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Related Concept Videos

Necrosis01:16

Necrosis

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 anucleated and die, but their...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

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Related Experiment Video

Updated: May 9, 2026

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System
08:15

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Published on: April 11, 2025

RIP3: a molecular switch for necrosis and inflammation.

Kenta Moriwaki1, Francis Ka-Ming Chan

  • 1Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.

Genes & Development
|August 6, 2013
PubMed
Summary

Receptor-interacting protein kinase 3 (RIPK3) regulates programmed necrosis (necroptosis) and inflammation. This review details RIPK3

Keywords:
FADDMLKLPGAM5RIP1caspase 8inflammation

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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

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Last Updated: May 9, 2026

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System
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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Biology

Background:

  • Receptor-interacting protein kinase 3 (RIPK3) is a key regulator of necroptosis, a form of inflammatory cell death.
  • RIPK3 activation involves complex post-translational modifications, including phosphorylation, ubiquitination, and caspase cleavage.
  • These modifications orchestrate the formation of the necrosome, a crucial signaling complex.

Purpose of the Study:

  • To review the mechanisms governing RIPK3-mediated necroptosis.
  • To explore the emerging role of RIPK3 in inflammation, independent of its cell death function.
  • To discuss RIPK3's involvement in various inflammatory diseases.

Main Methods:

  • Literature review of recent studies on RIPK3.
  • Analysis of molecular mechanisms regulating RIPK3.
  • Synthesis of data on RIPK3's role in inflammation and disease.

Main Results:

  • RIPK3 activation is precisely controlled by multiple post-translational modifications.
  • RIPK3 can drive inflammatory responses separately from its necroptotic function.
  • Evidence links RIPK3 to the pathogenesis of diverse inflammatory conditions.

Conclusions:

  • RIPK3 is a central node in both necroptosis and inflammatory signaling pathways.
  • Understanding RIPK3 regulation and function is critical for developing therapies for inflammatory diseases.