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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-11-18
pubmed:abstractText
Glomerulonephritis is paralleled by excessive formation of transforming growth factor-beta (TGF-beta), which participates in the pathophysiology of the disease. Recently, a novel downstream target of TGF-beta has been identified, i.e. the human serum and glucocorticoid-dependent kinase 1 (hSGK1), a serine/threonine kinase participating in the regulation of Na(+) transport. The present study was performed to elucidate transcriptional regulation of hSGK1 in glomerulonephritis. To this end, in situ hybridization was performed in biopsies from patients with clinical diagnosis of glomerulonephritis. hSGK1 transcript levels were moderately enhanced in 5 out of 9 patients and strongly enhanced in 4 out of 9 patients. Distal nephron epithelial cell hSGK1 transcript levels were low or absent in 7 of the 9 patients but markedly enhanced in 2 of the 9 patients. In conclusion, glomerulonephritis leads to glomerular and in some cases to epithelial up-regulation of hSGK1 transcription.
pubmed:language
eng
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:author
pubmed:copyrightInfo
Copyright 2002 S. Karger AG, Basel
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
303-7
pubmed:dateRevised
2011-11-2
pubmed:articleTitle
Up-regulation of the human serum and glucocorticoid-dependent kinase 1 in glomerulonephritis.
pubmed:affiliation
Department of Physiology, University of Tübingen, Germany.