CDKN2D / p19ink4d抗体

CDKN2D / p19ink4d抗体产品信息免疫原 : Recombinant Human CDKN2D / p19ink4d protein (Catalog#12558-H09E)

Antibody Type : Mouse Monoclonal Antibody ( Mouse mAb Service Platform )
克隆号 : 06
抗体宿主 : Mouse IgG1
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 : This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human CDKN2D / p19ink4d (rh CDKN2D / p19ink4d; Catalog#12558-H09E; P55273; Met 10-Leu 166). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
CDKN2D / p19ink4d抗体 Background
Cyclin-dependent kinase inhibitor 2D (also known as CDKN2D or p19ink4d), a member of the INK4 family of cyclin-dependent kinase (CDK) inhibitors, negatively regulates the cyclin D-CDK4/6 complexes, which promote G1/S transition by phosphorylating the retinoblastoma tumor-suppressor gene product. It is clearly shown that DNA repair is the main target of p19ink4d effect and that diminished apoptosis is a downstream event. Experiments has uncovered a role of p19INK4d as a regulator of DNA-damage-induced apoptosis and suggest that it protects cells from undergoing apoptosis by allowing a more efficient DNA repair. It has been demonstrated that p19INK4d expression enhances cell survival under genotoxic conditions. p19INK4d expression correlates with the cellular resistance to UV treatment with increased DNA repair activity against UV-induced lesions. On the contrary, cells transfected with p19INK4d antisense cDNA show reduced ability to repair DNA damage and increased sensitivity to genotoxic insult when compared with their p19INK4d-overexpressing counterparts. Previous work has shown that inactivation of the cyclin-dependent kinase inhibitor (CKI) p19 (Ink4d) leads to progressive hearing loss attributable to inappropriate DNA replication and subsequent apoptosis of hair cells. It may also involved in male reproductive function including testicular atrophy, alteration in serum follicle stimulating hormone, qualitative increase in germ cell apoptosis, and delayed kinetics of meiotic prophase markers.
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