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Publication : CAT2 arginine transporter deficiency significantly reduces iNOS-mediated NO production in astrocytes.

First Author  Manner CK Year  2003
Journal  J Neurochem Volume  85
Issue  2 Pages  476-82
PubMed ID  12675924 Mgi Jnum  J:82914
Mgi Id  MGI:2656016 Doi  10.1046/j.1471-4159.2003.01695.x
Citation  Manner CK, et al. (2003) CAT2 arginine transporter deficiency significantly reduces iNOS-mediated NO production in astrocytes. J Neurochem 85(2):476-82
abstractText  We have previously demonstrated that genetic ablation of cationic amino acid transporter 2 (Cat2) significantly inhibits nitric oxide (NO) production by inducible nitric oxide synthase (iNOS) in activated macrophages. Here we report that iNOS activity is impaired by 84% in activated Cat2-deficient astrocytes. Cat2 ablation appears to reduce astrocyte NO synthesis by decreasing the uptake of the sole precursor, arginine, as well as by reducing the expression of iNOS following activation. Excessive or dysregulated NO production by activated astrocytes and other CNS cell types has been implicated in the pathogenesis of neurological disorders. Our results support the idea that manipulation of CAT2 transporter function might be useful for the therapeutic modulation of iNOS activity.
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