Severe fibronectin-deposit renal glomerular disease in mice lacking uteroglobin

Zhongjian Zhang, Gopal C. Kundu, Chiun-Jye Yuan, Jerrold M. Ward, Eric J. Lee, Francesco DeMayo, Heiner Westphal, Anil B. Mukherjee*

*此作品的通信作者

研究成果: Article同行評審

116 引文 斯高帕斯(Scopus)

摘要

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.

原文English
頁(從 - 到)1408-1412
頁數5
期刊Science
276
發行號5317
DOIs
出版狀態Published - 30 5月 1997

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