ArticleJournal of molecular neuroscience : MN2015
CDK14 Contributes to Reactive Gliosis via Interaction with Cyclin Y in Rat Model of Spinal Cord Injury.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 30 citations in OpenAlex.
- Cyclins and Cyclin-Dependent Kinases: Structure, Biological Functions, and Innovative Targeting Strategies in Cancer.MedComm · 2026Review
- CDK6-PI3K signaling axis is an efficient target for attenuating ABCB1/P-gp mediated multi-drug resistance (MDR) in cancer cells.Molecular cancer · 2022Article
- Ribociclib Inhibits P-gp-Mediated Multidrug Resistance in Human Epidermoid Carcinoma Cells.Frontiers in pharmacology · 2022Article
- Identification of key genes and pathways downstream of the β-catenin-TCF7L1 complex in pancreatic cancer cells using bioinformatics analysis.Oncology letters · 2019Article
- The role of lncRNA MSC-AS1/miR-29b-3p axis-mediated CDK14 modulation in pancreatic cancer proliferation and Gemcitabine-induced apoptosis.Cancer biology & therapy · 2019Article
- Lentivirus-mediated silencing of the PTC1 and PTC2 genes promotes recovery from spinal cord injury by activating the Hedgehog signaling pathway in a rat model.Experimental & molecular medicine · 2017Article
- Temporal and Spatial Expression of LGR5 After Acute Spinal Cord Injury in Adult Rats.Neurochemical research · 2016Article
- The emerging roles and therapeutic potential of cyclin-dependent kinase 11 (CDK11) in human cancer.Oncotarget · 2016Review
Corrections and comments
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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
Cyclin-dependent kinases (CDKs) are perceived as the engine that drives cell cycle progression whereas cyclins are considered to be the gears that are changed to aid the transition between cycle phases. CDK14 is a cdc2-related serine/threonine 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 CDK14 during spinal cord injury (SCI). Western blot analysis revealed that the expression of CDK14 was gradually increased and reached a peak at 3 days after SCI. The expression of CDK14 was further analyzed by immunohistochemistry. Double immunofluorescence staining showed that CDK14 was co-expressed prominent in astrocytes. Co-localization CDK14/proliferating cell nuclear antigen (PCNA) were detected in glial cells. cyclin Y, which can interact with CDK14, was detected that had same expression trend was consistent with CDK14 Western blot results in SCI. Double-immunofluorescence staining indicated that CDK14 co-expressed with cyclin Y in some cells. Co-immunoprecipitation had been showed that CDK14 could interact with cyclin Y after acute SCI. Taken together, these data suggested that both CDK14 and cyclin Y may play important roles in spinal cord pathophysiology.
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