1-20 of 459 Search Results for

pkb-protein-kinase-b

Follow your search
Access your saved searches in your account

Would you like to receive an alert when new items match your search?
Close Modal
Sort by
Images
Proposed model for leucine's role in mitogenic signaling. α-KG,α-ketoglutar...
Published: 01 February 2001
FIG. 1. Proposed model for leucine's role in mitogenic signaling. α-KG,α-ketoglutarate; AOAA, aminooxyacetic acid; AT, aminotransferase; BCKDH,branched-chain α—keto-acid dehydrogenase; GDH, glutamate dehydrogenase; IR, insulin receptor; IRS, insulin receptor substrate;p70s6k, p70 S6 kinase; PHAS-I, phosphorylated heat- and acid-stable protein regulated by insulin; PKB, protein kinase B. FIG. 1. Proposed model for leucine's role in mitogenic signaling. α-KG,α-ketoglutarate; AOAA, aminooxyacetic acid; AT, aminotransferase; BCKDH,branched-chain α—keto-acid dehydrogenase; GDH, glutamate dehydrogenase; IR, insulin receptor; IRS, insulin receptor substrate;p70s6k, p70 S6 kinase; PHAS-I, phosphorylated heat- and acid-stable protein regulated by insulin; PKB, protein kinase B. More
Images
The three nutrient-sensing pathways, mTOR, AMPK, and SIRT1, may be independ...
Published: 12 December 2011
FIG. 2. The three nutrient-sensing pathways, mTOR, AMPK, and SIRT1, may be independently and coordinately involved in the pathogenesis of diabetic nephropathy. 4E-BP, 4E-binding protein; COX2, cyclooxygenase-2; eNOS, endothelial nitric oxide synthase; EPO, erythropoietin; FoxO, forkhead box class ... More
Images
Schema depicting roles of SS ceramides in insulin resistance under postabso...
Published: 08 May 2017
Figure 4 Schema depicting roles of SS ceramides in insulin resistance under postabsorptive conditions. There are two possible explanations for the data regarding SS ceramide concentrations and de novo synthesis of ceramides to insulin resistance. One model depicts the circumstance in which, when p... More
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(3):658–663
Published: 01 March 1999
... of Akt/protein kinase B (PKB) was diminished by 60%, compared with that of muscles preincubated in a glucose-free medium; whereas activation of phosphatidylinositol (PI) 3-kinase, an upstream regulator of Akt/PKB in the insulin-signaling cascade, and of mitogen-activated protein (MAP) kinase, a parallel...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(9):2691–2697
Published: 01 September 2002
..., and muscle biopsies were obtained immediately before and after the clamps. In the biopsies, insulin receptor kinase (IRK) activity, insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI3K) activity, Ser473 and Thr308 phosphorylation of protein kinase B (PKB...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(4):691–698
Published: 01 April 1999
...A Gagnon; C S Chen; A Sorisky Ectopic expression of activated protein kinase B (PKB) induces the differentiation of confluent 3T3-L1 preadipocytes into adipocytes. PKB is regulated by the lipid products of phosphoinositide 3-kinase (PI 3-kinase), phosphatidylinositol-3,4-bisphosphate [PI(3,4)P2...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(3):690–693
Published: 01 March 2001
... insulin response, intravenous glucose tolerance, insulin-mediated glucose uptake, and the prevalence of type 2 diabetes after 20 years of follow-up. We also expressed the variant in vitro to evaluate the impact on insulin-stimulated activation of protein kinase B (PKB). The Met326Ile variant of p85α...
Images
Integration of the metabolomics with transcriptomics data and their superim...
Published: 13 April 2012
FIG. 4. Integration of the metabolomics with transcriptomics data and their superimposition to build metabolic networks. A: Metabolic network of PPAR transcription pathway, which is connected to other metabolic processes such as lipid homeostasis, glucose, fatty acid metabolism, and inflammatory response. B: Network model of downstream of insulin-signaling pathways. The metabolites and the gene names shown in red are upregulated, and the same shown in blue are downregulated during insulin deficiency. B, binding; C, cleavage; CoA, coenzyme A; Erk, extracellular signal–related kinase; HPODE, hydroperoxylinoleic acid; IE, influence on expression; MAP, mitogen-activated protein; MAPK, MAP kinase; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; PKA, cAMP-dependent protein kinase; PKB, protein kinase B; P-, dephosphorylation; RXR, retinoid X receptor; SREBP1c, sterol regulatory element–binding protein 1c; T, transformation; TGF, transforming growth factor; TR, transcription regulation; +P, phosphorylation; Z, catalysis; GPCR, G protein-coupled receptor; 15d-PGJ2, deoxy-delta prostaglandin J2; PDK/PDK1, 3-phosphoinositide-dependent protein kinase -1; ACACA, acetyl-CoA carboxylase; ACSL, acyl-CoA synthetase long-chain family members; ACLY, ATP citrate lyase; BCAA, branch chain amino acid; CISY, citrate synthase; DAG, diacylglycerol; ELOVL, elongation-of-very-long-chain-fatty acids; EMT, epithelial-mesenchymal transition; BEH, ethylene-bridged hybrid; 4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FADS1, fatty acid desaturase 1; FASN, fatty acid synthase; GSK3β, glycogen synthase kinase 3; GNAS, G protein αs- dependent adenylate cyclase; GRB2, growth factor receptor-bound protein 2; H-Ras, Harvey rat sarcoma viral oncogene homolog; HGF, hepatocyte growth factor; HXK, hexokinase; HSS, high-strength silica; HODE, hydroxyoctadecadienoic acid; INSIG2, insulin-induced gene 2; IRS-1 and IRS-2, insulin receptor substrates-1 and -2; TRIP, mediator complex subunit 1; MEK/MAP1, mitogen-activated protein kinase kinase 1; NCOA1, nuclear receptor coactivator 1; NRC1/SRC1, nuclear receptor coactivator 1; N-CoR, nuclear receptor corepressor; SMRT, nuclear receptor corepressors; NUDT1, nudix (nucleoside diphosphate-linked moiety X)-type motif 1; PtdIns(3,4,5)P3, phosphatidylinositol 3,4,5-triphosphate; P13K, phospatidylinositol 3-kinase; PtdIns(4,5)P2, phosphatidylinositol 4,5-biphosphate; PGE, prostaglandin; PTGIS, prostaglandin I2 (prostacyclin) synthase; PDGHS, prostaglandin-endoperoxide synthase 2 prostaglandin G/H synthase; COX2, cyclooxygenase 2; PDHA, pyruvate dehydrogenase (lipoamide) α1; QCs, quality controls; RARs, retinoic acid receptors; RXRA, retinoid X nuclear receptor (α; SHC, Src homology 2 domain containing transforming protein 1; SHP, small heterodimer partner; SOS, son of sevenless protein homologs 1 and 2; c-Raf-1, gene homolog 1; XIAP, X-linked inhibitor of apoptosis. FIG. 4. Integration of the metabolomics with transcriptomics data and their superimposition to build metabolic networks. A: Metabolic network of PPAR transcription pathway, which is connected to other metabolic processes such as lipid homeostasis, glucose, fatty acid metabolism, and inflammatory response. B: Network model of downstream of insulin-signaling pathways. The metabolites and the gene names shown in red are upregulated, and the same shown in blue are downregulated during insulin deficiency. B, binding; C, cleavage; CoA, coenzyme A; Erk, extracellular signal–related kinase; HPODE, hydroperoxylinoleic acid; IE, influence on expression; MAP, mitogen-activated protein; MAPK, MAP kinase; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; PKA, cAMP-dependent protein kinase; PKB, protein kinase B; P-, dephosphorylation; RXR, retinoid X receptor; SREBP1c, sterol regulatory element–binding protein 1c; T, transformation; TGF, transforming growth factor; TR, transcription regulation; +P, phosphorylation; Z, catalysis; GPCR, G protein-coupled receptor; 15d-PGJ2, deoxy-delta prostaglandin J2; PDK/PDK1, 3-phosphoinositide-dependent protein kinase -1; ACACA, acetyl-CoA carboxylase; ACSL, acyl-CoA synthetase long-chain family members; ACLY, ATP citrate lyase; BCAA, branch chain amino acid; CISY, citrate synthase; DAG, diacylglycerol; ELOVL, elongation-of-very-long-chain-fatty acids; EMT, epithelial-mesenchymal transition; BEH, ethylene-bridged hybrid; 4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FADS1, fatty acid desaturase 1; FASN, fatty acid synthase; GSK3β, glycogen synthase kinase 3; GNAS, G protein αs- dependent adenylate cyclase; GRB2, growth factor receptor-bound protein 2; H-Ras, Harvey rat sarcoma viral oncogene homolog; HGF, hepatocyte growth factor; HXK, hexokinase; HSS, high-strength silica; HODE, hydroxyoctadecadienoic acid; INSIG2, insulin-induced gene 2; IRS-1 and IRS-2, insulin receptor substrates-1 and -2; TRIP, mediator complex subunit 1; MEK/MAP1, mitogen-activated protein kinase kinase 1; NCOA1, nuclear receptor coactivator 1; NRC1/SRC1, nuclear receptor coactivator 1; N-CoR, nuclear receptor corepressor; SMRT, nuclear receptor corepressors; NUDT1, nudix (nucleoside diphosphate-linked moiety X)-type motif 1; PtdIns(3,4,5)P3, phosphatidylinositol 3,4,5-triphosphate; P13K, phospatidylinositol 3-kinase; PtdIns(4,5)P2, phosphatidylinositol 4,5-biphosphate; PGE, prostaglandin; PTGIS, prostaglandin I2 (prostacyclin) synthase; PDGHS, prostaglandin-endoperoxide synthase 2 prostaglandin G/H synthase; COX2, cyclooxygenase 2; PDHA, pyruvate dehydrogenase (lipoamide) α1; QCs, quality controls; RARs, retinoic acid receptors; RXRA, retinoid X nuclear receptor (α; SHC, Src homology 2 domain containing transforming protein 1; SHP, small heterodimer partner; SOS, son of sevenless protein homologs 1 and 2; c-Raf-1, gene homolog 1; XIAP, X-linked inhibitor of apoptosis. More
Images
Integration of the metabolomics with transcriptomics data and their superim...
Published: 13 April 2012
FIG. 4. Integration of the metabolomics with transcriptomics data and their superimposition to build metabolic networks. A: Metabolic network of PPAR transcription pathway, which is connected to other metabolic processes such as lipid homeostasis, glucose, fatty acid metabolism, and inflammatory response. B: Network model of downstream of insulin-signaling pathways. The metabolites and the gene names shown in red are upregulated, and the same shown in blue are downregulated during insulin deficiency. B, binding; C, cleavage; CoA, coenzyme A; Erk, extracellular signal–related kinase; HPODE, hydroperoxylinoleic acid; IE, influence on expression; MAP, mitogen-activated protein; MAPK, MAP kinase; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; PKA, cAMP-dependent protein kinase; PKB, protein kinase B; P-, dephosphorylation; RXR, retinoid X receptor; SREBP1c, sterol regulatory element–binding protein 1c; T, transformation; TGF, transforming growth factor; TR, transcription regulation; +P, phosphorylation; Z, catalysis; GPCR, G protein-coupled receptor; 15d-PGJ2, deoxy-delta prostaglandin J2; PDK/PDK1, 3-phosphoinositide-dependent protein kinase -1; ACACA, acetyl-CoA carboxylase; ACSL, acyl-CoA synthetase long-chain family members; ACLY, ATP citrate lyase; BCAA, branch chain amino acid; CISY, citrate synthase; DAG, diacylglycerol; ELOVL, elongation-of-very-long-chain-fatty acids; EMT, epithelial-mesenchymal transition; BEH, ethylene-bridged hybrid; 4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FADS1, fatty acid desaturase 1; FASN, fatty acid synthase; GSK3β, glycogen synthase kinase 3; GNAS, G protein αs- dependent adenylate cyclase; GRB2, growth factor receptor-bound protein 2; H-Ras, Harvey rat sarcoma viral oncogene homolog; HGF, hepatocyte growth factor; HXK, hexokinase; HSS, high-strength silica; HODE, hydroxyoctadecadienoic acid; INSIG2, insulin-induced gene 2; IRS-1 and IRS-2, insulin receptor substrates-1 and -2; TRIP, mediator complex subunit 1; MEK/MAP1, mitogen-activated protein kinase kinase 1; NCOA1, nuclear receptor coactivator 1; NRC1/SRC1, nuclear receptor coactivator 1; N-CoR, nuclear receptor corepressor; SMRT, nuclear receptor corepressors; NUDT1, nudix (nucleoside diphosphate-linked moiety X)-type motif 1; PtdIns(3,4,5)P3, phosphatidylinositol 3,4,5-triphosphate; P13K, phospatidylinositol 3-kinase; PtdIns(4,5)P2, phosphatidylinositol 4,5-biphosphate; PGE, prostaglandin; PTGIS, prostaglandin I2 (prostacyclin) synthase; PDGHS, prostaglandin-endoperoxide synthase 2 prostaglandin G/H synthase; COX2, cyclooxygenase 2; PDHA, pyruvate dehydrogenase (lipoamide) α1; QCs, quality controls; RARs, retinoic acid receptors; RXRA, retinoid X nuclear receptor (α; SHC, Src homology 2 domain containing transforming protein 1; SHP, small heterodimer partner; SOS, son of sevenless protein homologs 1 and 2; c-Raf-1, gene homolog 1; XIAP, X-linked inhibitor of apoptosis. FIG. 4. Integration of the metabolomics with transcriptomics data and their superimposition to build metabolic networks. A: Metabolic network of PPAR transcription pathway, which is connected to other metabolic processes such as lipid homeostasis, glucose, fatty acid metabolism, and inflammatory response. B: Network model of downstream of insulin-signaling pathways. The metabolites and the gene names shown in red are upregulated, and the same shown in blue are downregulated during insulin deficiency. B, binding; C, cleavage; CoA, coenzyme A; Erk, extracellular signal–related kinase; HPODE, hydroperoxylinoleic acid; IE, influence on expression; MAP, mitogen-activated protein; MAPK, MAP kinase; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; PKA, cAMP-dependent protein kinase; PKB, protein kinase B; P-, dephosphorylation; RXR, retinoid X receptor; SREBP1c, sterol regulatory element–binding protein 1c; T, transformation; TGF, transforming growth factor; TR, transcription regulation; +P, phosphorylation; Z, catalysis; GPCR, G protein-coupled receptor; 15d-PGJ2, deoxy-delta prostaglandin J2; PDK/PDK1, 3-phosphoinositide-dependent protein kinase -1; ACACA, acetyl-CoA carboxylase; ACSL, acyl-CoA synthetase long-chain family members; ACLY, ATP citrate lyase; BCAA, branch chain amino acid; CISY, citrate synthase; DAG, diacylglycerol; ELOVL, elongation-of-very-long-chain-fatty acids; EMT, epithelial-mesenchymal transition; BEH, ethylene-bridged hybrid; 4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FADS1, fatty acid desaturase 1; FASN, fatty acid synthase; GSK3β, glycogen synthase kinase 3; GNAS, G protein αs- dependent adenylate cyclase; GRB2, growth factor receptor-bound protein 2; H-Ras, Harvey rat sarcoma viral oncogene homolog; HGF, hepatocyte growth factor; HXK, hexokinase; HSS, high-strength silica; HODE, hydroxyoctadecadienoic acid; INSIG2, insulin-induced gene 2; IRS-1 and IRS-2, insulin receptor substrates-1 and -2; TRIP, mediator complex subunit 1; MEK/MAP1, mitogen-activated protein kinase kinase 1; NCOA1, nuclear receptor coactivator 1; NRC1/SRC1, nuclear receptor coactivator 1; N-CoR, nuclear receptor corepressor; SMRT, nuclear receptor corepressors; NUDT1, nudix (nucleoside diphosphate-linked moiety X)-type motif 1; PtdIns(3,4,5)P3, phosphatidylinositol 3,4,5-triphosphate; P13K, phospatidylinositol 3-kinase; PtdIns(4,5)P2, phosphatidylinositol 4,5-biphosphate; PGE, prostaglandin; PTGIS, prostaglandin I2 (prostacyclin) synthase; PDGHS, prostaglandin-endoperoxide synthase 2 prostaglandin G/H synthase; COX2, cyclooxygenase 2; PDHA, pyruvate dehydrogenase (lipoamide) α1; QCs, quality controls; RARs, retinoic acid receptors; RXRA, retinoid X nuclear receptor (α; SHC, Src homology 2 domain containing transforming protein 1; SHP, small heterodimer partner; SOS, son of sevenless protein homologs 1 and 2; c-Raf-1, gene homolog 1; XIAP, X-linked inhibitor of apoptosis. More
Journal Articles
Journal: Diabetes
Diabetes 2001;50(10):2210–2218
Published: 01 October 2001
...Rosanna Cazzolli; Lee Carpenter; Trevor J. Biden; Carsten Schmitz-Peiffer We have shown previously that palmitate treatment of C2C12 skeletal muscle myotubes causes inhibition of the protein kinase B (PKB) pathway and hence reduces insulin-stimulated glycogen synthesis through the elevation...
Journal Articles
Journal: Diabetes
Diabetes 2007;56(9):2218–2227
Published: 01 September 2007
... by insulin, but this process is defective in diabetic subjects. Protein kinase B (PKB) is implicated in this action of insulin. An inhibitor of PKB, Akt inhibitor (Akti)-1/2, was recently reported; however, the specificity and efficacy against insulin-induced PKB was not reported. Our aim was to characterize...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2003;52(1):21–28
Published: 01 January 2003
...-associated phosphatidylinositol 3-kinase activity was also increased threefold. Protein kinase B (PKB) serine phosphorylation was increased sevenfold in liver of PTP1B ASO-treated mice upon insulin stimulation, while phosphorylation of PKB substrates, glycogen synthase kinase (GSK)-3α and -3β, was increased...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(2):421–427
Published: 01 February 2006
... transport. The effect on GLUT4 but not on GLUT1 is mediated by activation of protein kinase B (PKB). The serum- and glucocorticoid-inducible kinase SGK1, a further kinase downstream of PI3 kinase, regulates several transporters by enhancing their plasma membrane abundance. GLUT1 contains a consensus site...
Journal Articles
Journal: Diabetes
Diabetes 1997;46(12):2110–2114
Published: 01 December 1997
...Anna Krook; Yuichi Kawano; Xiao Mei Song; Suad Efendić; Richard A Roth; Harriet Wallberg-Henriksson; Juleen R Zierath The serine/threonine kinase Akt (protein kinase B [PKB] or related to A and C protein kinase [RAC] has recently been implicated to play a role in the signaling pathway to glucose...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(2):310–320
Published: 01 February 1999
... (PI) 3-kinase is necessary for insulin-stimulated GLUT4 translocation, and the serine/threonine kinase Akt/protein kinase B (PKB) is a downstream mediator of some actions of PI 3-kinase. To determine whether glucosamine-induced insulin resistance could be due to impaired signaling, we measured insulin...
Meeting Abstracts
Journal: Diabetes
Diabetes 1998;47(7):1006–1013
Published: 01 July 1998
... of GSK-3 is mediated by protein kinase B (PKB), a downstream target of PI 3-kinase, whose involvement in other insulin-stimulated responses remains poorly defined at present. In this study, we investigated whether the uptake of glucose, system A amino acid transport, and cellular protein synthesis...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(12):3221–3228
Published: 01 December 2006
... of phosphatidylinositol 3′-kinase (PI3K) and its downstream substrate protein kinase B (PKB)/Akt. However, its physiological protein substrates remain poorly characterized. In the present study, the effect of in vivo insulin action on phosphorylation of the PKB/Akt substrate 40 (PRAS40) was examined. In rat and mice...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(6):992–998
Published: 01 June 2000
..., and insulin receptor substrate 1-associated phosphatidylinositol 3-kinase (PI 3-kinase) activity were measured. Furthermore, insulin activation of protein kinase B (PKB) was compared with immunoblotting of serine residues at position 473. Basal glucose uptake (1.05 +/- 0.07 vs. 0.95 +/- 0.07 relative units...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(10):2936–2943
Published: 01 October 2002
... receptor substrate (IRS)-1-dependent phosphatidylinositol (PI) 3-kinase and its downstream effectors, atypical protein kinase Cs (aPKCs) (ζ/λ/ι) and protein kinase B (PKB) in muscles of nondiabetic monkeys. Insulin-induced increases in glucose disposal and aPKC activity diminished progressively...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(8):1926–1934
Published: 01 August 2003
... protein kinase C (aPKC) and protein kinase B (PKB), operating downstream of phosphatidylinositol (PI) 3-kinase and its lipid product, PI-3,4,5-(PO4)3 (PIP3), apparently mediate insulin effects on glucose transport. We examined these signaling factors during...