Cb1 PYXXM motifs activate the P85 subunit of phosphatidylinositol 3-kinase,Crk,atypical protein kinase C,and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes

Atsushi Miura; Mini P.Sajan; Mary L.Standaert; Gautam Bandyopadhyay; Dawn M.Franklin; Renee Lea-Currie; Robert V.Farese

首页> 外文期刊>Biochemistry >Cb1 PYXXM motifs activate the P85 subunit of phosphatidylinositol 3-kinase,Crk,atypical protein kinase C,and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes

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Cb1 PYXXM motifs activate the P85 subunit of phosphatidylinositol 3-kinase,Crk,atypical protein kinase C,and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes

机译：Cb1 PYXXM基序激活噻唑烷二酮在3T3 / L1和人脂肪细胞中的作用期间，激活磷脂酰肌醇3-激酶，Crk，非典型蛋白激酶C和葡萄糖转运的P85亚基

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The thiazolidinedione (TZD),rosiglitazone,has previously been found to tyrosine-phosphorylate Cbl and activate Cbl-dependent phosphatidylinositol (PI) 3-kinase and atypical protein kinase Cs (aPKCs) while stimulating glucose transport in 3T3/L1 adipocytes.Presently,the role of Cbl in rosigliazone action was further assessed in the 3T3/L1 and human adipocytes by expressing Y371F and/or Y731F mutant forms of Cbl that nullified the functionality of canonical pYXXM motifs in Cbl.These mutants diminished the interaction of Cbl with the p85 subunit of PI 3-kinase and inhibited subsequent increases in Cbl-dependent PI3-kinase activity,aPKC activity,and glucose transport.These mutants also inhibited the interaction of Cbl with Crk,which has been implicated in the activation of other PI 3-kinase-independent signaling factors that have been found to be required during activation of glucose transport by insulin and other agonists.We conclude that pYXXM motifs in Cb1 serve to activate PI 3-kinase-dependent and possibly PI 3-kinse-independent pathways that are required for TZD-dependent glucose transport in adipocytes.

机译：噻唑烷二酮（TZD）罗格列酮以前被发现可酪氨酸磷酸化Cbl并激活Cbl依赖性磷脂酰肌醇（PI）3-激酶和非典型蛋白激酶Cs（aPKCs），同时刺激3T3 / L1脂肪细胞中的葡萄糖转运。通过表达Cbl的Y371F和/或Y731F突变体形式使Cbl的典型pYXXM图案功能失效，进一步评估了Cbl在3T3 / L1和人类脂肪细胞中的作用，这些突变体减弱了Cbl与p85亚基的相互作用。抑制PI 3激酶的活性，并抑制随后的Cbl依赖性PI3激酶活性，aPKC活性和葡萄糖转运的增加。这些突变体还抑制Cbl与Crk的相互作用，这与其他PI 3激酶-的激活有关。已经发现胰岛素和其他激动剂激活葡萄糖转运过程中需要独立的信号传导因子。我们得出结论，Cb1中的pYXXM基序可激活PI 3-激酶-依赖和可能与PI 3激酶无关的途径，这是脂肪细胞中TZD依赖性葡萄糖转运所必需的。

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《Biochemistry》 |2003年第48期|共7页
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Atsushi Miura; Mini P.Sajan; Mary L.Standaert; Gautam Bandyopadhyay; Dawn M.Franklin; Renee Lea-Currie; Robert V.Farese;
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1. Cb1 PYXXM motifs activate the P85 subunit of phosphatidylinositol 3-kinase,Crk,atypical protein kinase C,and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes [J] . Atsushi Miura, Mini P.Sajan, Mary L.Standaert, Biochemistry . 2003,第48期

机译：Cb1 PYXXM基序激活噻唑烷二酮在3T3 / L1和人脂肪细胞中的作用期间，激活磷脂酰肌醇3-激酶，Crk，非典型蛋白激酶C和葡萄糖转运的P85亚基
2. The expression of the p85α subunit of phosphatidylinositol 3-Kinase is induced by activation of the peroxisome proliferator-activated receptor γ in human adipocytes [J] . J. Rieusset, C. Chambrier, K. Bouzakri, Diabetologia . 2001,第5期

机译：磷脂酰肌醇3-激酶的p85α亚基的表达是通过激活人脂肪细胞中的过氧化物酶体增殖物激活的受体γ来诱导的
3. Combined thiazolidinedione–metformin treatment synergistically improves insulin signalling to insulin receptor substrate-1-dependent phosphatidylinositol 3-kinase, atypical protein kinase C and protein kinase B/Akt in human diabetic muscle [J] . N. Temofonte, M. P. Sajan, S. Nimal, Diabetologia . 2009,第1期

机译：噻唑烷二酮-二甲双胍联合治疗可协同改善人糖尿病肌肉中胰岛素受体1依赖性磷脂酰肌醇3激酶，非典型蛋白激酶C和蛋白激酶B / Akt的胰岛素信号传导
4. THE GLUCOSE TRANSPORTER IS A GLYCOPROTEIN OF M(R) 55,000 AND IS PROBABLY NOT PHOSPHORYLATED IN RESPONSE TO BIOLOGICAL ACTIVATORS OF TRANSPORT (HUMAN ERYTHROCYTE, PROTEIN KINASE C, MONOCLONAL ANTIBODIES). [D] . ALLARD, W. JEFFREY. 1986

机译：葡萄糖转运蛋白是M（R）55,000的糖蛋白，可能不被磷酸化以响应生物转运因子（人类红细胞，蛋白激酶C，单克隆抗体）。
5. Combined thiazolidinedione–metformin treatment synergistically improves insulin signalling to insulin receptor substrate-1-dependent phosphatidylinositol 3-kinase atypical protein kinase C and protein kinase B/Akt in human diabetic muscle [O] . N. Temofonte, M. P. Sajan, S. Nimal, -1

机译：噻唑烷二酮-二甲双胍联合治疗可协同改善人糖尿病肌肉中胰岛素受体1依赖性磷脂酰肌醇3激酶非典型蛋白激酶C和蛋白激酶B / Akt的胰岛素信号传导
6. The expression of the p85α subunit of phosphatidylinositol 3-Kinase is induced by activation of the peroxisome proliferator-activated receptor γ in human adipocytes [O] . J. Rieusset, C. Chambrier, K. Bouzakri, 2001

机译：通过在人脂肪细胞中活化过氧酶体增殖物激活的受体γ诱导磷脂酰肌醇3-激酶P85α亚基的表达

Cb1 PYXXM motifs activate the P85 subunit of phosphatidylinositol 3-kinase,Crk,atypical protein kinase C,and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes

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