A Genetic Model for Deoxycytidine Kinase Deficiency
- 技術應用
- 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
- 詳細技術說明
- 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.
- *Abstract
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None
- *Principal Investigation
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Name: Wayne Austin
Department:
Name: Dean Campbell
Department:
Name: Johannes Czernin
Department:
Name: Hsiang I Liao
Department:
Name: Caius Radu
Department:
Name: Nagichettiar Satyamurthy
Department:
Name: Gerald Toy
Department:
Name: Owen Witte
Department:
- 其他
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State Of Development
The deoxycytidine kinase (dCK) conditional knockout mouse has been generated and validated.
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.
Related Materials
Nucleoside salvage pathway kinases regulate hematopoiesis by linking nucleotide metabolism with replication stress. J Exp Med. (2012)
Requirement for deoxycytidine kinase in T and B lymphocyte development. Proc Natl Acad Sci U S A. (2010)Tech ID/UC Case
22995/2010-015-0
Related Cases
2010-015-0
- 國家/地區
- 美國
