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Related Concept Videos

Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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Apoptosis01:30

Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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Phagocytosis of Apoptotic Cells

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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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Updated: Jun 13, 2025

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction
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Activity-dependent synapse elimination requires caspase-3 activation.

Zhou Yu1, Andrian Gutu1, Namsoo Kim1

  • 1Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, United States.

Elife
|June 10, 2025
PubMed
Summary
This summary is machine-generated.

Caspase-3 activation is crucial for removing excess synapses during brain development. This process is vital for normal neural circuit formation and may offer protection against neurodegenerative diseases like Alzheimer's.

Keywords:
caspase-3developmental biologymicrogliamouseneurosciencesynapse eliminationsynaptic activity

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Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Synapses are initially overproduced during brain development and subsequently eliminated via an activity-dependent process.
  • The precise mechanisms linking neuronal activity to synapse removal remain incompletely understood.
  • Weak synapses are preferentially targeted for elimination, but the molecular players are not fully elucidated.

Purpose of the Study:

  • To investigate the role of caspase-3 in activity-dependent synapse elimination during neural development.
  • To determine if caspase-3 deficiency impacts synapse elimination driven by spontaneous and experience-dependent neural activity.
  • To explore the potential of targeting caspase-3 to prevent synapse loss in neurodegenerative conditions like Alzheimer's disease.

Main Methods:

  • Utilized a developing mouse visual pathway model.
  • Manipulated synaptic transmission to induce postsynaptic caspase-3 activation.
  • Generated caspase-3 deficient mice to assess its role in synapse elimination.
  • Examined synapse elimination and microglial engulfment of inactive synapses.
  • Investigated synapse loss in a mouse model of Alzheimer's disease.

Main Results:

  • Inhibiting synaptic transmission led to postsynaptic caspase-3 activation in the developing mouse visual pathway.
  • Caspase-3 deficiency impaired synapse elimination mediated by both spontaneous and experience-dependent neural activity.
  • Activity-dependent synapse elimination was significantly blocked in caspase-3 deficient mice, with reduced engulfment of inactive synapses by microglia.
  • Caspase-3 deficiency provided protection against amyloid-β-induced synapse loss in an Alzheimer's disease mouse model.

Conclusions:

  • Caspase-3 activation is a critical molecular event in activity-dependent synapse elimination during brain development.
  • The findings highlight caspase-3 as a key regulator of synaptic pruning.
  • Targeting caspase-3 may represent a therapeutic strategy to mitigate synapse loss in neurodegenerative diseases.