ArticleMolecular and cellular biochemistry2008
Increased expression of CDK11p58 and cyclin D3 following spinal cord injury in rats.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Spatial and temporal activation of spinal glial cells: role of gliopathy in central neuropathic pain following spinal cord injury in rats.Experimental neurology · 2012Pooled it
- Activation of G-protein-coupled receptor 39 reduces neuropathic pain in a rat model.Neural regeneration research · 2024Article
- MicroRNA-138-5p Targets Pro-Apoptotic Factors and Favors Neural Cell Survival: Analysis in the Injured Spinal Cord.Biomedicines · 2022Article
- DKK3 ameliorates neuropathic pain via inhibiting ASK-1/JNK/p-38-mediated microglia polarization and neuroinflammation.Journal of neuroinflammation · 2022Article
- CDK11 Promotes Cytokine-Induced Apoptosis in Pancreatic Beta Cells Independently of Glucose Concentration and Is Regulated by Inflammation in the NOD Mouse Model.Frontiers in immunology · 2021Article
- Bilateral gene interaction hierarchy analysis of the cell death gene response emphasizes the significance of cell cycle genes following unilateral traumatic brain injury.BMC genomics · 2016Article
- The functional interaction between CDK11p58 and β-1,4-galactosyltransferase I involved in astrocyte activation caused by lipopolysaccharide.Inflammation · 2012Article
- Cyclin K goes with Cdk12 and Cdk13.Cell division · 2012Article
- CDK11(p58) promotes rat astrocyte inflammatory response via activating p38 and JNK pathways induced by lipopolysaccharide.Neurochemical research · 2012Article
- Cyclin D3/CDK11(p58) complex involved in Schwann cells proliferation repression caused by lipopolysaccharide.Inflammation · 2010Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinases are critical signalling molecules for normal cell growth and development. CDK11p58 is a p34cdc2-related protein kinase, and plays an important role in normal cell cycle progression. However its distribution and function in the central nervous system (CNS) lesion remain unclear. In this study, we mainly investigated the protein expression and cellular localization of CDK11 during spinal cord injury (SCI). Western blot analysis revealed that CDK11p58 was not detected in normal spinal cord. It gradually increased, reached a peak at 3 day after SCI, and then decreased. The protein expression of CDK11(p58) was further analyzed by immunohistochemistry. The variable immunostaining patterns of CDK11p58 were visualized at different periods of injury. Double immunofluorescence staining showed that CDK11 was co-expressed with NeuN, CNPase and GFAP. Co-localization of CDK11/active caspase-3 and CDK11/proliferating cell nuclear antigen (PCNA) were detected in some cells. Cyclin D3, which was associated with CDK11p58 and could enhance kinase activity, was detected in the normal and injured spinal cord. The cyclin D3 protein underwent a similar pattern with CDK11p58 during SCI. Double immunofluorescence staining indicated that CDK11 co-expressed with cyclin D3 in neurons and glial cells. Coimmunoprecipitation further showed that CDK11p58 and cyclin D3 interacted with each other in the damaged spinal cord. Thus, it is likely CDK11p58 and cyclin D3 could interact with each other after acute SCI. Another partner of CDK11p58 was beta-1,4-galactosyltransferase 1 (beta-1,4-GT 1). The co-localization of CDK11/beta-1,4-GT 1 in the damaged spinal cord was revealed by immunofluorescence analysis. The cyclin D3-CDK4 complexes were also present by coimmunoprecipitation analysis. Taken together, these data suggested that both CDK11 and cyclin D3 may play important roles in spinal cord pathophysiology.
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