NYGGF4&#160;homologous gene expression in 3T3-L1 adipocytes: regulation by FFA and adipokines (Q28513996)

GOA release 2020-03-11

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Ya-ping Zhao

1

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25 January 2017

Chun-mei Zhang

2

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25 January 2017

Chun Zhu

3

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25 January 2017

Xiao-hui Chen

4

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25 January 2017

Jia-lin Wang

5

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25 January 2017

Chen-bo Ji

6

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25 January 2017

Xia Chi

7

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25 January 2017

Qin Hong

8

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25 January 2017

Yu-zhu Peng

9

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25 January 2017

Xi-rong Guo

Molecular Biology Reports

10

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25 January 2017

1 October 2010

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25 January 2017

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25 January 2017

37

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25 January 2017

7

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25 January 2017

3291–3296

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25 January 2017

https://scigraph.springernature.com/pub.10.1007/s11033-009-9914-7

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Inhibition of insulin sensitivity by free fatty acids requires activation of multiple serine kinases in 3T3-L1 adipocytes

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Interleukin-6 enhances glucose transport in 3T3-L1 adipocytes

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Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects

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Over-expression of NYGGF4 inhibits glucose transport in 3T3-L1 adipocytes via attenuated phosphorylation of IRS-1 and Akt

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Identification and characterization of NYGGF4, a novel gene containing a phosphotyrosine-binding (PTB) domain that stimulates 3T3-L1 preadipocytes proliferation

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A phosphatidylinositol 3-kinase/Akt/mTOR pathway mediates and PTEN antagonizes tumor necrosis factor inhibition of insulin signaling through insulin receptor substrate-1.

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Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction.

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