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The Extrinsic Apoptotic Pathway01:17

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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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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.
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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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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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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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Cell death controlling complexes and their potential therapeutic role.

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Programmed cell death regulation involves multiprotein complexes. Targeting these platforms offers new therapeutic strategies for diseases like cancer and autoimmune disorders.

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Area of Science:

  • Cellular biology
  • Molecular mechanisms of cell death

Background:

  • Programmed cell death is crucial for multicellular organism homeostasis and development.
  • Aberrant cell death contributes to diseases such as cancer and autoimmune disorders.
  • Cell death initiation involves multiprotein complexes that dictate cellular fate.

Purpose of the Study:

  • To detail key cell-death complexes controlling apoptosis and necroptosis.
  • To discuss the regulation of these molecular platforms.
  • To explore the potential for pharmacological targeting of these complexes.

Main Methods:

  • Review and detailed discussion of known cell-death complexes.
  • Analysis of molecular interactions within these platforms.
  • Exploration of regulatory mechanisms governing cell death pathways.

Main Results:

  • Identified and described key complexes: DISC, complex II, TNFRI complex I/II, necrosome, RIPoptosome, apoptosome, and PIDDosome.
  • Highlighted the influence of complex composition and structure on cell death induction.
  • Underscored the role of these platforms in apoptosis and necroptosis pathways.

Conclusions:

  • Cell-death complexes are critical regulators of apoptosis and necroptosis.
  • Understanding these platforms is key to understanding cell death.
  • Pharmacological targeting of these high molecular weight platforms presents novel therapeutic avenues.