scholarly journals Cell Adhesion and Focal Adhesion Kinase Regulate Insulin Receptor Substrate-1 Expression

2000 ◽  
Vol 275 (49) ◽  
pp. 38371-38377 ◽  
Author(s):  
Patricia Lebrun ◽  
Véronique Baron ◽  
Christof R. Hauck ◽  
David D. Schlaepfer ◽  
Emmanuel Van Obberghen
Keyword(s):  
Cell Adhesion ◽  
Insulin Receptor ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1

scholarly journals Insulin Receptor Substrate-1 as a Signaling Molecule for Focal Adhesion Kinase pp125FAKand pp60src

1998 ◽  
Vol 273 (48) ◽  
pp. 32244-32253 ◽  
Author(s):  
Patricia Lebrun ◽  
Isabelle Mothe-Satney ◽  
Laurent Delahaye ◽  
Emmanuel Van Obberghen ◽  
Véronique Baron
Keyword(s):  
Insulin Receptor ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Signaling Molecule

scholarly journals MEK Kinase 1 Interacts with Focal Adhesion Kinase and Regulates Insulin Receptor Substrate-1 Expression

2002 ◽  
Vol 278 (6) ◽  
pp. 3846-3851 ◽  
Author(s):  
Toshiaki Yujiri ◽  
Ryouhei Nawata ◽  
Toru Takahashi ◽  
Yutaka Sato ◽  
Yukio Tanizawa ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Mek Kinase

scholarly journals Mechanisms of regulation of cell adhesion and motility by insulin receptor substrate-1 in prostate cancer cells

Oncogene ◽  
2001 ◽  
Vol 20 (4) ◽  
pp. 490-500 ◽  
Author(s):  
Krzysztof Reiss ◽  
Jin-Ying Wang ◽  
Gaetano Romano ◽  
Xiao Tu ◽  
Francesca Peruzzi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Adhesion ◽  
Insulin Receptor ◽  
Cancer Cells ◽  
Insulin Receptor Substrate ◽  
Prostate Cancer Cells ◽  
Insulin Receptor Substrate 1

Focal adhesion kinase mediates cell survival via NF-κB and ERK signaling pathways

2007 ◽  
Vol 292 (4) ◽  
pp. C1339-C1352 ◽  
Author(s):  
Danshan Huang ◽  
Michelle Khoe ◽  
Merone Befekadu ◽  
Sue Chung ◽  
Yasunori Takata ◽  
...  
Keyword(s):  
Growth Factor ◽  
Insulin Receptor ◽  
Cell Survival ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Erk Signaling ◽  
Insulin Receptor Substrate ◽  
Serum Withdrawal ◽  
Erk Phosphorylation

Focal adhesion kinase (FAK) is important to cellular functions such as proliferation, migration, and survival of anchorage-dependent cells. We investigated the role of FAK in modulating normal cellular responses, specifically cell survival in response to inflammatory stimuli and serum withdrawal, using FAK-knockout (FAK−/−) embryonic fibroblasts. FAK−/− fibroblasts were more vulnerable to TNF-α-induced apoptosis, as measured by terminal deoxynucleotidyl transferase positivity. FAK−/− fibroblasts also demonstrated increased procaspase-3 cleavage to p17 subunit, whereas this was undetectable in FAK+/+ fibroblasts. Insulin receptor substrate-1 expression was completely abolished and NF-κB activity was reduced, with a concomitant decrease in abundance of the anti-apoptotic protein Bcl-xL in FAK−/− cells. Upon serum withdrawal, FAK+/+ cells exhibited marked attenuation of basal ERK phosphorylation, while FAK−/− cells, in contrast, maintained high basal ERK phosphorylation. Moreover, inhibition of ERK phosphorylation potentiated serum withdrawal-induced caspase-3 activity. This was paralleled by increased insulin receptor substrate (IRS)-2 expression in FAK−/− cells, although both insulin- and IGF-1-mediated phosphorylation of Akt/PKB and GSK-3 were impaired. This suggests that IRS-2 protects against apoptosis upon serum withdrawal via the ERK signaling pathway. The specific role of FAK to protect cells from apoptosis is regulated by activation and phosphorylation of NF-κB and interaction between activated growth factor anti-apoptotic signaling pathways involving both phosphatidylinositol 3-kinase/Akt and MAPK/ERK1/2. We demonstrate that FAK is necessary for upregulation of the anti-apoptotic NF-κB response, as well as for normal expression of growth factor signaling proteins. Thus we propose a novel role for FAK in protection from cytokine-mediated apoptosis.

The Association between Maternal/Fetal Insulin Receptor Substrate 1 Gene Polymorphism rs1801278 and Gestational Diabetes Mellitus in a Chinese Population

2021 ◽  
pp. 1-8
Author(s):  
Lingling Wu ◽  
Changping Fang ◽  
Jun Zhang ◽  
Yanchou Ye ◽  
Haiyan Zhao
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gene Polymorphism ◽  
Gestational Diabetes Mellitus ◽  
Insulin Receptor ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Insulin Receptor Substrate ◽  
Single Center ◽  
Insulin Receptor Substrate 1

<b><i>Objectives:</i></b> Insulin receptor substrate 1 (IRS1) is a crucial factor in the insulin signaling pathway. IRS1 gene polymorphism rs1801278 in mothers has been reported to be associated with gestational diabetes mellitus (GDM). However, it is not clear whether IRS1 gene polymorphism rs1801278 in fetuses is associated with their mothers’ GDM morbidity. The purpose of this study is to analyze the association between maternal, fetal, or maternal/fetal <i>IRS1</i> gene polymorphism rs1801278 and GDM risk. <b><i>Design:</i></b> The study was a single-center, prospective cohort study. In total, 213 pairs of GDM mothers/fetuses and 191 pairs of control mothers/fetuses were included in this study. They were recruited after they underwent oral glucose tolerance test during 24–28 weeks of gestation and followed up until delivery. All participants received the conventional interventions (diet and exercise), and no special therapy except routine treatment. <b><i>Methods:</i></b> A total of 213 pairs of GDM mothers/fetuses and 191 pairs of normal blood glucose pregnant mothers/fetuses were ge­notyped using PCR and DNA sequencing from January 2015 to September 2016. Maternal/fetal <i>IRS1</i> gene polymorphism rs1801278 was analyzed and compared between 2 groups. <b><i>Results:</i></b> There were no significant differences in the frequency of individual mothers’ or fetuses’ <i>IRS1</i> rs1801278 polymorphisms between 2 groups; if both the mothers and fetuses carried A allele, significantly lower GDM morbidity was observed in the mothers. <b><i>Limitations:</i></b> The sample size was relatively small as a single-center study. <b><i>Conclusions:</i></b> Our study suggested that maternal/fetal rs1801278 polymorphism of <i>IRS1</i> is a modulating factor in GDM; both mothers/fetuses carrying the A allele of rs1801278 may protect the mothers against the development of GDM.

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