CDKN2D / p19ink4d Protein (GST Tag)

Cyclin-dependent kinase inhibitor 2D (p19, inhibits CDK4) Protein Datasheet

CDKN2D / p19ink4d Protein Product Information

• Synonym: INK4D, p19, p19-INK4D
• Protein Construction: A DNA sequence encoding the human CDKN2D (P55273) (Met 10-Leu 166) was fused with the GST tag at the N-terminus.
• Source: Human
• Expression Host: E.Coli

CDKN2D / p19ink4d Protein QC Testing

• Purity: >90 % as determined by SDS-PAGE.
• Endotoxin: Please contact us for more information.
• Stability: Samples are stable for up to twelve months from date of receipt at -70℃
• Predicted N terminal: Met
• Molecular Mass: The recombinant human CDKN2D/GST chimera consists of 400 amino acids and has a predicted molecular mass of 44.9 kDa. It migrates as an approxiamtely 46 KDa band in SDS-PAGE under reducing conditions.
• Formulation: Lyophilized from sterile PBS, pH7.5
  1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
  2. Please contact us for any concerns or special requirements.
• SDS-PAGE: CDKN2D / p19ink4d protein

CDKN2D / p19ink4d Protein Usage Guide

• Storage: Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

CDKN2D / p19ink4d Protein Description

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.

References

1. Buchold GM. et al., 2007, Mol Reprod Dev. 74 (8): 1008-20.
2. Laine H. et al., 2007, J Neurosci. 27 (6): 1434-44.
3. Ceruti JM. et al., 2005, Oncogene. 24 (25): 4065-80.