ArticleInflammation2009
Lipopolysaccharide induced upregulation of beta-1,4-galactosyltransferase-I in Schwann cell.
Article in Inflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Heat Shock Cognate Protein 70 Enhanced Integrin β1 Mediated Invasion in Cancer Cells.Cancer management and research · 2020Article
- The functional interaction between CDK11p58 and β-1,4-galactosyltransferase I involved in astrocyte activation caused by lipopolysaccharide.Inflammation · 2012Article
- β-1,4-Galactosyltransferase-involved in lipopolysaccharide-induced adhesion of Schwann cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
beta4 Galactosylation of glycoproteins is one of the most important post-translational modifications. Recent studies have demonstrated that aberrant galactosylation associates with some inflammation diseases. beta-1,4-galactosyltransferase-I (beta-1,4-GalT-I), which transfers galactose to the terminal N-acetylglucosamine of N- and O-linked glycans in a beta-1,4- linkage, considered to be the major galactosyltransferse among the seven members of the subfamily responsible for beta4 galactosylation. In the present study, we investigated the expression of beta-1,4-GalT-I in Schwann cells under Lipopolysaccharide (LPS) treatment. RT-PCR revealed that the beta-1,4-GalT-I mRNA was significant increased as early as 2 h after LPS stimulation. Immunofluorescence showed that beta-1,4-GalT-I was located in Golgi apparatus and membrane of Schwann cells. With the 1 microg/ml LPS treatment, expression levels of beta-1,4-GalT-I was much higher compared with control group. In addition, lectin blot indicated that the beta4 galactosylation of glycoproteins such as integrin alpha5 was enhanced, which may due to the induced beta-1,4-GalT-I expression. These results suggested that beta-1,4-GalT-I may play an important role in adhesion and migration of Schwann cells during inflammation.
Indexed as
Identifiers
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.