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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

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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...
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The Extrinsic Apoptotic Pathway01:17

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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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Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Autophagic Cell Death01:18

Autophagic Cell Death

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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.
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Cells of the Innate Immune Response01:28

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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
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Necrosis01:16

Necrosis

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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”.
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Related Experiment Video

Updated: Mar 3, 2026

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
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Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

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RIPK3-driven cell death during virus infections.

Jason W Upton1, Maria Shubina2, Siddharth Balachandran2

  • 1Department of Molecular Biosciences, LaMontagne Center for Infectious Disease, University of Texas, Austin, TX, USA.

Immunological Reviews
|May 3, 2017
PubMed
Summary
This summary is machine-generated.

Programmed cell death, including apoptosis and necroptosis, is vital for fighting infections. Receptor-interacting protein kinase 3 (RIPK3) activates necroptosis by phosphorylating MLKL, leading to cell death.

Keywords:
RIPK1RIPK3apoptosisnecroptosisnecrosisviruses

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Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Programmed cell death is a critical host defense against pathogens.
  • Apoptosis was long considered the primary cell death pathway in infected cells.
  • Newer mechanisms, like necroptosis, are increasingly recognized for their role in host defense.

Purpose of the Study:

  • To review the mechanisms by which viruses activate RIPK3.
  • To explore the pathways engaged by RIPK3 that drive cell death.
  • To highlight the role of RIPK3 in both necroptosis and apoptosis.

Main Methods:

  • Literature review of studies on RIPK3 activation and downstream pathways.
  • Analysis of viral strategies to manipulate RIPK3 signaling.
  • Examination of RIPK3's role in mediating cell death and inflammasome regulation.

Main Results:

  • Receptor-interacting protein kinase 3 (RIPK3) is a key mediator of necroptosis.
  • RIPK3 activation by viral infections leads to MLKL phosphorylation and membrane disruption.
  • RIPK3 also plays roles in apoptosis and inflammasome regulation.

Conclusions:

  • RIPK3 is a central regulator of programmed cell death pathways crucial for antiviral immunity.
  • Understanding RIPK3-mediated cell death mechanisms offers insights into host-pathogen interactions.
  • RIPK3's multifaceted roles in cell death and immunity warrant further investigation.