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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...
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...
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...
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,...

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Related Experiment Video

Updated: Jun 21, 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

RIP kinases initiate programmed necrosis.

Lorenzo Galluzzi1, Oliver Kepp, Guido Kroemer

  • 1INSERM, Villejuif, France.

Journal of Molecular Cell Biology
|August 15, 2009
PubMed
Summary
This summary is machine-generated.

Receptor-interacting serine-threonine kinase (RIP) 1 and RIP3 control cell death pathways, switching between apoptosis and necrosis. Understanding these molecular mechanisms is crucial for cell biology research.

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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

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Last Updated: Jun 21, 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

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Lethal stimuli can trigger distinct cell death pathways, including apoptosis and necrosis.
  • The molecular underpinnings of this cell death switch have remained largely elusive until recently.

Purpose of the Study:

  • To elucidate the molecular regulators governing the switch between apoptosis and necrosis.
  • To identify key proteins involved in controlling programmed cell death pathways.

Main Methods:

  • Investigated the roles of receptor-interacting serine-threonine kinase (RIP) family members.
  • Utilized cell-based assays to analyze cell death mechanisms.
  • Examined the signaling pathways controlled by RIP1 and RIP3.

Main Results:

  • Demonstrated that RIP1 and RIP3 are critical mediators of the apoptosis-necrosis switch.
  • Provided evidence for the involvement of RIP kinases in regulating cell fate decisions.
  • Identified RIP1 and RIP3 as key players in programmed cell death.

Conclusions:

  • RIP1 and RIP3 play a central role in determining whether a cell undergoes apoptosis or necrosis.
  • Further research is needed to fully resolve the controversial mechanistic details of RIP kinase-mediated cell death.