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BRENDA support

Literature summary for 2.7.1.91 extracted from

  • Ren, S.; Babelova, A.; Moreth, K.; Xin, C.; Eberhardt, W.; Doller, A.; Pavenstaedt, H.; Schaefer, L.; Pfeilschifter, J.; Huwiler, A.
    Transforming growth factor-beta2 upregulates sphingosine kinase-1 activity, which in turn attenuates the fibrotic response to TGF-beta2 by impeding CTGF expression (2009), Kidney Int., 76, 857-867.
    View publication on PubMed

Application

Application Comment Organism
medicine in a mouse model of streptozotocin-induced diabetic nephropathy, isoform Sk1 and connective tisuue grwoth factor CTGF are upregulated in podocytes. In Sk1 deficient mice, exacerbation of diesease is detected by increased albuminuria and CTGF expression when compared to wild-type Mus musculus
medicine isoform Sk1 expression is increased in the podocytes of kidney sections of patients with diabetic nephropathy Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
kidney
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Mus musculus
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podocyte podocyte cell line Homo sapiens
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Expression

Organism Comment Expression
Homo sapiens transforming growth factor TGF-beta2 activates the promoter of isoform Sk1, resulting in upregulation of its mRNa and protein expression up

General Information

General Information Comment Organism
physiological function depletion of isoform Sk1 by siRNA or inhibitors leads to accelerated connective tissue growth factor CTGF induction, mediated by sphingosine 1-phosphate Homo sapiens