CDKN2A/p19ARF Rabbit pAb
CDKN2A/p19ARF Rabbit pAb
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Application
| IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | P51480 |
| Reactivity | Rat |
| Predicted | Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 17941 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from mouse CDKN2A/p19ARF |
| Epitope Specificity | 65-169/169 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Cytoplasm. Nucleus. |
| DISEASE | Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:155601]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites. Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:606719]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:151623]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. [DISEASE] Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:155755]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene. [provided by RefSeq, Sep 2012]. |
| Gene ID | 12578 |
|---|---|
| Other Names | Cyclin-dependent kinase inhibitor 2A {ECO:0000312|MGI:MGI:104738}, Cyclin-dependent kinase 4 inhibitor A, CDK4I, p16-INK4a, p16-INK4, Cdkn2a {ECO:0000312|MGI:MGI:104738}, P16ink4a |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | Cdkn2a {ECO:0000312|MGI:MGI:104738} |
|---|---|
| Synonyms | P16ink4a |
| Function | Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein. |
| Cellular Location | Cytoplasm. Nucleus. |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
REFERENCES
Quelle D.E.,et al.Oncogene 11:635-645(1995).
Zhang S.,et al.Proc. Natl. Acad. Sci. U.S.A. 95:2429-2434(1998).
Gong Z.,et al.Submitted (DEC-2000) to the EMBL/GenBank/DDBJ databases.
Carninci P.,et al.Science 309:1559-1563(2005).
Church D.M.,et al.PLoS Biol. 7:E1000112-E1000112(2009).
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