Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Necrosis01:16

Necrosis

5.2K
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...
5.2K
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

63
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,...
63
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

70
Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
70
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.2K
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...
6.2K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.2K
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...
6.2K
Cell Motility through Blebbing01:16

Cell Motility through Blebbing

1.9K
Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
Blebbing Through the Matrix
In multicellular...
1.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Metabolic control of autophagy.

Cell·2014
Same author

A phase I/II trial of Erlotinib in higher risk myelodysplastic syndromes and acute myeloid leukemia after azacitidine failure.

Leukemia research·2014
Same author

Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation.

Autophagy·2014
Same author

Cancer cell-autonomous contribution of type I interferon signaling to the efficacy of chemotherapy.

Nature medicine·2014
Same author

Entosis, a key player in cancer cell competition.

Cell research·2014
Same author

Cytokines reinstate NK cell-mediated cancer immunosurveillance.

The Journal of clinical investigation·2014
Same journal

Why microglial repair programs fade.

Cell research·2026
Same journal

Atypical signaling, ligand recognition and selective agonist discovery of complement receptor C5aR2.

Cell research·2026
Same journal

One drug, five targets.

Cell research·2026
Same journal

Smooth emotional response: amygdalar neurovascular coupling drives stress encoding.

Cell research·2026
Same journal

Liquid surrogates of spatial tumor ecosystems.

Cell research·2026
Same journal

MitoCatch directs mitochondria delivery and prevents cell degeneration.

Cell research·2026
See all related articles

Related Experiment Video

Updated: May 4, 2026

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

10.1K

MLKL regulates necrotic plasma membrane permeabilization.

Lorenzo Galluzzi1, Oliver Kepp2, Guido Kroemer3

  • 11] Gustave Roussy, Villejuif, France [2] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [3] Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France.

Cell Research
|January 15, 2014
PubMed
Summary
This summary is machine-generated.

New research reveals how mixed lineage kinase domain-like (MLKL) triggers necroptosis. Phosphorylation by RIPK3 causes MLKL to form membrane-damaging oligomers, disrupting cell ion balance.

More Related Videos

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
05:30

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

603
High-throughput Measurement of Plasma Membrane Resealing Efficiency in Mammalian Cells
10:07

High-throughput Measurement of Plasma Membrane Resealing Efficiency in Mammalian Cells

Published on: January 7, 2019

7.1K

Related Experiment Videos

Last Updated: May 4, 2026

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

10.1K
Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
05:30

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

603
High-throughput Measurement of Plasma Membrane Resealing Efficiency in Mammalian Cells
10:07

High-throughput Measurement of Plasma Membrane Resealing Efficiency in Mammalian Cells

Published on: January 7, 2019

7.1K

Area of Science:

  • Cellular biology
  • Molecular mechanisms of cell death

Background:

  • Necroptosis is a regulated form of necrosis.
  • The role of mixed lineage kinase domain-like (MLKL) in necroptosis is under investigation.

Purpose of the Study:

  • To elucidate the molecular mechanisms of MLKL-mediated necroptosis.
  • To understand how MLKL activation leads to plasma membrane permeabilization.

Main Methods:

  • Investigated MLKL oligomerization upon RIPK3 phosphorylation.
  • Examined the localization and function of MLKL oligomers at the plasma membrane.

Main Results:

  • MLKL phosphorylation by RIPK3 induces MLKL oligomer formation.
  • These MLKL oligomers accumulate at the plasma membrane.
  • MLKL oligomers disrupt the plasma membrane's ability to maintain ionic homeostasis, leading to necroptosis.

Conclusions:

  • MLKL oligomerization is a critical step in necroptosis.
  • RIPK3-mediated phosphorylation of MLKL is essential for its oligomerization and subsequent membrane damage.
  • The disruption of ionic homeostasis by MLKL oligomers is a key event in necroptotic cell death.