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Publication : Severe fibronectin-deposit renal glomerular disease in mice lacking uteroglobin.

First Author  Zhang Z Year  1997
Journal  Science Volume  276
Issue  5317 Pages  1408-12
PubMed ID  9162006 Mgi Jnum  J:40748
Mgi Id  MGI:892088 Doi  10.1126/science.276.5317.1408
Citation  Zhang Z, et al. (1997) Severe fibronectin-deposit renal glomerular disease in mice lacking uteroglobin. Science 276(5317):1408-12
abstractText  Despite myriads of biological activities ascribed to uteroglobin (UG), a steroid-inducible secreted protein, its physiological functions are unknown. Mice in which the uteroglobin gene was disrupted had severe renal disease that was associated with massive glomerular deposition of predominantly multimeric fibronectin (Fn), The molecular mechanism that normally prevents Fn deposition appears to involve high-affinity binding of UG with Fn to form Fn-UG heteromers that counteract Fn self-aggregation,which is required for abnormal tissue deposition, Thus, UG is essential for maintaining normal renal function in mice, which raises the possibility that an analogous pathogenic mechanism may underlie genetic Fn-deposit human glomerular disease.
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