ArticleInflammation2012
The functional interaction between CDK11p58 and β-1,4-galactosyltransferase I involved in astrocyte activation caused by lipopolysaccharide.
Article in Inflammation, 2012. 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
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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.
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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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Dysbindin-1A modulation of astrocytic dopamine and basal ganglia dependent behaviors relevant to schizophrenia.Molecular psychiatry · 2022Article
- β4GalT1 Mediates PPARγ N-Glycosylation to Attenuate Microglia Inflammatory Activation.Inflammation · 2018Article
- Cyclin-dependent kinase 11 (CDK11) is crucial in the growth of liposarcoma cells.Cancer letters · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glial cells are mediating the main activation of the central nervous system (CNS), being astrocytes the mayor glial cells in the brain. Glial activation may result beneficial since it could promote tissue repair and pathogen elimination. However, excessive glial activation mechanism can also have do harm to the tissue. β-1,4-Galactosyltransferase I (β-1,4-GalT-I) is a key inflammatory mediator that participates in the initiation and maintenance of inflammatory reaction in some diseases. Moreover, CDK11(p58) has been reported to be associated with β-1,4-GalT-I. We have found that CDK11(p58) and β-1,4-GalT-I are induced in lipopolysaccharide (LPS)-challenged rat primary astrocytes in a affinis dose- and time-dependent manner. CDK11(p58) regulates the expression of β-1,4-GalT-I by interacting with it. After the knockdown of CDK11(p58) expression, the expression of β-1,4-GalT-I decreases, and astrocyte activation downregulates. Inversely, the expression of β-1,4-GalT-I increases, and astrocyte activation enhances due to the overexpression of CDK11(p58). Knockdown of β-1,4-GalT-I reduces the activation potentiation caused by the overexpression of CDK11(p58), illustrating the function of CDK11(p58) to promote astrocyte activation depends on β-1,4-GalT-I. The interaction between CDK11(p58) and β-1,4-GalT-I to upregulate astrocyte activation is related to activating p38 and JNK pathways. These findings indicated that the functional interaction between CDK11(p58) and β-1,4-GalT-I may play an important role during astrocyte activation after LPS administration.
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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.