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- source_evidence_literature type ECO_0000212 NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- source_evidence_literature label "DisGeNET evidence - LITERATURE" NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- source_evidence_literature comment "Gene-disease associations inferred from text-mining the literature." NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_assertion description "[We conclude the following: 1) physiological hyperinsulinemia induces sustained activation of insulin-signaling molecules in human skeletal muscle; 2) the more distal insulin-signaling components (Akt, GSK-3) are activated much more rapidly than the proximal signaling molecules (IRTK as well as insulin receptor substrate 1 and phosphatidylinositol 3-kinase [Wojtaszewski et al., Diabetes 46:1775-1781, 1997]); and 3) prior exercise increases insulin stimulation of both glucose uptake and glycogen synthase activity in the absence of an upregulation of signaling events in human skeletal muscle.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_assertion evidence source_evidence_literature NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_assertion SIO_000772 10868952 NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_assertion wasDerivedFrom befree-20150227 NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_assertion wasGeneratedBy ECO_0000203 NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.
- befree-20150227 importedOn "2015-02-27" NP515445.RAWUwdNP3_5h-mIZy88iFm8EafcR1-N7hhVLXnXXJOSJc130_provenance.