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

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...
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...
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.
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

You might also read

Related Articles

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

Sort by
Same author

Planar InAs avalanche photodiodes with high gain and low noise factor.

Optics express·2026
Same author

Operational management of X-ray protective devices in radiology: An integrated practice protocol for integrity, functionality, and infection control.

Radiography (London, England : 1995)·2025
Same author

No One Left Behind: The Design of Young Biomedical Science Programme (YBMS) on Medical Education for Postdoctoral Fellows.

Medical science educator·2025
Same author

Cognitive frailty in older adults: examining the impact of frailty criteria on neuropsychological profile, functional outcomes, activity levels, and quality of life.

European geriatric medicine·2024
Same author

Cardioneuroablation: the known and the unknown.

Frontiers in cardiovascular medicine·2024
Same author

Effects of Fitlight training on cognitive-motor performance in élite judo athletes.

Heliyon·2024

Related Experiment Video

Updated: May 14, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

IF1 limits the apoptotic-signalling cascade by preventing mitochondrial remodelling.

D Faccenda1, C H Tan, A Seraphim

  • 1Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, London, UK.

Cell Death and Differentiation
|January 26, 2013
PubMed
Summary

Mitochondrial protein IF1 protects cells from apoptosis by regulating Cytochrome c release. Overexpression of IF1 delays programmed cell death, suggesting it

More Related Videos

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Related Experiment Videos

Last Updated: May 14, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Area of Science:

  • Mitochondrial biology
  • Cell death regulation
  • Cancer research

Background:

  • Mitochondrial structure is crucial for energy conversion and cell death.
  • IF1 (inhibitor of F1Fo-ATP synthase) protects against necrotic cell death and maintains mitochondrial cristae structure.
  • IF1 is upregulated in many human cancers.

Purpose of the Study:

  • To investigate the role of IF1 in the progression of apoptosis.
  • To determine if IF1 expression influences the release of Cytochrome c (Cyt c) and subsequent apoptotic events.
  • To explore IF1's potential as a predictive marker for chemotherapy response.

Main Methods:

  • Examined the effect of IF1 expression levels on apoptosis progression.
  • Investigated the role of IF1 in regulating Cytochrome c (Cyt c) release.
  • Analyzed the amplification pathway involved in apoptosis, including ER Ca(2+) release, Dynamin-related protein 1 (Drp1) recruitment, and Bax insertion.
  • Assessed mitochondrial morphology and ultrastructure in relation to IF1 expression.

Main Results:

  • Increased IF1 expression protects cells from apoptotic death by acting as a checkpoint for Cytochrome c (Cyt c) release.
  • IF1 overexpression delays an amplification pathway involving Ca(2+) signaling, Drp1 recruitment, and Bax insertion, which promotes further Cyt c release.
  • IF1 overexpression preserves mitochondrial morphology and ultrastructure, impacting Cyt c release regulation.

Conclusions:

  • IF1 acts as an antiapoptotic factor and may promote tumorigenesis.
  • IF1's role in regulating mitochondrial architecture and preventing Cyt c release is critical in controlling apoptosis.
  • IF1 may serve as a valuable predictor of patient response to chemotherapy.