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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 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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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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Antigen Processing Pathways01:31

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MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
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NF-κB-dependent Signaling Pathway02:26

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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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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Related Experiment Video

Updated: Jul 6, 2025

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
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HDAC6/aggresome processing pathway importance for inflammasome formation is context-dependent.

Longlong Wang1, Shihua Shi1, Adeline Unterreiner2

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The Journal of Biological Chemistry
|January 10, 2024
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Summary
This summary is machine-generated.

Histone deacetylase 6 (HDAC6) importance in inflammasome activation varies by cell type and experimental conditions. Its role is context-dependent, not universally essential for inflammasome assembly.

Keywords:
DARPinHDAC6degraderinflammasomeinhibitorsinterleukin

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • The inflammasome is a crucial protein complex for innate immunity, mediating inflammatory responses.
  • Previous studies suggested histone deacetylase 6 (HDAC6) and the aggresome processing pathway (APP) are essential for inflammasome assembly in immortalized macrophages.
  • The precise role of HDAC6 in inflammasome activation across different cellular contexts remains unclear.

Purpose of the Study:

  • To investigate the role of HDAC6 in inflammasome activation using various cellular models.
  • To determine if HDAC6 dependency for inflammasome assembly is conserved in primary cells and human systems.
  • To clarify the context-dependent nature of HDAC6's contribution to inflammasome function.

Main Methods:

  • Utilized primary bone marrow-derived macrophages (BMDMs) from HDAC6-ablated or impaired mice.
  • Employed human peripheral blood mononuclear cells and monocyte cell lines with impaired HDAC6-ubiquitin interaction and APP.
  • Applied a novel HDAC6 degrader in human macrophage cell lines to deplete HDAC6.

Main Results:

  • Inflammasome activation was largely normal in primary BMDMs lacking functional HDAC6.
  • Inflammasome activation was moderately affected in human cells with impaired HDAC6-ubiquitin interaction and APP.
  • Depletion of HDAC6 using a degrader partially impaired inflammasome activation in human macrophage cell lines.

Conclusions:

  • HDAC6 is not universally required for inflammasome activation.
  • The importance of HDAC6 in inflammasome assembly is context-dependent, varying with cell type and experimental manipulation.
  • These findings refine our understanding of inflammasome regulation and highlight the need for context-specific investigation.