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

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.4K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.4K
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

2.0K
2.0K
Exon Recombination02:32

Exon Recombination

3.1K
The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
Exon shuffling follows “splice frame rules.” Each exon...
3.1K

You might also read

Related Articles

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

Sort by
Same author

Glycine or Muscimol Might Limit the Release of DAMPs by Inhibiting NINJ1-Mediated Plasma Membrane Rupture in Platelets.

Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion·2026
Same author

Pyroptosis in Ovarian Aging, and Its Influence on Female Reproductive Health in Aged Ovaries.

American journal of reproductive immunology (New York, N.Y. : 1989)·2026
Same author

Ethanol-induced NINJ1 oligomerization might contribute to the lytic death of granulosa cells in PCOS.

Human cell·2026
Same author

Synthesis of new rhodanine derivative molecules, their biological properties and sensor applications in environmental samples.

BMC chemistry·2026
Same author

Phosphatidylinositol (PI)-mediated release of LDH might be due to increased interaction of NINJ1 with membrane lipids based on PI accumulation in the granulosa cell membrane.

Irish journal of medical science·2026
Same author

Downregulation of DACH2 Expression in an Adrenocortical Cell Model of PCOS with Adrenal Hyperandrogenism, and in Human Granulosa Cells from Patients with Hyperandrogenic-PCOS: a Link Between Ovaries and Adrenal Glands in PCOS.

Reproductive sciences (Thousand Oaks, Calif.)·2026

Related Experiment Video

Updated: Apr 28, 2026

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition
06:12

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Published on: March 3, 2023

1.5K

In Silico Transcriptomic Analysis Suggests That Nickel Exposure Upregulates NINJ1 Expression: Implications for Lytic

Sukran Yagmur Avcioglu1, Busra Nur Ozdemir1, Caglar Berkel1

  • 1Department of Molecular Biology and Genetics, Tokat Gaziosmanpasa University, Tokat, Türkiye.

Environmental Toxicology
|April 26, 2026
PubMed
Summary

Nickel exposure increases NINJ1 (Ninjurin 1) mRNA, potentially causing cell death and inflammation. This NINJ1 involvement in nickel allergy and toxicity warrants further experimental investigation.

Keywords:
NINJ1cell deathcell lysisinflammationnickelplasma membrane rupturepyroptosis

More Related Videos

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
05:51

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Published on: June 15, 2013

12.4K
A Rapid In Vivo Bioassay for Developmentally Active Enhancers
00:08

A Rapid In Vivo Bioassay for Developmentally Active Enhancers

1.1K

Related Experiment Videos

Last Updated: Apr 28, 2026

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition
06:12

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Published on: March 3, 2023

1.5K
Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
05:51

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Published on: June 15, 2013

12.4K
A Rapid In Vivo Bioassay for Developmentally Active Enhancers
00:08

A Rapid In Vivo Bioassay for Developmentally Active Enhancers

1.1K

Area of Science:

  • Toxicology
  • Cell Biology
  • Immunology

Background:

  • Nickel (Ni) induces cell death via apoptosis and pyroptosis.
  • NINJ1 (Ninjurin 1) mediates plasma membrane rupture in lytic cell death.
  • NINJ1's role in nickel-induced cell death is unstudied.

Purpose of the Study:

  • Investigate NINJ1's role in nickel-induced cell death.
  • Analyze NINJ1 mRNA expression in nickel-exposed cells and tissues.
  • Hypothesize NINJ1's contribution to nickel toxicity and allergy.

Main Methods:

  • In silico transcriptomics analysis of public datasets.
  • Utilized R programming environment for data analysis.
  • Compared NINJ1 mRNA levels in nickel-exposed vs. control cells and skin biopsies.

Main Results:

  • Nickel exposure elevated NINJ1 mRNA in human PBMCs, endothelial cells, and rat liver cells.
  • Higher NINJ1 mRNA expression observed in nickel-allergic skin biopsies.
  • Computational analysis suggests increased NINJ1 expression correlates with nickel exposure.

Conclusions:

  • Nickel exposure upregulates NINJ1 mRNA expression.
  • NINJ1 may mediate plasma membrane rupture and lytic cell death in nickel toxicity.
  • Findings suggest NINJ1's potential role in nickel allergy and inflammation, requiring experimental validation.