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

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

484
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
484
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

483
Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
483
T Cell Types and Functions01:24

T Cell Types and Functions

2.1K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.1K
Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

496
Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
496
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.4K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.4K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

10.5K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.5K

You might also read

Related Articles

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

Sort by
Same author

Reamed and unreamed intramedullary nailing for the treatment of open and closed tibial fractures: a subgroup analysis of randomised trials.

International orthopaedics·2009
Same author

Selective COX-2 inhibitor versus nonselective COX-1 and COX-2 inhibitor in the prevention of heterotopic ossification after total hip arthroplasty: a meta-analysis of randomised trials.

International orthopaedics·2009
Same author

[Study on evaluating sex determining region of the Y as an engrafting track of BMSCs transplantation for repairing osteonecrosis of the femoral head of rabbit].

Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery·2009
Same author

Positive association between benign familial infantile convulsions and LGI4.

Brain & development·2009
Same author

Catalytic enantioselective synthesis of chiral phthalides by efficient reductive cyclization of 2-acylarylcarboxylates under aqueous transfer hydrogenation conditions.

Organic letters·2009
Same author

Significance of urinary liver-fatty acid-binding protein in cardiac catheterization in patients with coronary artery disease.

Internal medicine (Tokyo, Japan)·2009

Related Experiment Video

Updated: Jan 14, 2026

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

3.1K

TRIM16 Inhibits Inflammation by Interacting With and Ubiquitinating TRAF2 in a Colitis Model.

Dong-Liang Li1, Li Zhou2, Bo Zhang1

  • 1Department of General Surgery, The First People's Hospital of Zhangjiagang City, Suzhou, China.

Journal of Cellular and Molecular Medicine
|October 24, 2025
PubMed
Summary

Tripartite motif 16 (TRIM16) acts as an anti-inflammatory factor by inhibiting the TRAF2/NF-ĸB pathway. Its reduced expression is linked to colitis, suggesting TRIM16 as a potential therapeutic target for inflammatory bowel disease.

Keywords:
IBDNF‐ĸBTRAF2TRIM16ubiquitination

More Related Videos

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

17.4K
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.6K

Related Experiment Videos

Last Updated: Jan 14, 2026

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

3.1K
Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

17.4K
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.6K

Area of Science:

  • Immunology
  • Molecular Biology
  • Gastroenterology

Background:

  • Tripartite motif 16 (TRIM16) is an E3 ubiquitin ligase involved in immunity and inflammation.
  • Its role in inflammatory bowel disease (IBD) and specific regulatory mechanisms remain underexplored.

Purpose of the Study:

  • To investigate the expression and regulatory mechanisms of TRIM16 in inflammatory conditions, particularly IBD.
  • To elucidate the role of TRIM16 in modulating inflammatory signaling pathways.

Main Methods:

  • Utilized dextran sulfate sodium (DSS)-induced mouse colitis model and lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages.
  • Assessed TRIM16 expression, inflammatory mediator mRNA levels (iNOS, TNF-α, IL-6), and NF-ĸB pathway activation.
  • Investigated TRIM16 interaction with TRAF2 and its ubiquitination effects.

Main Results:

  • TRIM16 expression was significantly decreased in DSS-induced colitis and LPS-stimulated macrophages.
  • TRIM16 knockdown exacerbated inflammation by increasing iNOS, TNF-α, and IL-6 mRNA levels and activating the NF-ĸB pathway.
  • TRIM16 directly interacted with TRAF2, promoting its ubiquitination and subsequently inhibiting NF-ĸB signaling and IL-6 expression.

Conclusions:

  • TRIM16 plays a critical role in suppressing inflammation by modulating the TRAF2/NF-ĸB signaling pathway.
  • Downregulation of TRIM16 is associated with colitis development, positioning TRIM16 as a potential therapeutic target for IBD.