Publication Date:
1997-05-30
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Z -- Kundu, G C -- Yuan, C J -- Ward, J M -- Lee, E J -- DeMayo, F -- Westphal, H -- Mukherjee, A B -- HL47620/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 May 30;276(5317):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Developmental Genetics, Heritable Disorders Branch, National Institute of Child Health and Human Development (NICHD), National Insitutes of Health (NIH), Bethesda, MD 20892-1830, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162006" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Cells, Cultured
;
Crosses, Genetic
;
Fibronectins/*metabolism
;
Gene Targeting
;
Humans
;
Kidney Diseases/embryology/genetics/pathology
;
*Kidney Glomerulus/embryology/metabolism/ultrastructure
;
Mice
;
Mice, Inbred C57BL
;
Uteroglobin/deficiency/genetics/*physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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