Loss of the ??-Isoform of Calcineurin Is Sufficient to Induce Nephrotoxicity and Altered Expression of Transforming Growth Factor-??
Author(s) -
Jennifer L. Gooch,
Brian R. Roberts,
Scott L. Cobbs,
James A. Tumlin
Publication year - 2007
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/01.tp.0000251423.78124.51
Subject(s) - calcineurin , fibronectin , nephrotoxicity , fibrosis , downregulation and upregulation , transforming growth factor , transforming growth factor beta , extracellular matrix , biology , in vivo , gene isoform , endocrinology , microbiology and biotechnology , medicine , chemistry , kidney , transplantation , biochemistry , gene
Use of calcineurin inhibitors is frequently limited by fibrosis, closely linked with increased transforming growth factor (TGF)-beta. However, mechanisms of extracellular matrix expansion and TGFbeta regulation following calcineurin inhibition are unknown. Mice lacking specific calcineurin catalytic subunit isoforms may offer important insight into this pathway.
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