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PMID:22120654

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Citation

Liu, X, Cheng, C, Shao, B, Wu, X, Ji, Y, Liu, Y, Lu, X and Shen, A (2012) CDK11(p58) promotes rat astrocyte inflammatory response via activating p38 and JNK pathways induced by lipopolysaccharide. Neurochem. Res. 37:563-73

Abstract

In response to a variety of neural damages in the CNS, quiescent astrocytes become reactive astrocytes. Astrocytes are the major glial subtype and are important effectors that participate in the pathogenesis of numerous neural disorders, including trauma, stroke, aging, and developmental, genetic, idiopathic or acquired neurodegenerative diseases. CDK11(p58) (Cyclin-dependent kinases 11 protein 58/PITSLRE) is a p34cdc2-related protein kinase that plays an important role in normal cell cycle progression. In the process of LPS stimulus, the expression of CDK11(p58) in astrocytes was increased. Induced CDK11(p58) was parallel to astrocyte inflammatory response. Knockdown of CDK11(p58) by small-interfering RNAs (siRNAs) reduced the LPS-induced astrocyte inflammatory response, while overexpression CDK11(p58) enhanced the process. CDK11(p58) exerted its functions via activating p38 and JNK MAPK pathways. This study delineates that CDK11(p58) may be a significant regulatory factor for host defenses in central nervous system (CNS) inflammation.

Links

PubMed Online version:10.1007/s11064-011-0643-7

Keywords

Animals; Astrocytes/drug effects; Astrocytes/enzymology; Astrocytes/immunology; Base Sequence; Blotting, Western; Cyclin-Dependent Kinases/metabolism; DNA Primers; Flow Cytometry; Lipopolysaccharides/pharmacology; MAP Kinase Kinase 4/metabolism; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; p38 Mitogen-Activated Protein Kinases/metabolism

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

RAT:D3ZDM6

involved_in

GO:0050729: positive regulation of inflammatory response

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

Notes

See also

References

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