AKT thr308 phosphorylation related to total AKT2 protein in SOL muscle (m. soleus) (A) and EDL muscle (m. extensor digitorum longus) (D) and AKT ser472.

Slides:

Advertisements

Similar presentations

Volume 18, Issue 3, Pages (September 2013)

Advertisements

Jaya Sahni, Andrew M. Scharenberg Cell Metabolism

Volume 21, Issue 11, Pages (November 2014)

IHC analyses of levels and/or phosphorylation status of selected proteins from representative sections of ventral prostate of Hi-Myc mice. IHC analyses.

Control of IL‐6 synthesis by ζPKC and RelA Ser311 phosphorylation.

TFE3 regulates glucose homeostasis

Volume 16, Issue 10, Pages (September 2016)

Irs1 Serine 307 Promotes Insulin Sensitivity in Mice

DH E2 infusion significantly increased phosphorylation of the p42 isoform of ERK (A) and of Akt (B) in the DH of OVX females, but not sham GDX males. DH.

Volume 8, Issue 5, Pages (November 2008)

Volume 7, Issue 5, Pages (May 2001)

IRS1-Independent Defects Define Major Nodes of Insulin Resistance

Volume 16, Issue 7, Pages (August 2016)

Volume 82, Issue 4, Pages (August 2012)

mGPDH is not essential to muscle development

The selective PI3K inhibitor A66 suppresses PIP3 accumulation, AKT phosphorylation at Thr308, and YAP/TAZ–regulated gene expression in PDAC cells. The.

p38 MAPK activation is required for phosphorylation of Akt at Ser473.

Supraphysiological levels of GDF11 cause atrophy of striated muscle in vivo Supraphysiological levels of GDF11 cause atrophy of striated muscle in vivo.

Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.

Cyp8b1−/− mice have improved islet insulin secretion and increased islet insulin content but unchanged β-cell mass. Cyp8b1−/− mice have improved islet.

Immobilization decreases the global rates of protein synthesis and muscle mass, but activates mTOR signaling and cap-dependent translation. Immobilization.

Impaired Mitochondrial Fat Oxidation Induces FGF21 in Muscle

Volume 23, Issue 8, Pages (August 2015)

Effects of insulin administration in streptozotocin-treated mice.

WASH cKO mice display a normal pancreatic development.

P38 activation mediates chronic insulin-induced IRS1 and IRS2 degradation and is involved in myocardial insulin resistance in vitro. p38 activation mediates.

TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin resistance. TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin.

Activation of β-adrenoceptors improves glucose tolerance in diabetic animals and increases glucose uptake in vivo, ex vivo, and in vitro. Activation of.

Effects of canagliflozin on AMPK, lipid synthesis, and fatty acid oxidation in intact cells. Effects of canagliflozin on AMPK, lipid synthesis, and fatty.

FGF21 signaling in hypothalamus is blocked by FGFR1 neutralizing antibody. FGF21 signaling in hypothalamus is blocked by FGFR1 neutralizing antibody. Twelve-week-old.

N-3 resolution mediators improve insulin signaling by blunting JNK and iNOS in muscle and liver. n-3 resolution mediators improve insulin signaling by.

Modulation of insulin sensitivity by IL-6 in mice: A lack of PTP1B prevents chronic effects of IL-6. Modulation of insulin sensitivity by IL-6 in mice:

Angiotensin-(1-7) activates the IGF-1/Akt signalling pathway during muscle disuse through the Mas receptor. Angiotensin-(1-7) activates the IGF-1/Akt signalling.

IGF-II and IGFBP-5 rescue the atrophy of myotubes induced by adipocytes. IGF-II and IGFBP-5 rescue the atrophy of myotubes induced by adipocytes. A–D:

Smad3-KO adipose tissues have increased FA uptake and β-oxidation.

Measurement of insulin release from islets evoked by glucose, diazoxide, and high K+. Measurement of insulin release from islets evoked by glucose, diazoxide,

Glucose tolerance in WT and TRPM2-KO mice.

Fasting-induced lipolysis is impaired in weight-matched Ugcgf/f//CamKCreERT2 mice 3–4 weeks pi. Fasting-induced lipolysis is impaired in weight-matched.

Stimulation of cells with FFAR4 agonist.

Phosphorylation of AMPK-Thr172 before and after metformin treatment in muscle from subjects with type 2 diabetes. Phosphorylation of AMPK-Thr172 before.

The effect of VSG on body weight and body fat in GLP-1r KO mice.

Chop deletion preserves β-cell function in P58IPK−/− mice.

Disruption of MAM integrity and insulin signaling in liver of diet-induced diabetic mice. Disruption of MAM integrity and insulin signaling in liver of.

Reduced OXPHOS expression and increased UCP expression.

Increased phosphorylation of Akt, Girdin S1416, and NR2B of NMDA receptor in the hippocampus of mouse after fear conditioning. Increased phosphorylation.

HFD feeding induced insulin resistance in TRIB3 MOE mice.

High-glucose–induced insulin resistance in TRIB3 MOE mice.

Hepatic fuel metabolism in male 5αR1-KO and WT mice

Mice fed GP-SPI diet show improved fasting glucose and oral glucose tolerance. Mice fed GP-SPI diet show improved fasting glucose and oral glucose tolerance.

Insulin resistance and hepatic steatosis in ASKO mice.

PEDF inhibits Wnt/T-cell factor/β-catenin signaling in resting and wounded skin. PEDF inhibits Wnt/T-cell factor/β-catenin signaling in resting and wounded.

Identification of divergent effects of FEN in fully differentiated adipocytes. Identification of divergent effects of FEN in fully differentiated adipocytes.

Urinary albumin excretion and histology of glomeruli.

Energy stores in quadriceps muscles at rest (white bars) and after treadmill exercise (black bars) in WT and HSL KO mice. Energy stores in quadriceps muscles.

Metabolic effects of VSG in GLP-1r KO mice.

Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,

Expression of PKCδ in islets and other tissues of control and PKCδKN-overexpressing mice. Expression of PKCδ in islets and other tissues of control and.

GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. GTTs and ITTs. A: GTTs.

Loss of Phb2 in β-cells induces development of diabetes over a 3-week period in β-Phb2−/− mice. Loss of Phb2 in β-cells induces development of diabetes.

β-Cell–specific deletion of Phb2 renders mice diabetic.

Pioglitazone lowers glucose overload but only partially improves cardiac function. Pioglitazone lowers glucose overload but only partially improves cardiac.

Inducible liver-specific insulin receptor knockout (iLIRKO) shows insulin resistance in the liver and extrahepatic tissues. Inducible liver-specific insulin.

TBS- and HFS activate different signaling pathways.

M-MDSC:mast cell cross-talk in the regulation of TNFα production.

Imatinib mesylate inhibits PDGF-mediated ERK and Akt activation.

Fig. 3 Active p38γ dissociates PSD-95/tau/Fyn/NR complexes.

Volume 25, Issue 12, Pages e5 (December 2018)

Effect of CDV on human SF7796 xenografts in vivo.

Effects of UVB on AKT in SKH-1 mouse epidermis.

Fig. 4 Systemic AAV9 delivery of gene editing components to ΔEx44 mice rescues dystrophin expression. Systemic AAV9 delivery of gene editing components.

Presentation transcript:

AKT thr308 phosphorylation related to total AKT2 protein in SOL muscle (m. soleus) (A) and EDL muscle (m. extensor digitorum longus) (D) and AKT ser472 phosphorylation related to total AKT2 protein in SOL muscle (B) and EDL muscle (E). AKT thr308 phosphorylation related to total AKT2 protein in SOL muscle (m. soleus) (A) and EDL muscle (m. extensor digitorum longus) (D) and AKT ser472 phosphorylation related to total AKT2 protein in SOL muscle (B) and EDL muscle (E). AS-160 phosphorylation in SOL muscle (C) and EDL muscle (F), in the presence of no insulin and during 100 µU/mL insulin stimulation at rest (white bars) and 90-min POST EX (PEX) (black bars) in WT and HSL KO mice. A representative blot is shown above each graph, measured between 16 and 25 weeks of age (n = 7–9 in each group). Data are expressed as the mean ± SEM. **Significant effect of 100 µU/mL insulin (P < 0.01). Annette Karen Serup et al. Diabetes 2016;65:2932-2942 ©2016 by American Diabetes Association