|Immunohistochemistry (Paraffin) (IHC (P))||1:25|
|Tested Species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide derived from C-terminus of human p14|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS, pH 7.6, with 1% BSA|
|Contains||<0.1% sodium azide|
|Storage conditions||4° C, do not freeze|
Heat-mediated antigen retrieval is recommended prior to staining, using a 10mM citrate buffer, pH 6.0, for 10 minutes followed by cooling at room temperature for 20 min. Following antigen retrieval, incubate samples with primary antibody for 30 min at room temperature. A suggested positive control is lymphoma.
The INK4a-ARF locus encodes two unrelated proteins both of which function in tumor suppression. p14ARF arrests the cell cycle in a p53-dependent manner. p14ARF binds to mdm2 and promotes the rapid degradation of mdm2 proteinrequired for mdm2 modification and concurrent p53 stabilization and accumulation. This interaction is mediated by the exon 1Beta-encoded N-terminal domain of p14ARF and a C-terminal region of mdm2. Deletion of the ARF-INK4a locus simultaneously impairs both the INK4a-cyclin D/cdk4-RB and the ARF-mdm2-p53 pathways.
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Protein Aliases: Alternative reading frame; ARF; CDK4 inhibitor p16-INK4; CDK4I; CDKN2; cell cycle negative regulator beta; CMM2; Cyclin-dependent kinase 4 inhibitor A; Cyclin-dependent kinase inhibitor 2A; cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4); cyclin-dependent kinase inhibitor 2A melanoma; inhibits CDK4; INK4; INK4A; MLM; MTS-1; MTS1; Multiple tumor suppressor 1; P14ARF; P16; p16-INK4; P16-INK4A; P16INK4; P16INK4A; P19ARF; TP16; Tumor suppressor ARF
Gene Aliases: ARF; CDK4I; CDKN2; CDKN2A; CMM2; INK4; INK4A; MLM; MTS-1; MTS1; P14; P14ARF; P16; P16-INK4A; P16INK4; P16INK4A; P19; P19ARF; TP16
UniProt ID: (Human) P42771
Entrez Gene ID: (Human) 1029
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