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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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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
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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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Proteins can form homomeric complexes with another unit of the same protein or heteromeric complexes with different types.  Most protein complexes self-assemble spontaneously via ordered pathways, while some proteins need assembly factors that guide their proper assembly. Despite the crowded intracellular environment, proteins usually interact with their correct partners and form functional complexes.
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Related Experiment Video

Updated: May 2, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Inflammasome: putting the pieces together.

Jürgen Ruland1

  • 1Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.

Cell
|March 18, 2014
PubMed
Summary

Inflammasome activation triggers prion-like ASC polymerization into filaments, forming platforms for inflammatory cytokine production. This reveals a unified mechanism for inflammasome assembly and cytokine release.

Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Biology

Background:

  • Inflammasome activation by microbial and danger signals is crucial for innate immunity.
  • The precise mechanisms underlying inflammasome activation and subsequent inflammatory cytokine release remain incompletely understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms of inflammasome activation.
  • To identify the structural basis for inflammatory cytokine production following inflammasome sensor triggering.

Main Methods:

  • Investigated the role of the adaptor ASC in inflammasome assembly.
  • Utilized techniques to observe the polymerization of ASC into filaments upon inflammasome sensor activation.

Main Results:

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  • Demonstrated that inflammasome sensor activation induces prion-like polymerization of the ASC adaptor protein into higher-order filaments.
  • Showed that these ASC filaments serve as platforms essential for the production of inflammatory cytokines.

    • Conclusions:

    • Proposed a unified mechanism for inflammasome assembly, highlighting the critical role of ASC prion-like polymerization.
    • These findings provide new insights into the regulation of inflammatory responses and cytokine production.