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Matches in Nanopublications for { ?s ?p "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." ?g. }

• _4 value "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." provenance.
• _7 value "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." provenance.
• _4 value "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." provenance.
• _5 value "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." provenance.
• _7 value "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." provenance.
• _5 value "Conversely, insulin-stimulated PI(3)K activity was increased by 80% in muscle of both Rbp+/- and Rbp4-/- mice compared with control mice (Fig. 5b). However, PI(3)K activity was not altered in the liver of RBP4-Tg (Fig. 5c) or Rbp4-/- mice (Fig. 5d). Consistent with these observations, RBP4 injection for 21 days in wild-type mice caused a 34% reduction in insulin-stimulated PI(3)K activity in muscle, but no alteration in liver (Fig. 5e). Furthermore, RBP4 treatment resulted in a 24% reduction in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS1) at tyrosine residue 612 (Fig. 5f), an important docking site for the p85 subunit of PI(3)K23." provenance.