...
首页> 外文期刊>Biological chemistry >FAM134B promotes adipogenesis by increasing vesicular activity in porcine and 3T3-L1 adipocytes
【24h】

FAM134B promotes adipogenesis by increasing vesicular activity in porcine and 3T3-L1 adipocytes

机译:FAM134B通过增加猪和3T3-L1脂肪细胞中的囊泡活性来促进脂肪组织

获取原文
获取原文并翻译 | 示例
           

摘要

Family with sequence similarity 134, Member B (FAM134B), is a cis-Golgi transmembrane protein that is known to be necessary for the long-term survival of nociceptive and autonomic ganglion neurons. Recent work has shown that FAM134B plays a pivotal role in autophagy-mediated turnover of endoplasmic reticulum (ER) membranes, tumor inhibition and lipid homeostasis. In this study, we provide mechanistic links between FAM134B and ARF-related protein 1 (ARFRP1) and further show that FAM134B resides in the Golgi apparatus. Here, we found that FAM134B increased lipid accumulation in adipocytes. Transport vehicle number and ADP-ribosylation factor (ARF) family gene expression were also increased by FAM134B overexpression, suggesting that vesicular transport activity enhanced lipid accumulation. ARF-related protein 1 (ARFRP1) is a GTPase that promotes protein trafficking. We show that FAM134B regulates the expression of ARFRP1, and the knockdown of ARFRP1 abolishes enhancement on lipid accumulation caused by FAM134B. In addition, FAM134B upregulates the PAT family protein (PAT), which associates with the lipid droplets (LDs) surface and promotes lipolysis by recruiting adipocyte triglyceride lipase (ATGL). These findings indicate that FAM134B promotes lipid accumulation and adipogenic differentiation by increasing vesicle transport activity in the Golgi apparatus and inhibiting the lipolysis of LDs.
机译:具有序列相似性134,成员B(FAM134B)的家庭是CIS-GOLGI跨膜蛋白,该蛋白已知是伤害性和自主神经神经节神经元的长期存活所必需的。最近的工作表明,FAM134B在自噬介导的内质网(ER)膜,肿瘤抑制和脂质稳态的自噬介导周转中起着枢轴作用。在这项研究中,我们提供FAM134B和ARF相关蛋白1(ARFRP1)之间的机械链接,进一步表明FAM134B位于GOLGI设备中。在这里,我们发现FAM134B增加了脂肪细胞中的脂质积累。通过FAM134B过表达也增加了运输车辆数量和ADP-核糖化因子(ARF)家族基因表达,表明囊泡传输活性增强了脂质积累。 arf相关蛋白1(Arfrp1)是促进蛋白质贩运的GTP酶。我们表明FAM134B规范了ARFRP1的表达,ARFRP1的敲低取消了FAM134B引起的脂质积累的增强。此外,FAM134B上调了与脂液滴(LDS)表面​​相关联的PAT系列蛋白(PAT),并通过募集脂肪细胞甘油三酯脂肪酶(ATG1)来促进脂解。这些发现表明,通过增加高尔基装置中的囊泡运输活性并抑制LDS的脂肪解来,FAM134B通过增加囊泡运输活性来促进脂质积累和脂肪切分化。

著录项

  • 来源
    《Biological chemistry》 |2019年第4期|共10页
  • 作者单位

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

    College of Animal Sciences Zhejiang University Zhejiang P.R. China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    arfrp1; fam134b; Golgi apparatus; lipid droplets; vesicular transport;

    机译:ARFRP1;FAM134B;GOLGI装置;脂液滴;浆果运输;

相似文献

  • 外文文献
  • 中文文献
  • 专利
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