The insulin‐PI3K‐Rac1 axis contributes to terminal adipocyte differentiation through regulation of actin cytoskeleton dynamics
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- Haruko Kunitomi
- Division of Gene Regulation Institute for Advanced Medical Research Keio University School of Medicine Tokyo Japan
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- Yoshinao Oki
- Laboratory of Cell and Tissue Biology College of Bioresource Sciences Nihon University Fujisawa Japan
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- Nobuyuki Onishi
- Division of Gene Regulation Institute for Advanced Medical Research Keio University School of Medicine Tokyo Japan
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- Koichiro Kano
- Laboratory of Cell and Tissue Biology College of Bioresource Sciences Nihon University Fujisawa Japan
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- Kouji Banno
- Department of Obstetrics and Gynecology Keio University School of Medicine Tokyo Japan
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- Daisuke Aoki
- Department of Obstetrics and Gynecology Keio University School of Medicine Tokyo Japan
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- Hideyuki Saya
- Division of Gene Regulation Institute for Advanced Medical Research Keio University School of Medicine Tokyo Japan
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- Hiroyuki Nobusue
- Division of Gene Regulation Institute for Advanced Medical Research Keio University School of Medicine Tokyo Japan
書誌事項
- 公開日
- 2020-01-29
- 資源種別
- journal article
- 権利情報
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- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
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- 10.1111/gtc.12747
- 公開者
- Wiley
この論文をさがす
説明
<jats:title>Abstract</jats:title><jats:p>Adipocyte differentiation is accompanied by a pronounced change in the actin cytoskeleton characterized by the reorganization of filamentous (F)‐actin stress fibers into cortical F‐actin structures. We previously showed that depolymerization of F‐actin stress fibers induced by inactivation of RhoA–ROCK (Rho‐associated kinase) signaling acts as a trigger for adipocyte differentiation. The relevance and underlying mechanism of the formation of cortical F‐actin structures from depolymerized actin during adipocyte differentiation have remained unclear, however. We have now examined the mechanistic relation between actin dynamics and adipogenic induction. Transient exposure to the actin‐depolymerizing agent latrunculin A (LatA) supported the formation of adipocyte‐associated cortical actin structures and the completion of terminal adipocyte differentiation in the presence of insulin, whereas long‐term exposure to LatA prevented such actin reorganization as well as terminal adipogenesis. Moreover, these effects of insulin were prevented by inhibition of phosphatidylinositol 3‐kinase (PI3K)–Rac1 signaling and the actin‐related protein 2/3 (Arp2/3) complex which is a critical component of the cortical actin networks. Our findings thus suggest that the insulin‐PI3K‐Rac1 axis leads to the formation of adipocyte‐associated cortical actin structures which is essential for the completion of adipocyte differentiation.</jats:p>
収録刊行物
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- Genes to Cells
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Genes to Cells 25 (3), 165-174, 2020-01-29
Wiley
