相关实验视频

Updated: Jun 22, 2025

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body

Published on: August 4, 2022

Atg8/LC3控制了和人类系统营养余信号

Aditi Madan¹, Kevin P Kelly¹, Patrick Bahk¹

¹Basic Sciences Division, Fred Hutch, Seattle, WA 98109, USA.

Current biology : CB

|July 2, 2024

概括

自蛋白 (Atg8/LC3) 通过促进营养余期间的皮分泌和响应缺乏,来管理营养的流动. 营养感应中的这种双向作用是代谢平衡的关键,并可能为肥胖症的治疗提供信息.

科学领域:

细胞生物学细胞生物学
代谢调节代谢调节代谢调节
分子机制的分子机制

背景情况:

生物必须在营养物质的可用性波动的情况下保持能量恒温.
脂肪细胞分泌像勒一样的皮蛋白来信号营养状况,但人体细胞的勒分泌机制尚不清楚.
肥胖症涉及代谢失调,与改变的瘦素分泌有关.

研究的目的:

研究Atg8/LC3蛋白质在人类脂肪细胞中的脂蛋白分泌中的作用.
为了阐明在营养余条件下控制勒素释放的分子机制.
了解Atg8/LC3在营养感应中的双向功能.

主要方法:

在人类脂肪细胞和多虫模型中研究了Atg8/LC3家族蛋白质.
利用蛋白质组分析来识别蛋白质相互作用和通路.
研究了细胞外囊泡 (EV) 介导的分泌途径.

主要成果:

在营养过剩期间,Atg8/LC3蛋白质促进了叶丁及其Drosophila ortholog,未配对2 (Upd2) 的分泌.
LC3将瘦素引导到一个特定的分泌途径,涉及LC3依赖的细胞外囊泡载荷和分泌 (LDELS).
影响Drosophila中Atg8与Upd2相互作用的突变导致阿迪波金保留,改变脂质储存,饥饿反应和转录组变化.

结论:

Atg8/LC3蛋白质在营养感知中发挥着保守的双向作用,在过剩时促进脂蛋白分泌,并在缺乏时作出反应.
在人类脂肪细胞中,LDELS代表了一种新的瘦素分泌途径.
了解Atg8/LC3的功能为代谢障碍提供了潜在的治疗点.

关键词:

在Upd2中,我们可以使用Upd2.这是一种阿迪波基因 (adipokine).自独立自独立自独立外基因组是外基因组的组成部分.勒普丁是一种素.肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖和感和感是一种感觉.抗饥饿能力抗饥饿能力抗饥饿能力非传统的分泌物

更多相关视频

Combining Quantitative Food-intake Assays and Forcibly Activating Neurons to Study Appetite in Drosophila

Combining Quantitative Food-intake Assays and Forcibly Activating Neurons to Study Appetite in Drosophila

Published on: April 24, 2018

Quantification of Macronutrients Intake in a Thermogenetic Neuronal Screen using Drosophila Larvae

Quantification of Macronutrients Intake in a Thermogenetic Neuronal Screen using Drosophila Larvae

Published on: June 11, 2020

相关概念视频

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...