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Genes (Basel). 2010 Sep 30;1(3):335-48. doi: 10.3390/genes1030335.

Role of Cell Division Autoantigen 1 (CDA1) in Cell Proliferation and Fibrosis.

Genes

Ban-Hock Toh, Yugang Tu, Zemin Cao, Mark E Cooper, Zhonglin Chai

Affiliations

  1. Autoimmunity Laboratory, Centre for Inflammatory Diseases, Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria 3168, Australia. [email protected].
  2. Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. [email protected].
  3. Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. [email protected].
  4. Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. [email protected].
  5. Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. [email protected].

PMID: 24710090 PMCID: PMC3966230 DOI: 10.3390/genes1030335

Abstract

Cell Division Autoantigen 1 (CDA1) was discovered following screening a human expression library with serum from a patient with Discoid Lupus Erythematosus. CDA1, encoded by TSPYL2 on the X chromosome, shares anti-proliferative and pro‑fibrotic properties with TGF-b. It inhibits cell growth through p53, pERK1/2 and p21‑mediated pathways and is implicated in tumorigenesis and the DNA damage response. Its pro-fibrotic property is mediated through cross-talk with TGF-b that results in upregulation of extracellular matrix proteins. The latter properties have identified a key role for CDA1 in diabetes associated atherosclerosis. These dual properties place CDA1 as an attractive molecular target for treating tumors and vascular fibrosis including atherosclerosis and other vascular disorders associated with enhanced TGF-β action and tissue scarring.

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