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

Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

2.4K
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...
2.4K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.4K
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...
6.4K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.3K
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...
6.3K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.2K
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...
6.2K
Apoptosis01:30

Apoptosis

11.3K
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...
11.3K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

5.3K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.3K

You might also read

Related Articles

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

Sort by
Same author

A bibliometric approach to worldwide scientific production of familial hypophosphataemic rickets in Scopus (2000-2022).

Orphanet journal of rare diseases·2025
Same author

Gene Expression Analysis of HPRT-Deficient Cells Maintained with Physiological Levels of Folic Acid.

Cells·2025
Same author

The Crosstalk Between Cartilage and Bone in Skeletal Growth.

Biomedicines·2025
Same author

Bone Development and Growth.

International journal of molecular sciences·2024
Same author

A new physiological medium uncovers biochemical and cellular alterations in Lesch-Nyhan disease fibroblasts.

Molecular medicine (Cambridge, Mass.)·2024
Same author

ThyroidPrint®: clinical utility for indeterminate thyroid cytology.

Endocrine-related cancer·2023

Related Experiment Video

Updated: Jun 16, 2025

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

8.6K

p38α and p38β regulate osmostress-induced apoptosis.

Nabil Ben Messaoud1, José M López1

  • 1Institut de Neurociències, Departament de Bioquímica i Biologia Molecular, Unitat de Bioquímica, Facultad de Medicina, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Barcelona, Spain.

The Journal of Biological Chemistry
|December 9, 2024
PubMed
Summary
This summary is machine-generated.

Hyperosmotic shock triggers apoptosis in Xenopus oocytes via mitochondrial pathways. Specific p38 isoforms (p38α, p38β) and their sustained activation accelerate this osmostress-induced cell death process.

Keywords:
Xenopusapoptosiscaspasecell deathoocyteosmotic shockp38stress

More Related Videos

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

898
Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

1.8K

Related Experiment Videos

Last Updated: Jun 16, 2025

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

8.6K
Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

898
Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

1.8K

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Apoptosis Research

Background:

  • Hyperosmotic shock initiates cell death pathways in Xenopus oocytes, involving mitochondria.
  • Mitogen-activated protein kinases (MAPKs), including JNK1-1 and JNK1-2, are activated early by osmostress.
  • While sustained JNK activation accelerates apoptosis, the specific p38 isoforms involved in osmostress-induced cell death remain poorly characterized.

Purpose of the Study:

  • To investigate the expression and activation patterns of Xenopus p38 isoforms under hyperosmotic stress.
  • To elucidate the role of specific p38 isoforms in accelerating osmostress-induced apoptosis.
  • To explore the interplay between caspases and p38 kinases in the apoptotic feedback loop.

Main Methods:

  • Hyperosmotic shock applied to Xenopus oocytes.
  • Analysis of p38 isoform expression and activation.
  • Microinjection of cytochrome c to assess caspase-3 activation and p38 phosphorylation.

Main Results:

  • p38α, p38β, and p38γ isoforms are rapidly activated by hyperosmotic shock.
  • Sustained activation of p38α and p38β significantly accelerates osmostress-induced apoptosis.
  • Cytochrome c injection leads to caspase-3 activation and p38α/p38β phosphorylation, indicating a positive feedback loop.

Conclusions:

  • Osmostress-induced apoptosis in Xenopus oocytes involves early activation of multiple p38 isoforms.
  • Sustained p38α and p38β activity plays a key role in accelerating the apoptotic process.
  • A positive feedback mechanism exists between caspases and p38 kinases, amplifying cell death signaling.