ArticleInflammation2018
β4GalT1 Mediates PPARγ N-Glycosylation to Attenuate Microglia Inflammatory Activation.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Effect ofBiomolecules & biomedicine · 2024Article
- Article
- Article
- Analysis of N- and O-Linked Glycosylation: Differential Glycosylation after Rat Spinal Cord Injury.Journal of neurotrauma · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The inflammatory activation of microglia has double-edged effects in central nervous system (CNS) diseases. The ligand-activated transcriptional factor peroxisome proliferator-activated receptor γ (PPARγ) inhibits the inflammatory response. β-1,4-Galactosyltransferase Ι (β1, 4GalT1) mediates N-glycosylation. In this study, the N-glycosylation of PPARγ, as well as two N-linked glycosylation sites in its DNA binding domain (DBD), was identified. Disruption of both sites by site-directed mutagenesis completely abrogated the N-glycosylation of PPARγ. PPAR wild-type (WT) transfection inhibited the inflammatory activation of microglia, while the anti-inflammatory function of unglycosylated PPARγ was down-regulated. In addition, β1, 4GalT1 was shown to interact with PPARγ and to mediate PPARγ glycosylation. β1, 4GalT1 promoted PPARγ's anti-transcription and anti-inflammatory functions. Collectively, our findings define that β-1, 4GalT1 mediated PPARγ glycosylation to attenuate the inflammatory activation of microglia, which has implications for potential therapies for CNS inflammatory diseases.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.