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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.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
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...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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,...
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...
Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...

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Related Experiment Video

Updated: Jun 16, 2026

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
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Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

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Lysosome dysfunction triggers Atg7-dependent neural apoptosis.

Ken C Walls1, Arindam P Ghosh, Aimee V Franklin

  • 1Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0017, USA. kcwalls@uab.edu

The Journal of Biological Chemistry
|February 4, 2010
PubMed
Summary
This summary is machine-generated.

Lysosome dysfunction triggers neural precursor cell death through autophagy mediator Atg7, distinct from its protective role in starvation. This highlights Atg7

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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
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Published on: October 28, 2019

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Last Updated: Jun 16, 2026

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
06:58

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Published on: October 18, 2024

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

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

Published on: October 28, 2019

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Neuroscience

Background:

  • Macroautophagy (autophagy) degrades cellular components via lysosomes; its dysfunction is linked to neural tube defects, neurodegeneration, and cancer.
  • Lysosome integrity is crucial for autophagy completion, and its disruption can lead to autophagic vacuole accumulation and caspase activation.
  • The tumor suppressor p53, prevalent in neural precursor cells (NPCs), regulates both autophagy and apoptosis.

Purpose of the Study:

  • To investigate the hypothesis that impaired lysosome function induces NPC death through interactions between autophagy and apoptosis pathways.
  • To elucidate the specific roles of autophagy-related proteins, such as Atg7 and Beclin1, in lysosome dysfunction-induced cell death.

Main Methods:

  • Utilized FGF2-expanded NPCs and the C17.2 neural stem cell line.
  • Treated cells with lysosomotropic agent chloroquine (CQ) and vacuolar ATPase inhibitor bafilomycin A1 (Baf A1) to induce lysosome dysfunction.
  • Employed short hairpin RNA (shRNA) to knock down Atg7 and Beclin1 expression.
  • Assessed autophagic vacuole (AV) accumulation, p53 phosphorylation, caspase-3 activation, and cell death.

Main Results:

  • CQ and Baf A1 induced concentration- and time-dependent AV accumulation, p53 phosphorylation, caspase-3 activation, and cell death in NPCs.
  • Knockdown of Atg7, but not Beclin1, significantly inhibited CQ- and Baf A1-induced cell death, identifying Atg7 as an upstream mediator.
  • Cell death and caspase-3 activation were attenuated by protein synthesis inhibition, p53 deficiency, or Bax deficiency, implicating the intrinsic apoptotic pathway.
  • In contrast to lysosome dysfunction, Atg7 or Beclin1 knockdown inhibited starvation-induced AV accumulation, and Atg7 knockdown did not affect starvation-induced death.

Conclusions:

  • Atg7 and Beclin1-mediated autophagy plays a protective role during starvation.
  • Atg7 exhibits a distinct pro-apoptotic function specifically in response to lysosome dysfunction.
  • Lysosome dysfunction can trigger NPC death via a pathway involving Atg7 and the intrinsic apoptotic machinery.