Key features and details
- Rabbit polyclonal to CDKN2A/p14ARF
- Suitable for: IHC-P, IHC-Fr, WB, ICC/IF
- Reacts with: Human
- Isotype: IgG
CDKN2A/p14ARF 一次抗体 製品一覧
製品の詳細Rabbit polyclonal to CDKN2A/p14ARF
アプリケーション適用あり: IHC-P, IHC-Fr, WB, ICC/IFmore details
Synthetic peptide within Human CDKN2A/p14ARF (C terminal). The exact sequence is proprietary.
- ICC/IF: HeLa cells. IHC-P: Lymphoma tissue.
This product is FOR RESEARCH USE ONLY. For commercial use, please contact firstname.lastname@example.org.
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保存方法Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Preservative: 0.1% Sodium azide
Constituents: PBS, 1% BSA
Concentration information loading...
精製度Immunogen affinity purified
Our Abpromise guarantee covers the use of ab3642 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/25. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.|
|IHC-Fr||Use at an assay dependent concentration.|
|WB||Use a concentration of 1 - 2 µg/ml. Detects a band of approximately 14 kDa (predicted molecular weight: 14 kDa).|
|ICC/IF||Use a concentration of 1 µg/ml.|
関連性The gene for CDK2NA generates several transcripts/proteins which differ from each other in their first exons. Three of these transcripts are generated by alternative splicing (isoform 1 a.k.a p16INK4A, isoform 2 and isoform 3 a.k.a p12), two of which are known to function as inhibitors of CDK4 kinase. One other transcript that is generated from this gene contains an alternate reading frame (ARF), with the first exon located 20kb upstream of the remainder of the gene(isoform 4 a.k.a. p14ARF, p19ARF, ARF). In spite of the structural and some functional differences, all the proteins encoded by the CDKN2A gene are involved in cell cycle G1 control.
細胞内局在Cytoplasmic and Nuclear
- ARF antibody
- CDK4 inhibitor p16 INK4 antibody
- CDK4I antibody
Confocal image showing nuclear staining increased after HeLa cells transfected with CDKN2A/p14ARF.
ICC/IF image of ab3642 stained HeLa cells. The cells were 4% paraformaldehyde fixed and then incubated in 0.1% trixtonX-100 to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with primary antibody ab3642 at a dilution of 1/250. An AlexaFluor®594 goat anti-mouse secondary IgG (ab150077) was used at a 1/1000 dilution. Anti-tubulin (ab7291) and an AlexaFluor®594 goat anti-mouse IgG (ab150120) were used as counterstains, both at a dilution of 1/1000. DAPI was used to stain the cell nuclei blue.
This image was kindly supplied as part of the review submitted by Joost van Galen.
ICC/IF image of ab3642 stained HeLa cells. The cells were 4% formaldehyde fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody ab3642 at 1µg/ml overnight at +4°C. The secondary antibody (green) was DyLight® 488 goat anti- rabbit (ab96899) IgG (H+L) used at a 1/250 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
ab3642 は 15 報の論文で使用されています。
- Cui L et al. Overexpression of CCDC69 activates p14ARF/MDM2/p53 pathway and confers cisplatin sensitivity. J Ovarian Res 12:4 (2019). PubMed: 30651135
- Sargen MR et al. Biomarker discovery analysis: Alterations in p14, p16, p53, and BAP1 expression in nevi, cutaneous melanoma, and metastatic melanoma. Pigment Cell Melanoma Res 32:474-478 (2019). PubMed: 30672662
- Liang J et al. CDKN2A inhibits formation of homotypic cell-in-cell structures. Oncogenesis 7:50 (2018). PubMed: 29904067
- Xie H & Wang H PRL-3 promotes breast cancer progression by downregulating p14ARF-mediated p53 expression. Oncol Lett 15:2795-2800 (2018). PubMed: 29435006
- Yosef R et al. Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL. Nat Commun 7:11190 (2016). PubMed: 27048913