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Related Concept Videos

Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal

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Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

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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The Intrinsic Apoptotic Pathway

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Related Experiment Video

Updated: May 20, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Inflammasomes and Intestinal Tumorigenesis.

Md Hasan Zaki1, Mohamed Lamkanfi, Thirumala-Devi Kanneganti

  • 1Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.

Drug Discovery Today. Disease Mechanisms
|July 7, 2012
PubMed
Summary

The inflammasome, a key regulator of intestinal inflammation, plays a crucial role in preventing colorectal cancer development. Understanding inflammasome signaling is vital for developing new strategies against this major health problem.

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Last Updated: May 20, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

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Published on: May 21, 2018

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
08:41

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

Published on: April 6, 2022

Area of Science:

  • Gastroenterology and Oncology
  • Immunology
  • Molecular Biology

Background:

  • Colorectal cancer (CRC) is a significant global health concern, particularly in developed nations.
  • Chronic intestinal inflammation is a known risk factor for CRC development.
  • Intracellular NOD-like receptors (NLRs) are critical in regulating intestinal inflammation and CRC tumorigenesis.

Purpose of the Study:

  • To review the current understanding of inflammasome function in the context of colorectal cancer.
  • To elucidate the mechanisms by which inflammasome signaling protects against colorectal tumorigenesis.

Main Methods:

  • This review synthesizes existing research on inflammasome pathways and their involvement in intestinal inflammation and CRC.
  • Key signaling molecules, including NLRs, caspase-1, and cytokines IL-1β/IL-18, are discussed in relation to their roles.

Main Results:

  • Inflammasome activation leads to the formation of a protein complex crucial for processing inflammatory cytokines.
  • Defects in gut inflammasome signaling are linked to increased epithelial barrier permeability, altered cell proliferation, and oncogenic mediator induction, contributing to colitis and CRC.
  • The inflammasome acts as a protective mechanism against the development of colorectal cancer.

Conclusions:

  • The inflammasome is a critical component in maintaining intestinal homeostasis and preventing colorectal cancer.
  • Dysregulation of inflammasome signaling pathways contributes to the pathogenesis of colitis and colorectal cancer.
  • Further research into inflammasome-targeted therapies holds promise for CRC prevention and treatment.