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Related Concept Videos

Caspases01:24

Caspases

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 cells.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Apoptosis01:30

Apoptosis

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 reduction of the tissue.
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...
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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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

C. elegans EIF-3.K promotes programmed cell death through CED-3 caspase.

Chun-Yi Huang1, Jia-Yun Chen, Shu-Chun Wu

  • 1Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan.

Plos One
|May 17, 2012
PubMed
Summary
This summary is machine-generated.

A newly identified protein, eukaryotic translation initiation factor 3 subunit k (eIF-3.K), promotes programmed cell death (apoptosis) in C. elegans. This protein acts upstream of the CED-3 caspase, and its function is conserved in humans.

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Programmed cell death (apoptosis) is crucial for metazoan development and homeostasis.
  • Caspases are central executioners of apoptosis, activated by an inhibitory cascade involving EGL-1, CED-9, and CED-4 in C. elegans.

Purpose of the Study:

  • To identify novel regulators of programmed cell death in C. elegans.
  • To elucidate the role and mechanism of eukaryotic translation initiation factor 3 subunit k (eIF-3.K) in apoptosis.

Main Methods:

  • Genetic screens in C. elegans to identify new cell death regulators.
  • Loss-of-function and overexpression studies of eif-3.K.
  • Cell-specific promoter analysis.
  • Analysis of genetic interactions with known apoptosis pathway components (ced-3, ced-4).
  • Structure-function analysis of the EIF-3.K protein, including domain mapping.
  • Cross-species functional complementation using human eIF3k.

Main Results:

  • The loss of eif-3.K reduced cell death in both somatic and germ cells.
  • Overexpression of eif-3.K led to a significant increase in cell death.
  • eIF-3.K promotes cell death in a cell-autonomous manner.
  • Loss of eIF-3.K suppressed ced-4-induced but not ced-3-induced cell death.
  • eIF-3.K acts upstream of CED-3 caspase activation.
  • The WH domain of EIF-3.K is necessary and sufficient for its cell death-promoting activity.
  • Human eIF3k partially substituted for C. elegans eif-3.K, indicating conserved function.

Conclusions:

  • eIF-3.K is a novel pro-apoptotic factor in C. elegans that functions upstream of CED-3.
  • The cell death-promoting function of EIF-3.K, particularly its WH domain, is conserved across species.
  • This discovery expands our understanding of the molecular machinery regulating apoptosis.