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Related Concept Videos

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.
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Autophagy01:27

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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,...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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Autophagic Cell Death01:18

Autophagic Cell Death

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Receptor-mediated Endocytosis01:38

Receptor-mediated Endocytosis

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Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

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Related Experiment Video

Updated: Jun 19, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

Autophagy induction by the pathogen receptor CD46.

Pierre-Emmanuel Joubert1, Grégory Meiffren, Isabel Pombo Grégoire

  • 1Université de Lyon, Lyon, F-69003, France.

Cell Host & Microbe
|October 20, 2009
PubMed
Summary
This summary is machine-generated.

CD46 engagement triggers autophagy, an innate immune response. This pathway, involving CD46-Cyt-1 and GOPC, helps control infections by initiating cellular clearance mechanisms against pathogens like measles virus.

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Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
10:33

Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages

Published on: October 25, 2017

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Autophagy is a cellular process for clearing and recycling components, crucial for innate immunity against pathogens.
  • Pathogens often evade or exploit autophagy, and the induction pathways remain unclear.
  • CD46 is a cell surface receptor that binds various pathogens.

Purpose of the Study:

  • To investigate the molecular mechanisms by which CD46 engagement induces autophagy.
  • To identify the specific CD46 splice variant and interacting proteins involved in autophagy induction.
  • To determine if CD46-mediated autophagy is a general mechanism for controlling CD46-binding pathogens.

Main Methods:

  • Studied autophagy induction upon CD46 engagement using cell-based assays.
  • Investigated the interaction between CD46-Cyt-1, GOPC, and the VPS34/Beclin1 complex.
  • Examined the role of this pathway in response to measles virus and group A Streptococcus infection.

Main Results:

  • CD46 engagement alone is sufficient to induce autophagy.
  • The CD46-Cyt-1 splice variant interacts with GOPC, linking CD46 to the VPS34/Beclin1 autophagosome formation complex.
  • Measles virus and group A Streptococcus utilize this CD46-Cyt-1/GOPC pathway to induce autophagy.

Conclusions:

  • Cell surface receptor engagement, specifically CD46, can directly trigger autophagy as an innate immune response.
  • The CD46-Cyt-1/GOPC pathway is a key mechanism for initiating autophagy against certain microbial pathogens.
  • This discovery provides insights into host-pathogen interactions and autophagy regulation during infection.