A Genetic Model for Deoxycytidine Kinase Deficiency

Tech ID: 22995 / UC Case 2010-015-0

Background

Production and maintenance of a balanced pool of deoxyribonucleoside triphosphates (dNTPs) for DNA synthesis is of critical importance for cell division.  Cellular dNTP pools are generated by two biosynthetic pathways: de novo synthesis and deoxyribonucleoside salvage.  Amongst salvage pathway enzymes, deoxycytidine kinase (dCK) has unique properties: it provides cells with all 4 dNTPs required for DNA synthesis (dATP, dCTP, dGTP, dTTP) and activates many pro-drugs that are widely used in cancer, autoimmunity and viral infections such as gemcitabine, fludarabine and cladribine.  dCK is highly expressed in hematopoietic/lymphoid cells and is also overexpressed in lymphoid malignancies and in some solid tumors.  These properties make dCK an attractive therapeutic and imaging target.

Innovation

Researchers at UCLA have generated a novel deoxycytidine kinase (dCK) conditional knockout mouse to better understand the function of the deoxyribonucleoside salvage pathway and identify new therapeutic targets for immune disorders and cancer.

Applications

  • Develop new therapeutics for cancer and autoimmune disorders
  • Identify and characterize agents that bind deoxycytidine kinase and/or modulate its activity
  • Identify biological processes in which dCK plays a critical role
  • Indentify small molecule dCK inhibitors

State Of Development

The deoxycytidine kinase (dCK) conditional knockout mouse has been generated and validated.

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Inventors

  • Radu, Caius G.

Other Information

Keywords

Research tool, mouse model, deoxycytidine kinase, dCK, knockout mouse, immune disorders, deoxyribonucleoside salvage, cancer

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