Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.26 (GSK)
 6,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Influx of [(3)H]-L-proline into renal OK cells revealed that basal transport was mediated by the transporter SIT1. When cells were submitted for 8 h to amino acid deprivation, uptake of L-proline was now dominated by a low-affinity system with an apparent K (m) of 4.4 +/- 0.6 mM and a V (max) of 10.2 +/- 0.6 nmol/mg of protein/min operating in addition to the high-affinity SIT1 system with a K (m) of 0.12 +/- 0.01 mM and a V (max) of 0.28 +/- 0.04 nmol/mg of protein/min. The low- and high-affinity proline transporting systems were sensitive to inhibitors of JNK and PI-3 kinases, whereas a GSK-3 inhibitor affected only the upregulated transport system. Ion-replacement studies and experiments assessing substrate specificities for both systems provided strong evidence that SNAT2, that showed two- to threefold increased mRNA levels, is the responsible transporter mediating the increased proline influx under conditions of amino acid deprivation.
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PMID:L-Proline transport into renal OK epithelial cells: a second renal proline transport system is induced by amino acid deprivation. 1933 19