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|Tested species reactivity||Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide conjugated to KLH, derived from a sequence within residues 50-150 of mouse p19ARF. [Swiss-Prot #P51480]|
|Purification||Antigen affinity chromatography|
|Storage buffer||tris citrate, pH 7-8|
|Contains||0.1% sodium azide|
|Storage Conditions||Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Tested Applications||Dilution *|
|Immunohistochemistry (IHC)||1 µg/ml|
|Immunohistochemistry (Frozen) (IHC (F))||1 µg/ml|
|Immunohistochemistry (Paraffin) (IHC (P))||1 µg/ml|
|Western Blot (WB)||2 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
The target sequence has 93% sequence homology with rat, 86% sequence homology with porcine and 80% sequence homology with human.
The INK4a/ARF locus encodes two unrelated tumor suppressor proteins, p16INK4a and p19ARF. These proteins restrain cell growth by modifying the functions of the retinoblastoma protein and p53, respectively. INK4a/ARF is among the most frequently mutated tumor suppressor loci in human cancer. Both p16INK4a and p19ARF act as cell proliferation inhibitors. The ARF gene, p19ARF in mouse and p14ARF in human, has become an important player in cell cycle regulation. In mice, tumor suppressor effects appear to be mediated by interactions between p19ARF and the p53 tumor suppressor protein. p19ARF counters uncontrolled proliferation and oncogenic signals in p53 dependent pathways. Proteins encoded by the INK4a/ARF locus also play a role in Abelson virus transformation. Both p16INK4a and p19ARF are expressed in many cells as they emerge from the apoptotic crisis that characterizes the transformation process. p19ARF is an important part in cellular defense against transforming signals from the Abl oncoprotein, providing direct evidence that the p19ARF-p53 regulatory loop plays an important role in lymphoma induction.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
alternative reading frame; Arf; ARF-INK4a; CDK4I; cdkn2a; cyclin-dependent kinase 4 inhibitor A; cyclin-dependent kinase inhibitor 2A; cyclin-dependent kinase inhibitor 2A (p16, inhibits CDK4); cyclin-dependent kinase inhibitor 2A, isoform 3; cyclin-dependent kinase inhibitor 2A, isoforms 1/2; cyclin-dependent kinase inhibitor protein; INK4a-ARF; Ink4a/Arf; mitochondrial smARF; MTS1; p16; p16(INK4a); p16-INK4; p16-INK4a; p16INK4a; p19<ARF>; Pctr1; RP23-166I8.5
Arf; ARF-INK4a; Cdkn2a; INK4a-ARF; Ink4a/Arf; MTS1; p16; p16(INK4a); P16ink4a; p19<ARF>; p19ARF; Pctr1