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Cell adhesion and focal adhesion kinase regulate insulin receptor substrate-1 expression

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2000

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Lebrun, Patricia
Baron, Véronique
Schlaepfer, David D.
Obberghen, Emmanuel van

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Published

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Journal of Biological Chemistry. 2000, 275(49), pp. 38371-38377. ISSN 0021-9258. Available under: doi: 10.1074/jbc.M006162200

Zusammenfassung

bIntegrins are transmembrane receptors involved in interactions between cells and extracellular matrix proteins. Here we show that cell adhesion regulates insulin receptor substrate-1 (IRS-1) mRNA synthesis. When fibroblasts are held in suspension, lower levels of IRS-1 mRNA, but not of IRS-2 mRNA, are detected, and this effect is due to the negative regulation of IRS-1 transcription rather than to decreased mRNA stability. Upon fibronectin- or vitronectin-mediated integrin stimulation, the level of IRS-1 mRNA was restored within 4 h. The focal adhesion kinase (FAK) is known to be activated upon integrin stimulation, and we found that IRS-1 was not expressed in FAK-/- cells. Stable re-expression of epitope-tagged FAK in FAK-/- fibroblasts (DA2 cells) restored normal levels of IRS-1 expression, confirming that IRS-1 mRNA expression is regulated by FAK. It is known that integrins activate the JNK pathway. However, in adherent FAK-/- cells, we failed to detect activation of JNK, whereas JNK was stimulated in DA2 cells. This confirms the role of FAK in integrin-induced JNK stimulation. FAK-independent stimulation of JNK with anisomycin treatment both in FAK-/- cells and in suspended FAK+/+ cells confirmed that IRS-1 mRNA transcription can be partially regulated by JNK. We suggest that integrins can modulate insulin and insulin-like growth factor-1 signaling pathways by regulating the levels of IRS-1 in cells and that FAK-mediated signaling to JNK is one pathway involved in this process.

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Fachgebiet (DDC)
570 Biowissenschaften, Biologie

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NH2-terminal kinase, FAK, focal adhesion kinase, ERK, extracellular signal-regulated kinase

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ISO 690LEBRUN, Patricia, Véronique BARON, Christof R. HAUCK, David D. SCHLAEPFER, Emmanuel van OBBERGHEN, 2000. Cell adhesion and focal adhesion kinase regulate insulin receptor substrate-1 expression. In: Journal of Biological Chemistry. 2000, 275(49), pp. 38371-38377. ISSN 0021-9258. Available under: doi: 10.1074/jbc.M006162200
BibTex
@article{Lebrun2000adhes-7657,
  year={2000},
  doi={10.1074/jbc.M006162200},
  title={Cell adhesion and focal adhesion kinase regulate insulin receptor substrate-1 expression},
  number={49},
  volume={275},
  issn={0021-9258},
  journal={Journal of Biological Chemistry},
  pages={38371--38377},
  author={Lebrun, Patricia and Baron, Véronique and Hauck, Christof R. and Schlaepfer, David D. and Obberghen, Emmanuel van}
}
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    <dcterms:abstract xml:lang="deu">bIntegrins are transmembrane receptors involved in interactions between cells and extracellular matrix proteins. Here we show that cell adhesion regulates insulin receptor substrate-1 (IRS-1) mRNA synthesis. When fibroblasts are held in suspension, lower levels of IRS-1 mRNA, but not of IRS-2 mRNA, are detected, and this effect is due to the negative regulation of IRS-1 transcription rather than to decreased mRNA stability. Upon fibronectin- or vitronectin-mediated integrin stimulation, the level of IRS-1 mRNA was restored within 4 h. The focal adhesion kinase (FAK) is known to be activated upon integrin stimulation, and we found that IRS-1 was not expressed in FAK-/- cells. Stable re-expression of epitope-tagged FAK in FAK-/- fibroblasts (DA2 cells) restored normal levels of IRS-1 expression, confirming that IRS-1 mRNA expression is regulated by FAK. It is known that integrins activate the JNK pathway. However, in adherent FAK-/- cells, we failed to detect activation of JNK, whereas JNK was stimulated in DA2 cells. This confirms the role of FAK in integrin-induced JNK stimulation. FAK-independent stimulation of JNK with anisomycin treatment both in FAK-/- cells and in suspended FAK+/+ cells confirmed that IRS-1 mRNA transcription can be partially regulated by JNK. We suggest that integrins can modulate insulin and insulin-like growth factor-1 signaling pathways by regulating the levels of IRS-1 in cells and that FAK-mediated signaling to JNK is one pathway involved in this process.</dcterms:abstract>
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