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CDKN2D / p19ink4d Antibody, Mouse MAb

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    Human CDKN2D/p19ink4d Antibody Product Information
    Immunogen:Recombinant Human CDKN2D / p19ink4d protein (Catalog#12558-H09E)
    Clone ID:06
    Ig Type:Mouse IgG1
    Concentration:
    Endotoxin:
    Formulation:0.2 μm filtered solution in PBS with 5% trehalose
    Preparation: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.
    Other CDKN2D/p19ink4d Antibody Products
    CDKN2D/p19ink4d 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. 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. 

    Human CDKN2D/p19ink4d References
  • Buchold GM, et al. (2007) Mice lacking cyclin-dependent kinase inhibitor p19Ink4d show strain-specific effects on male reproduction. Mol Reprod Dev. 74 (8): 1008-20.
  • Laine H, et al. (2007) p19(Ink4d) and p21(Cip1) collaborate to maintain the postmitotic state of auditory hair cells, their codeletion leading to DNA damage and p53-mediated apoptosis. J Neurosci. 27 (6): 1434-44.
  • Ceruti JM, et al. (2005) Induction of p19INK4d in response to ultraviolet light improves DNA repair and confers resistance to apoptosis in neuroblastoma cells. Oncogene. 24 (25): 4065-80.
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    Catalog: 12558-MM06-50
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    Datasheet & Documentation

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    Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"