...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation
【24h】

Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation

机译：Mitogen-Dependent DUSP1支配ERK的监管和p38信号在早期3 t3-l1脂肪细胞分化

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Knowledge concerning mechanisms that control proliferation and differentiation of preadipocytes is essential to our understanding of adipocyte hyperplasia and the development of obesity. Evidence has shown that temporal regulation of mitogen-activated protein kinase (MAPK) phosphorylation and dephosphorylation is critical for coupling extracellular stimuli to cellular growth and differentiation. Using differentiating 3T3-L1 preadipocytes as a model of adipocyte hyperplasia, we examined a role for dual-specificity phosphatase 1 (DUSP1) on the timely modulation of MAPK signaling during states of growth arrest, proliferation, and differentiation. Using real-time reverse transcription PCR (qRT-PCR), we report that DUSP1 is induced during early preadipocyte proliferation concomitant with ERK and p38 dephosphorylation. As deactivation of ERK and p38 is essential for the progression of adipocyte differentiation, we further showed that de novo mRNA synthesis was required for ERK and p38 dephosphorylation, suggesting a role for inducible phosphatases in regulating MAPK signaling. Pharmacological and genetic inhibition of DUSP1 markedly increased ERK and p38 phosphorylation during early adipocyte differentiation. Based on these findings, we postulated that loss of DUSP1 would block adipocyte hyperplasia. However, genetic loss of DUSP1 was not sufficient to prevent preadipocyte proliferation or differentiation, suggesting a role for other phosphatases in the regulation of adipogenesis. In support of this, qRT-PCR identified several MAPK-specific DUSPs induced during early (DUSP2, -4, -5, & -6), mid (DUSP4 & -16) and late (DUSP9) stages of adipocyte differentiation. Collectively, these data suggest an important role for DUSPs in regulating MAPK dephosphorylation, with an emphasis on DUSP1, during early adipogenesis. J. Cell. Physiol. 231: 1562-1574, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：有关机制,管理知识增殖和分化preadipocytes对我们理解至关重要脂肪细胞增生和的发展肥胖。增殖调节蛋白激酶(MAPK)磷酸化和去磷酸化耦合的关键细胞外刺激细胞生长和分化。区分3 t3-l1 preadipocytes作为一个模型脂肪细胞增生,我们检查的作用dual-specificity磷酸酶1 (DUSP1)期间及时调制MAPK信号状态增长的逮捕、扩散和分化。转录PCR(存在),我们报告DUSP1在早期诱导preadipocyte吗伴随ERK和p38增殖去磷酸化。对脂肪细胞的发展至关重要分化,我们进一步表明新创信使rna合成ERK和p38所需去磷酸化,暗示的作用在调节MAPK诱导磷酸酶信号。ERK和p38 DUSP1显著增加磷酸化在早期脂肪细胞分化。假定DUSP1将阻止的损失脂肪细胞增生。DUSP1并不足以防止preadipocyte增殖或分化,暗示为其他监管磷酸酶的作用脂肪形成。确定几个MAPK-specific DUSPs诱导在早期(DUSP2, 4、5、6),中期(DUSP4 &-16年)和后期(DUSP9)的脂肪细胞阶段分化。一个重要的角色在调节MAPK DUSPs去磷酸化,强调DUSP1,在早期脂肪形成。1562 - 1574年,2016年。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号