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

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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...
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...
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...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
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...
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...

You might also read

Related Articles

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

Sort by
Same author

Serum amyloid A1 directly engages TLR4/MD-2 to trigger neuroinflammatory signaling in microglia cultures.

International immunopharmacology·2026
Same author

Attentional Functioning in Healthy Older Adults and aMCI Patients: Results from the Attention Network Test with a Focus on Sex Differences.

Brain sciences·2025
Same author

Fentanyl enhances immune cell response through TLR4/MD-2 complex.

Frontiers in pharmacology·2024
Same author

Unilateral tactile agnosia as an onset symptom of corticobasal syndrome.

Frontiers in human neuroscience·2024
Same author

2-Pentadecyl-2-oxazoline inhibits lipopolysaccharide-induced microglia activation interfering with TLR4 signaling.

Life sciences·2023
Same author

Pre- and Early Post-treatment With <i>Arthrospira platensis</i> (Spirulina) Extract Impedes Lipopolysaccharide-triggered Neuroinflammation in Microglia.

Frontiers in pharmacology·2021

Related Experiment Video

Updated: Jul 7, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

MAP kinase pathways in neuronal cell death.

Karen L Philpott1, Laura Facci

  • 1Neurology Centre of Excellence for Drug Discovery, GlaxoSmithKline Research & Development Limited, New Frontiers Science Park, Third Avenue, CM19 5AW, Harlow, Essex, UK. Karen.L.philpott@gsk.com

CNS & Neurological Disorders Drug Targets
|February 22, 2008
PubMed
Summary

Mitogen-activated protein kinase pathways, particularly c-Jun N-terminal kinases (JNKs), are implicated in neuronal death across aging and disease. Inhibiting JNKs shows therapeutic potential for neurodegenerative conditions like Parkinson's disease.

More Related Videos

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

Related Experiment Videos

Last Updated: Jul 7, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Neuronal death is a critical process in development, aging, and disease.
  • Mitogen-activated protein kinase (MAPK) pathways, especially c-Jun N-terminal kinases (JNKs), are increasingly recognized for their role in human neuropathology.
  • JNKs are activated by extracellular stimuli, including cellular stress.

Purpose of the Study:

  • To review the evidence linking JNK signaling pathways to neuronal loss.
  • To explore the therapeutic potential of JNK inhibition in neurological diseases.

Main Methods:

  • Review of existing literature on JNK signaling and neuronal death.
  • Analysis of data from knockout mouse studies modeling neurodegenerative diseases.
  • Examination of JNK activation in human disease tissues.

Main Results:

  • JNK pathways are significant regulators of neuronal death.
  • Knockout studies demonstrate JNK gene removal reduces disease severity in models of Parkinson's disease and cerebral ischemia.
  • JNK activation is observed in human neuropathological tissues.

Conclusions:

  • JNK signaling is a key factor in regulating neuronal loss.
  • Small molecule inhibitors targeting JNK pathways represent a promising avenue for future therapeutic interventions in neurological disorders.