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Related Concept Videos

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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...
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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In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
08:40

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

Published on: November 22, 2017

BH3 mimetics activate multiple pro-autophagic pathways.

S A Malik1, I Orhon, E Morselli

  • 1INSERM, U848, Institut Gustave Roussy, Villejuif, France.

Oncogene
|April 5, 2011
PubMed
Summary
This summary is machine-generated.

BH3 mimetics like ABT737 trigger autophagy by disrupting Bcl-2 interactions and activating multiple signaling pathways, including AMPK and IKK. These compounds exhibit pleiotropic effects on cellular signaling, promoting autophagy through diverse routes.

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Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy
09:59

Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy

Published on: May 3, 2013

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • BH3 mimetics are known to induce autophagy by targeting anti-apoptotic proteins.
  • The interaction between Beclin 1 and Bcl-2/Bcl-X(L) is crucial for regulating autophagy.
  • The precise signaling pathways modulated by BH3 mimetics beyond Bcl-2 inhibition require further investigation.

Purpose of the Study:

  • To investigate whether the BH3 mimetic ABT737 stimulates other pro-autophagic signal-transduction pathways.
  • To identify novel signaling targets of ABT737 involved in autophagy induction.
  • To explore the pleiotropic effects of BH3 mimetics on cellular signaling.

Main Methods:

  • Treatment of cells with ABT737 and HA14-1 (another BH3 mimetic).
  • Analysis of protein phosphorylation status using Western blotting.
  • Assessment of kinase activities and protein dephosphorylation.
  • Pharmacological and genetic inhibition of key signaling molecules (IKK, Sirtuin, MDM2).

Main Results:

  • ABT737 induced activating phosphorylation of AMP-dependent kinase (AMPK) and acetyl CoA carboxylase.
  • ABT737 caused activating phosphorylation of inhibitor of NF-κB (IκB) kinase (IKK) and hyperphosphorylation of IκB.
  • ABT737 inhibited mammalian target of rapamycin (mTOR) activity and dephosphorylated p53, glycogen synthase kinase-3, and Akt.
  • These effects were shared by HA14-1, indicating a class effect of BH3 mimetics.
  • Inhibition of IKK, Sirtuin, or MDM2 prevented ABT737-induced autophagy.

Conclusions:

  • BH3 mimetics like ABT737 exert unexpected and pleiotropic pro-autophagic effects.
  • These compounds modulate multiple signaling pathways, including AMPK, IKK, mTOR, p53, and Akt, to induce autophagy.
  • The findings reveal a broader impact of BH3 mimetics on cellular signaling than previously understood, with implications for therapeutic strategies.