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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...
Overview of Cell Death01:30

Overview of Cell Death

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.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
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...

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Related Experiment Video

Updated: May 7, 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

Necroptosis: STAT3 kills?

Vassilis Georgiadis1, Richard A Knight

  • 1Medical Molecular Biology Unit; University College London; London, UK.

JAK-STAT
|September 24, 2013
PubMed
Summary
This summary is machine-generated.

Tumor necrosis factor (TNF)-induced necroptosis involves RIPK1 and mitochondrial reactive oxygen species (ROS). A new study identifies STAT3 as a key mediator, linking RIPK1 to STAT3 mitochondrial translocation in this programmed cell death pathway.

Keywords:
GRIM-19RIP1ROS productionSTAT3necroptosis

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Neutrophil Lifespan Extension with CLON-G and an In Vitro Spontaneous Death Assay
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Neutrophil Lifespan Extension with CLON-G and an In Vitro Spontaneous Death Assay

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Last Updated: May 7, 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

Neutrophil Lifespan Extension with CLON-G and an In Vitro Spontaneous Death Assay
05:52

Neutrophil Lifespan Extension with CLON-G and an In Vitro Spontaneous Death Assay

Published on: May 12, 2023

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • TNF-induced necroptosis is a programmed cell death pathway.
  • This process is mediated by RIPK1 and involves mitochondrial reactive oxygen species (ROS).
  • The precise signaling molecules linking RIPK1 activation to ROS production in necroptosis remain unclear.

Purpose of the Study:

  • To elucidate the role of STAT3 in TNF-induced necroptosis.
  • To identify the signaling intermediates connecting RIPK1 to mitochondrial ROS production.

Main Methods:

  • The study investigated the interaction between RIPK1 and STAT3.
  • Mitochondrial translocation of STAT3 was examined.
  • The role of GRIM-19 in this process was analyzed.

Main Results:

  • RIPK1 mediates STAT3 phosphorylation at Ser727.
  • Phosphorylated STAT3 translocates to the mitochondria.
  • STAT3 interacts with GRIM-19, a component of mitochondrial complex I.

Conclusions:

  • STAT3 is a crucial mediator in TNF-induced necroptosis.
  • The RIPK1-STAT3 signaling axis contributes to ROS production in necroptosis.
  • This finding provides new insights into the molecular mechanisms of programmed necrosis.