Related Experiment Video

Updated: May 15, 2026

Study of Protein-protein Interactions in Autophagy Research
14:08

Study of Protein-protein Interactions in Autophagy Research

Published on: September 9, 2017

MIR181A regulates starvation- and rapamycin-induced autophagy through targeting of ATG5

Kumsal Ayse Tekirdag1, Gozde Korkmaz, Deniz Gulfem Ozturk

  • 1Faculty of Engineering and Natural Sciences, Biological Sciences and Bioengineering Program, Sabanci University, Istanbul, Turkey.

Autophagy
|January 17, 2013
PubMed

Insights

MicroRNAs regulate cellular recycling through autophagy. MIR181A, a specific microRNA, inhibits autophagy by targeting ATG5, a key protein in the process.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Macroautophagy (autophagy) is a vital cellular process for degrading damaged components, crucial for maintaining cell health.
  • Dysregulation of autophagy is implicated in various diseases, including cancer and neurodegenerative disorders.
  • MicroRNAs (miRNAs) have emerged as critical regulators of cellular processes, including autophagy.

Purpose of the Study:

  • To identify and characterize novel microRNAs that regulate autophagy.
  • To investigate the role of MIR181A in controlling autophagic activity.
  • To elucidate the molecular mechanism by which MIR181A modulates autophagy.

Main Methods:

  • Overexpression of MIR181A in human cancer cell lines (MCF-7, Huh-7, K562).
  • Inhibition of endogenous miRNA activity using antagomirs.
  • Identification of ATG5 as a direct target of MIR181A using luciferase reporter assays and Western blotting.
  • Rescue experiments using miRNA-insensitive ATG5 constructs.

Main Results:

  • MIR181A overexpression significantly attenuated starvation- and rapamycin-induced autophagy.
  • Inactivation of endogenous miRNAs using antagomirs enhanced autophagic activity.
  • MIR181A directly targets ATG5, leading to decreased ATG5 protein levels.
  • Restoration of ATG5 expression rescued the autophagic defects caused by MIR181A.

Conclusions:

  • MIR181A is a novel and significant regulator of macroautophagy.
  • ATG5 acts as a rate-limiting target for MIR181A-mediated autophagy regulation.
  • Understanding the MIR181A-ATG5 axis provides new insights into autophagy control and potential therapeutic strategies.
Keywords:
ATG5MTORhsa-miR-181amacroautophagymammalian autophagy regulationmicroRNArapamycinstarvation

More Related Videos

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body06:02

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

Published on: August 4, 2022

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

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 Pathway01:22

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 rapamycin-insensitive companion...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...