ArticleInflammation2017
CDK11p58 Promotes Microglia Activation via Inducing Cyclin D3 Nuclear Localization.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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Who cites it
0 citing papers in PubMed, 2 citations in OpenAlex.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia activation has been implicated in the pathogenesis of many neurological diseases. These reactive microglia are capable of producing a variety of proinflammatory mediators and potentially neurotoxic compounds. The increase of cell number and expression of CD11b are the main features of activated microglia. In this study, we examined the suppressive effects of CDK11p58 on microglia activation induced by lipopolysaccharide (LPS) in vitro. We found that in the activated microglia, the expression of CDK11p58 increased and the overexpression of CDK11p58 could reduce the increased proliferation and CD11b expression in LPS-activated microglia. Such suppressive effects might be resulted from the interaction with cyclin D3 which promoted CDK11p58 nuclear localization. Our results suggested that CDK11p58 acted to regulate microglia activation through CDK11p58 and cyclin D3 interaction.
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