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

Cell Polarization by Rho Proteins01:21

Cell Polarization by Rho Proteins

4.0K
Cell polarity is the asymmetric distribution of cellular and membrane components, making one side of the cell different from the other. This polarity is essential to many processes such as embryogenesis, axon migration, glucose transport across epithelial cells, and directional cell migration. A migrating cell responds to intracellular or extracellular signals via molecular cascades that reorganize the actin cytoskeleton to establish this polarity. In these cells, the Rho family proteins Cdc42,...
4.0K
Overview of Cell Death01:30

Overview of Cell Death

11.0K
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...
11.0K
Cell Motility through Blebbing01:16

Cell Motility through Blebbing

2.7K
Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
Blebbing Through the Matrix
In multicellular...
2.7K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

3.0K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
3.0K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

9.2K
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...
9.2K
Mechanism of Lamellipodia Formation01:31

Mechanism of Lamellipodia Formation

4.0K
Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
4.0K

You might also read

Related Articles

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

Sort by
Same author

Integrating multimodal prehabilitation into enhanced recovery after surgery programs (MPhERAS) for elderly patients: a systematic review and meta-analysis of randomized controlled trials and cohort studies.

Techniques in coloproctology·2025
Same author

<i>Meso</i>-Modified Porphyrinoids: Stimuli-Driven Conformational Plasticity, Modulation of π-Conjugation, and Bis-Rh(I) Complexation.

Inorganic chemistry·2025
Same author

Nonalternant Acenaphthylene-Fused Carbaporphyrins: Topological Modulation of π-Delocalization, (Anti)aromaticity, and B<sup>III</sup> Coordination.

Organic letters·2025
Same author

Siamese Twin Homocarbaporphyrin Dimer: Nonplanar Architecture, Localized Conjugation and Bis-B<sup>III</sup> Complex.

Chemistry, an Asian journal·2025
Same author

<i>E</i>-Stilbene-Imprinted Cyclic Diphyrin and Its B<sup>III</sup> Complex.

Organic letters·2025
Same author

Ectopic expression of the cation-chloride cotransporter KCC2 in blood exosomes as a biomarker for functional rehabilitation.

Frontiers in molecular neuroscience·2025

Related Experiment Video

Updated: Mar 23, 2026

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells
09:32

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells

Published on: February 27, 2020

9.7K

Eiger-induced cell death relies on Rac1-dependent endocytosis.

W Ruan1, A Srinivasan1, S Lin1

  • 1Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.

Cell Death & Disease
|April 8, 2016
PubMed
Summary
This summary is machine-generated.

Tumor necrosis factor receptor (TNFR) superfamily signaling controls cell death. This study reveals Rac1 GTPase and endosomal trafficking are crucial for Eiger-induced JNK activation and cell death in Drosophila.

More Related Videos

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
09:15

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

Published on: October 20, 2022

2.9K
Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System
08:15

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Published on: April 11, 2025

1.0K

Related Experiment Videos

Last Updated: Mar 23, 2026

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells
09:32

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells

Published on: February 27, 2020

9.7K
Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
09:15

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

Published on: October 20, 2022

2.9K
Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System
08:15

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Published on: April 11, 2025

1.0K

Area of Science:

  • Cellular biology
  • Molecular signaling
  • Developmental biology

Background:

  • Tumor necrosis factor receptor (TNFR) superfamily members regulate cell fate.
  • p75 neurotrophin receptor (p75NTR) signaling activates c-Jun N-terminal kinases (JNKs) to induce cell death.
  • Receptor-proximal signaling events remain unclear.

Purpose of the Study:

  • Identify conserved signaling events in Eiger (Egr)-induced JNK activation and cell death.
  • Elucidate the role of Rac1 GTPase in Egr-mediated cell death.
  • Characterize upstream regulators and downstream effectors of Rac1 in this pathway.

Main Methods:

  • Utilized Drosophila as a model system to study Egr-induced cell death.
  • Investigated the function of Rac1 using loss-of-function and overexpression approaches.
  • Identified Guanine nucleotide Exchange Factor (GEF) for Rac1 and negative regulators.
  • Analyzed the role of endosomal trafficking proteins (Rab21, Rab7) in the pathway.

Main Results:

  • Rac1 GTPase is essential for Egr-induced JNK activation and cell death.
  • Vav acts as a GEF for Rac1, while dLRRK negatively regulates Rac1.
  • Rac1-dependent endosomal entry of Egr is required for JNK activation and cell death.
  • Rab21 and Rab7 are critical for Egr entry into early endosomes.

Conclusions:

  • Rac1 GTPase is a key mediator of Egr-induced cell death.
  • Endosomal trafficking, regulated by Rab proteins, is a critical step for JNK pathway activation.
  • This study reveals novel regulatory mechanisms of Rac1 in cell death signaling.