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Severe Fibronectin-Deposit Renal Glomerular Disease in Mice Lacking Uteroglobin

  1. Author:
    Zhang, Z. J.
    Kundu, G. C.
    Yuan, C. J.
    Ward, J. M.
    Lee, E. J.
    Demayo, F.
    Westphal, H.
    Mukherjee, A. B.

  2. Author Address

    Mukherjee AB NICHHD SECT DEV GENET HERITABLE DISORDERS BRANCH NIH BETHESDA, MD 20892 USA NICHHD SECT DEV GENET HERITABLE DISORDERS BRANCH NIH BETHESDA, MD 20892 USA NCI VET & TUMOR PATHOL SECT OFF LAB ANIM SCI FREDERICK, MD 21702 USA NICHHD LAB MAMMALIAN GENET & DEV NIH BETHESDA, MD 20892 USA BAYLOR COLL MED DEPT CELL BIOL HOUSTON, TX 77030 USA
    1. Year: 1997
  2. Journal: Science
    1. 276
    2. 5317
    3. Pages: 1408-1412
  4. Type of Article: Article
  1. Abstract:

    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. [References: 42]

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