreatic adenocarcinoma, and gliomas. Its inducible expression and short half-life offer experimental precision for synthetic lethality screens targeting MDM2, with therapeutic restoration via gene therapy showing promise in p53-wildtype malignancies.

Background

CDKN2A/p14ARF, encoded by the INK4a/ARF locus, functions as a pivotal tumor suppressor protein that diverges from its p16INK4a sibling through alternative reading frame usage, primarily stabilizing p53 to enforce cell cycle checkpoints and apoptosis. It features a compact structure with two α-helical domains that mediate high-affinity binding to MDM2, sequestering this E3 ligase in the nucleolus to prevent p53 ubiquitination and degradation, thereby amplifying p53-dependent transcription of p21 and BAX while licensing DNA damage-induced G1 arrest and caspase activation. This nucleolar detention of MDM2 integrates p14ARF into the ARF-MDM2-p53 signaling axis, where hyperproliferative signals like oncogenic MYC or RAS trigger ARF induction via E2F1 derepression, creating a surveillance mechanism that couples aberrant mitogenic drive to p53 restoration; concurrently, p14ARF binds E2F1 to directly blunt its transactivation of S-phase genes and interacts with TOP1 to enhance rRNA synthesis while promoting NPM1 polyubiquitination for ribosome biogenesis control. p14ARF inhibits cyclin B1-CDK1 complexes for G2/M blockade and represses BCL6 transcriptional activity, ensuring robust antiproliferative barriers in epithelial and hematopoietic contexts. This position p14ARF as a guardian of tissue homeostasis during development and regeneration, ideal for researchers probing oncogene-induced senescence in co-culture assays or dissecting nucleolar stress responses with isoform-specific knockdowns. Inactivation via homozygous deletion or methylation unleashes MDM2 hyperactivity in cancers like melanoma, pancreatic adenocarcinoma, and gliomas. Its inducible expression and short half-life offer experimental precision for synthetic lethality screens targeting MDM2, with therapeutic restoration via gene therapy showing promise in p53-wildtype malignancies.

References
https://pubmed.ncbi.nlm.nih.gov/11876522/ https://pubmed.ncbi.nlm.nih.gov/9724636/

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%