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Related Concept Videos

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,...
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...
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...
Intralumenal Vesicles and Multivesicular Bodies01:38

Intralumenal Vesicles and Multivesicular Bodies

Intraluminal vesicles (ILVs) are small vesicles 50-80 nm in diameter formed during the maturation of early endosomes. A specialized endosome containing numerous ILVs is called a multivesicular body (MVB). ILVs contain internalized molecules such as antigens, nucleic acids, proteins, and metabolites. Some of these molecules are released from the MVBs inside exosomes and are transported to other cells. Other MVBs contain molecules that are retained in the ILVs and are later degraded within the...
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...

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Related Experiment Video

Updated: Jun 9, 2026

The Lactate Dehydrogenase Sequestration Assay &#8212; A Simple and Reliable Method to Determine Bulk Autophagic Sequestration Activity in Mammalian Cells
09:34

The Lactate Dehydrogenase Sequestration Assay — A Simple and Reliable Method to Determine Bulk Autophagic Sequestration Activity in Mammalian Cells

Published on: July 27, 2018

Endogenous HMGB1 regulates autophagy.

Daolin Tang1, Rui Kang, Kristen M Livesey

  • 1Damage Associated Molecular Pattern Molecule Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15219, USA. tangd2@upmc.edu

The Journal of Cell Biology
|September 8, 2010
PubMed
Summary
This summary is machine-generated.

High mobility group box 1 (HMGB1) regulates autophagy, a cellular process crucial for survival during stress. HMGB1

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

Published on: October 28, 2019

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Immunology

Background:

  • Autophagy is a vital cellular process for degrading damaged components and producing energy during stress.
  • High-mobility group box 1 (HMGB1) is a nuclear protein with roles in DNA binding and extracellular signaling.
  • HMGB1 acts as a damage-associated molecular pattern (DAMP) molecule, influencing immune responses.

Purpose of the Study:

  • To investigate the role of High-mobility group box 1 (HMGB1) in regulating autophagy.
  • To elucidate the molecular mechanisms by which HMGB1 influences autophagic flux.
  • To determine the therapeutic potential of targeting HMGB1 for autophagy modulation.

Main Methods:

  • Investigated HMGB1's translocation to the cytosol upon reactive oxygen species (ROS) stimulation.
  • Examined the interaction between HMGB1 and Beclin1, a key autophagy protein, using biochemical assays.
  • Utilized site-directed mutagenesis of HMGB1 (C106, C23/45) to assess its impact on autophagy.
  • Assessed the effect of pharmacological inhibition of HMGB1 cytoplasmic translocation on autophagy.

Main Results:

  • HMGB1 promotes autophagic flux, particularly under conditions of cellular stress.
  • Cytosolic translocation of HMGB1, induced by ROS, enhances autophagy.
  • HMGB1 directly interacts with Beclin1, displacing Bcl-2 and promoting autophagy.
  • Mutation of C106 in HMGB1 facilitates cytosolic localization and sustained autophagy.
  • The disulfide bridge (C23/45) in HMGB1 is essential for Beclin1 binding and autophagy.
  • Inhibition of HMGB1 translocation reduces starvation-induced autophagy.

Conclusions:

  • Endogenous HMGB1 is a critical positive regulator of autophagy.
  • HMGB1 enhances cell survival and mitigates programmed cell death by promoting autophagy.
  • Targeting HMGB1's interaction with Beclin1 presents a potential therapeutic strategy for modulating autophagy.