| http://purl.uniprot.org/citations/12933351 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12933351 | http://www.w3.org/2000/01/rdf-schema#comment | "We previously found that disruption of Kir6.2-containing ATP-sensitive K+ (KATP) channels increases glucose uptake in skeletal muscle, but the mechanism is not clear. In the present study, we generated knockout mice lacking both Kir6.2 and insulin receptor substrate-1 (IRS-1). Because IRS-1 is the major substrate of insulin receptor kinase, we expected disruption of the IRS-1 gene to reduce glucose uptake in Kir6.2 knockout mice. However, the double-knockout mice do not develop insulin resistance or glucose intolerance. An insulin tolerance test reveals the glucose-lowering effect of exogenous insulin in double-knockout mice and in Kir6.2 knockout mice to be similarly enhanced compared with wild-type mice. The basal 2-deoxyglucose uptake rate in skeletal muscle of double-knockout mice is increased similarly to the rate in Kir6.2 knockout mice. Accordingly, disruption of the IRS-1 gene affects neither systemic insulin sensitivity nor glucose uptake in skeletal muscles of Kir6.2-deficient mice. In addition, no significant changes were observed in phosphatidylinositol 3-kinase (PI3K) activity and its downstream signal in skeletal muscle due to lack of the Kir6.2 gene. Disruption of Kir6.2-containing Katp channels clearly protects against IRS-1-associated insulin resistance by increasing glucose uptake in skeletal muscles by a mechanism separate from the IRS-1/PI3K pathway."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpendo.00278.2003"xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Miki T."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Minami K."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Kadowaki T."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Morita M."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Seino S."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Yano H."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Terauchi Y."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Kuriyama T."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/author | "Saraya A."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/name | "Am J Physiol Endocrinol Metab"xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/pages | "E1289-96"xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/title | "ATP-sensitive K+ channel-mediated glucose uptake is independent of IRS-1/phosphatidylinositol 3-kinase signaling."xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://purl.uniprot.org/core/volume | "285"xsd:string |
| http://purl.uniprot.org/citations/12933351 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12933351 |
| http://purl.uniprot.org/citations/12933351 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/12933351 |
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| http://purl.uniprot.org/uniprot/#_P35569-mappedCitation-12933351 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/12933351 |
| http://purl.uniprot.org/uniprot/#_Q543V3-mappedCitation-12933351 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/12933351 |
| http://purl.uniprot.org/uniprot/#_Q61743-mappedCitation-12933351 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/12933351 |