ArticlePloS one2016
Enhanced Expression of Trib3 during the Development of Myelin Breakdown in dmy Myelin Mutant Rats.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 3 citations in OpenAlex.
- Expression and distribution of tribbles pseudokinase 3 in oxidative stress-mediated acute liver and kidney injury models.Journal of toxicologic pathology · 2026Article
- Exposure to Frontline Antiretroviral Dolutegravir Disrupts Oligodendrocyte Development Across Differentiation Stages.ASN neuro · 2026Article
- Deciphering the Genetic Crosstalk between Microglia and Oligodendrocyte Precursor Cells during Demyelination and Remyelination Using Transcriptomic Data.International journal of molecular sciences · 2022Article
- Role of endoplasmic reticulum stress-associated gene TRIB3 in rats following kainic acid-induced seizures.International journal of clinical and experimental pathology · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The demyelination (dmy) rat exhibits hind limb ataxia and severe myelin breakdown in the central nervous system. The causative gene of dmy rats is the MRS2 magnesium transporter gene. Tribbles homolog 3 (Trib3) is a pseudokinase molecule that modifies certain signal pathways, and its expression is increased in response to various stresses. Here we sought to clarify the mechanism of myelin breakdown by focusing Trib3, which is remarkably up-regulated in dmy rats. The expression of Trib3 mRNA was significantly increased at 4, 5, 6, 7 and 8 weeks of age in the dmy rats, prior to the prominent myelin breakdown between 7 and 10 weeks of age. The expression level of Trib3 was increased concurrently with the progression of the clinical and pathological conditions in the dmy rats. Double immunofluorescence demonstrated that TRIB3 was mainly expressed in neurons and oligodendrocytes and localized in the Golgi apparatus. Our findings indicate that Trib3 may be associated with the pathogenic mechanism of dmy rats.
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