- Tel: 858.663.9055
-
Email: info@nsjbio.com
- Tel: 858.663.9055
- Email: info@nsjbio.com
CDKN2A Antibody Recombinant Mouse MAb / P16INK4a [clone rCDKN2A/8004] (V5277)
Email: info@nsjbio.com
| Catalog No | Formulation | Size | Price (USD) | ||
|---|---|---|---|---|---|
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V5277-100UG | 0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced), 0.05% sodium azide | 100 ug | 559 | |
|
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V5277-20UG | 0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced), 0.05% sodium azide | 20 ug | 259 | |
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V5277SAF-100UG | 1 mg/ml in 1X PBS; BSA free, sodium azide free | 100 ug | 559 |
|
| Availability | 1-3 business days |
| Species Reactivity | Human |
| Format | Purified |
| Host | Mouse |
| Clonality | Recombinant Mouse Monoclonal |
| Isotype | Mouse IgG1, kappa |
| Clone Name | rCDKN2A/8004 |
| Purity | Protein A/G affinity |
| UniProt | P42771 |
| Localization | Nucleus, Cytoplasm |
| Applications | Immunohistochemistry (FFPE) : 1-2ug/ml for 30 min at RT |
| Limitations | This CDKN2A antibody is available for research use only. |
|
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CDKN2A antibody recognizes Cyclin-dependent kinase inhibitor 2A, the tumor suppressor protein commonly referred to as p16INK4a, encoded by the CDKN2A gene on chromosome 9p21.3. CDKN2A Antibody Recombinant Mouse MAb is developed for detection of this critical cell cycle regulator in research applications involving normal and neoplastic tissues. The p16INK4a protein localizes predominantly to the nucleus, with additional cytoplasmic presence, where it binds CDK4 and CDK6 to inhibit phosphorylation of the retinoblastoma protein and block transition from G1 to S phase.
p16INK4a antibody, also referred to as CDKN2A antibody and INK4a antibody in the literature, targets a central component of the RB pathway. The CDKN2A locus is complex and produces multiple distinct proteins through alternative reading frames, including p14ARF, but p16INK4a specifically functions as an inhibitor of cyclin D-CDK4 and cyclin D-CDK6 complexes. Loss of CDKN2A function through deletion, mutation, or promoter methylation is one of the most common molecular events in melanoma, pancreatic carcinoma, glioma, bladder carcinoma, and other human malignancies.
In normal tissues, p16INK4a expression is typically low but can increase during cellular senescence or in response to oncogenic stress. Marked overexpression is frequently observed in high-risk human papillomavirus-associated lesions, including cervical intraepithelial neoplasia and carcinoma, where viral oncoproteins inactivate RB, leading to compensatory upregulation of p16INK4a. As a result, CDKN2A antibody is widely used in research examining viral oncogenesis, cell cycle dysregulation, and tumor suppressor pathway alterations.
Structurally, p16INK4a contains ankyrin repeat motifs that mediate interaction with CDK4 and CDK6. By maintaining RB in a hypophosphorylated, growth-suppressive state, p16INK4a enforces cell cycle arrest and prevents inappropriate entry into S phase. Disruption of this regulatory axis contributes directly to uncontrolled cellular proliferation and tumor progression.
The recombinant mouse monoclonal clone rCDKN2A/8004 provides specific detection of p16INK4a in formalin-fixed tissues and cell-based systems. Visualization of nuclear and cytoplasmic staining patterns supports evaluation of CDKN2A expression status and investigation of RB pathway integrity in research settings at NSJ Bioreagents.
Optimal dilution of the CDKN2A antibody recombinant mouse mAb should be determined by the researcher.
Purified recombinant prokaryotic full-length human protein was used as the immunogen for the CDKN2A antibody recombinant mouse mAb.
Aliquot the CDKN2A antibody and store frozen at -20oC or colder. Avoid repeated freeze-thaw cycles.
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