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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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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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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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Overview of Cell Death01:30

Overview of Cell Death

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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...
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Necrosis01:16

Necrosis

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
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In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening
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The caspase-activated DNase: apoptosis and beyond.

Brian D Larsen1, Claus S Sørensen1

  • 1Biotech Research and Innovation Centre, University of Copenhagen, Denmark.

The FEBS Journal
|November 20, 2016
PubMed
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Subapoptotic caspase signaling, through caspase-activated DNase (CAD), triggers DNA damage responses that influence cell fate, including differentiation and senescence. This pathway also presents a potential source for oncogenic mutations.

Keywords:
CADDNA breaksICADapoptosiscaspasecell fate control

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Area of Science:

  • Cellular biology
  • Molecular signaling

Background:

  • Cellular development relies on precise signal transduction for homeostasis.
  • Apoptotic caspase signaling is crucial for cell death and balance.
  • Subapoptotic caspase signaling influences diverse cellular fates.

Purpose of the Study:

  • To review mechanisms of CAD-induced DNA breaks.
  • To highlight how CAD activity promotes varied cell fates.

Main Methods:

  • Review of existing literature on caspase signaling and DNA damage response.
  • Analysis of CAD activation via ICAD cleavage.
  • Examination of downstream effects including p53 signaling.

Main Results:

  • Subapoptotic caspase signaling activates CAD, leading to DNA breaks.
  • CAD-induced DNA breaks trigger DNA damage responses and p53 signaling.
  • Cell differentiation and senescence are demonstrated outcomes of CAD activity.

Conclusions:

  • CAD-induced DNA breaks are a key mechanism in subapoptotic caspase signaling.
  • CAD activity contributes to diverse cell fate decisions.
  • CAD's role in oncogenesis warrants further investigation.