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jnk-jun-nh2-terminal-kinase

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Molecular constituents of autophagy. Autophagy requires more than 30 Atg pr...
Published: 17 January 2012
FIG. 1. Molecular constituents of autophagy. Autophagy requires more than 30 Atg proteins that orchestrate the formation of a de novo limiting membrane, which sequesters cytosolic cargo and then seals upon itself to form an autophagosome. The fusion of autophagosomes to lysosomes leads to cargo degradation and release of nutrients into the cytosol. JNK, Jun NH2-terminal kinase 1; PE, phosphatidylethanolamine; P, phosphorylation of JNK. FIG. 1. Molecular constituents of autophagy. Autophagy requires more than 30 Atg proteins that orchestrate the formation of a de novo limiting membrane, which sequesters cytosolic cargo and then seals upon itself to form an autophagosome. The fusion of autophagosomes to lysosomes leads to cargo degradation and release of nutrients into the cytosol. JNK, Jun NH2-terminal kinase 1; PE, phosphatidylethanolamine; P, phosphorylation of JNK. More
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A schematic representation of the proposed mechanisms by which resveratrol ...
Published: 01 March 2010
FIG. 1. A schematic representation of the proposed mechanisms by which resveratrol improves insulin sensitivity. Working through the energy-sensing AMPK, resveratrol (RSV) may act to increase mitochondrial β-oxidation, which in turn increases the NAD+-to-NAHD ratio, triggering the activation of SIRT1 and the deacetylation of PGC-1α and resulting in mitochondrial biogenesis. AMPK-α1 and -α2–dependent increases in fatty acid oxidation and mitochondrial capacity decrease reactive lipid intermediates such as diacyglycerol (DAG) and ceramides, thereby improving insulin-stimulated glucose disposal. Ac, acetylation; ACC, acetyl-CA carboxylase; Akt, protein kinase B; CPT-1, carnitine palmitoyl transferase; IKK, inhibitor of κ kinase; FA, fatty acid; IRS-1, insulin receptor substrate-1; JNK, Jun NH2-terminal kinase; GCN5, histone acetyltransferase GCN5; P, phosphate; PP2A, protein phosphatase 2A; PDK, 3-phosphoinositide-dependent kinase; PKC, protein kinase C; TAG, triacylglycerol. FIG. 1. A schematic representation of the proposed mechanisms by which resveratrol improves insulin sensitivity. Working through the energy-sensing AMPK, resveratrol (RSV) may act to increase mitochondrial β-oxidation, which in turn increases the NAD+-to-NAHD ratio, triggering the activation of SIRT1 and the deacetylation of PGC-1α and resulting in mitochondrial biogenesis. AMPK-α1 and -α2–dependent increases in fatty acid oxidation and mitochondrial capacity decrease reactive lipid intermediates such as diacyglycerol (DAG) and ceramides, thereby improving insulin-stimulated glucose disposal. Ac, acetylation; ACC, acetyl-CA carboxylase; Akt, protein kinase B; CPT-1, carnitine palmitoyl transferase; IKK, inhibitor of κ kinase; FA, fatty acid; IRS-1, insulin receptor substrate-1; JNK, Jun NH2-terminal kinase; GCN5, histone acetyltransferase GCN5; P, phosphate; PP2A, protein phosphatase 2A; PDK, 3-phosphoinositide-dependent kinase; PKC, protein kinase C; TAG, triacylglycerol. More
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Molecular mechanism by which HFHSD leads to hepatic insulin resistance and ...
Published: 31 December 2014
Figure 5 Molecular mechanism by which HFHSD leads to hepatic insulin resistance and imeglimin’s action mode. A: HFHSD increases intracellular lipids (triglyceride and DAG), leading to alterations of mitochondrial function, which results in inhibition of insulin signaling. B: Imeglimin improves mitochondrial function by modulating mitochondrial lipid composition, increasing mitochondrial respiration associated with energy waste in succinate, decreasing ROS production, restoring CIII activity, decreasing CI activity, and reorienting oxidative fluxes to fatty acid oxidation. As a consequence, imeglimin leads to improved insulin signaling and decreased liver steatosis, insulin resistance, and glucose intolerance. CIV, complex IV; CoQ, coenzyme Q; CytC, cytochrome c; FADH2, flavin adenine dinucleotide; FFA, free fatty acid; IMM, inner mitochondrial membrane; IRS, insulin receptor substrate; JNK, Jun NH2-terminal kinase; mtDNA, mitochondrial DNA; OMM, outer mitochondrial membrane; PKC, protein kinase C; Ser-Thre, serine-threonine; TG, triglyceride. Figure 5. Molecular mechanism by which HFHSD leads to hepatic insulin resistance and imeglimin’s action mode. A: HFHSD increases intracellular lipids (triglyceride and DAG), leading to alterations of mitochondrial function, which results in inhibition of insulin signaling. B: Imeglimin improves mitochondrial function by modulating mitochondrial lipid composition, increasing mitochondrial respiration associated with energy waste in succinate, decreasing ROS production, restoring CIII activity, decreasing CI activity, and reorienting oxidative fluxes to fatty acid oxidation. As a consequence, imeglimin leads to improved insulin signaling and decreased liver steatosis, insulin resistance, and glucose intolerance. CIV, complex IV; CoQ, coenzyme Q; CytC, cytochrome c; FADH2, flavin adenine dinucleotide; FFA, free fatty acid; IMM, inner mitochondrial membrane; IRS, insulin receptor substrate; JNK, Jun NH2-terminal kinase; mtDNA, mitochondrial DNA; OMM, outer mitochondrial membrane; PKC, protein kinase C; Ser-Thre, serine-threonine; TG, triglyceride. More
Journal Articles
Journal: Diabetes
Diabetes 2005;54(8):2351–2359
Published: 01 August 2005
.../55/50, protein kinase C (PKC)-θ activity, levels of pSer307 insulin receptor substrate (IRS)-1 and p-Jun NH2-terminal kinase (JNK)-1, and myosin heavy chain IIx fibers. Increased basal phosphorylation of Ser307 IRS-1 in the obese and type 2 diabetic subjects...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(10):2678–2687
Published: 01 October 2006
... phosphorylation, and GLUT4 translocation. In contrast, insulin-stimulated extracellular signal–regulated kinase1/2 and Jun NH2-terminal kinase (JNK) activation were decreased in the presence of bradykinin, accompanied by decreased IRS-1 Ser307 phosphorylation. Furthermore, bradykinin did...
Journal Articles
Journal: Diabetes
Diabetes 2008;57(4):846–859
Published: 01 April 2008
...) led to early Jun NH2-terminal kinase (JNK) activation that preceded induction of ER stress markers and apoptosis. Foxo1 activity was increased with fatty acid administration and by pharmacological inducers of ER stress, and this increase was prevented by JNK inhibition. Fatty acids induced...
Includes: Supplementary data
Meeting Abstracts
Journal: Diabetes
Diabetes 2020;69(Supplement_1):222-LB
Published: 01 June 2020
...-induced Kupffer cell activation, and pJNK1 inhibition decreases Kupffer cell activation induced by diabetes. We aim to study the involvement c-Jun NH2-terminal kinase pathways in the regulatory mechanisms of liver inflammation and FGF-21 in diabetes. Type 1 diabetic Akita mice (C57BL/6J...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(1):77–82
Published: 01 January 2001
...Christophe Bonny; Anne Oberson; Stéphanie Negri; Christelle Sauser; Daniel F. Schorderet Stress conditions and proinflammatory cytokines activate the c-Jun NH2-terminal kinase (JNK), a member of the stress-activated group of mitogen-activated protein kinases (MAPKs). We recently...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(11):2720–2730
Published: 01 November 2003
...@showa.gunma-u.ac.jp 30 7 2003 23 4 2003 DIABETES 2003 ERK, extracellular signal-regulated kinase GAPDH, glyceraldehyde-6-phosphate dehydrogenase GLP, glucagon-like polypeptide IRI, immunoreactive insulin JIP, c-jun NH2-terminal kinase–interacting protein JNK, c-jun...
Journal Articles
Journal: Diabetes
Diabetes 2008;57(5):1205–1215
Published: 01 May 2008
... through activation of the c-Jun NH2-terminal kinase (JNK) pathway. This study was designed to investigate whether the long-acting agonist of the hormone glucagon-like peptide 1 (GLP-1) receptor exendin-4 (ex-4), which mediates protective effects against cytokine-induced β-cell apoptosis, could...
Journal Articles
Journal: Diabetes
Diabetes 2013;62(2):471–477
Published: 17 January 2013
...), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH2-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn−/− mice. Chromatin immunoprecipitation assays were used to identify a 12-O...
Includes: Supplementary data
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(9):1468–1476
Published: 01 September 2000
... MAPKs extracellular signal-regulated kinases (ERKs)-1/2, c-Jun NH2-terminal kinase (JNK), and p38 MAPK (p38). This led to increased phosphorylation of the transcription factors c-Jun, Elk-1, and ATF2 and of heat shock protein 25. Inhibition of ERK-1/2 and p38 did not prevent but aggravated IL-1beta...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(4):881–889
Published: 01 April 1999
... includes c-jun NH2-terminal kinase (JNK) or stress-activated protein kinase (SAPK1) and extracellular signal-regulated kinases (ERKs) 1 and 2. Diabetes induced a significant three- to fourfold (P < 0.05) increase in phosphorylation of a 54-kDa isoform of JNK in DRG and sural nerve, and this correlated...
Journal Articles
Journal: Diabetes
Diabetes 2018;67(4):624–635
Published: 09 January 2018
... mitogen-activated protein kinases (MAPKs), p38 MAPK, and c-Jun NH2-terminal kinase (JNK). Stress also induces expression of MAPK phosphatase-1 (MKP-1), which inactivates both JNK and p38 MAPK. However, the equilibrium between JNK/p38 MAPK and MKP-1 signaling in the development of obesity...
Includes: Supplementary data
Meeting Abstracts
Journal: Diabetes
Diabetes 2021;70(Supplement_1):388-P
Published: 01 June 2021
...) were evaluated by enzyme-linked immunosorbent assay (ELISA). GLP-1R, HMGB1, TGF-β1, phosphorylated and total extracellular signal-regulated kinases (ERK), c-Jun NH2-terminal kinases (JNK), p38 mitogen-activated protein kinases (p38MAPK), and NF-κB p65 were measured by western blot analysis. Results...
Journal Articles
Journal: Diabetes
Diabetes 2010;59(3):551–553
Published: 01 March 2010
.... Ac, acetylation; ACC, acetyl-CA carboxylase; Akt, protein kinase B; CPT-1, carnitine palmitoyl transferase; IKK, inhibitor of κ kinase; FA, fatty acid; IRS-1, insulin receptor substrate-1; JNK, Jun NH2-terminal kinase; GCN5, histone acetyltransferase GCN5; P, phosphate; PP2A, protein...
Journal Articles
Journal: Diabetes
Diabetes 2012;61(12):3181–3188
Published: 15 November 2012
... inhibitors and agonists in the amelioration of endothelial function. Protein expression and phosphorylation of p38, c-Jun NH2-terminal kinase (JNK), and extracellular signal–regulated kinase (Erk) were assessed in mesenteric arteries of 3- (3M) and 9-month-old (9M) male diabetic and control mice...
Journal Articles
Journal: Diabetes
Diabetes 2014;63(10):3497–3511
Published: 15 September 2014
... cytokines via inactivation of nuclear factor-κB in both H9c2 cells and neonatal cardiomyocytes. Furthermore, we showed that the inhibition of Jun NH2-terminal kinase (JNK) phosphorylation contributed to the protection of C66 from inflammation and cell apoptosis, which was validated by the use...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2008;57(7):1896–1904
Published: 01 July 2008
...Dariush Mokhtari; Jason W. Myers; Nils Welsh OBJECTIVE— The transcription factor nuclear factor-κB (NF-κB) and the mitogen-activated protein kinases (MAPKs) c-Jun NH2-terminal kinase (JNK) 1/2 are known to play decisive roles in cytokine-induced damage of rodent β-cells. The upstream...
Journal Articles
Journal: Diabetes
Diabetes 2004;53(6):1436–1444
Published: 01 June 2004
...Ying Leng; Tatiana L. Steiler; Juleen R. Zierath Effects of diverse stimuli, including insulin, muscle contraction, and phorbol 12-myristate-13-acetate (PMA), were determined on phosphorylation of mitogen-activated protein kinase (MAPK) signaling modules (c-Jun NH2-terminal kinase [JNK...