Recombinant Mouse Cyclin-dependent kinase 5 activator 1 (Cdk5r1)

1. This study demonstrated that a complete deletion of p35 normalized the accelerating Rotarod performance relative to their non-transgenic littermates at four months of age. PMID: 28391013
2. Loss of endothelial NO plays an important role in the generation of p25 and resulting tau phosphorylation in neuronal tissue. Endothelial nitric oxide synthase (eNOS)-deficient (eNOS-/-) mice display increased levels of p25, an aberrant activator of cyclin-dependent kinase 5, which is one of the primary kinases responsible for tau hyperphosphorylation, and a statistically higher p25/p35 ratio. PMID: 27601478
3. These data suggest p35 and p39 have specific and overlapping roles in oligodendrocyte development, some of which may be independent of Cdk5 activation. PMID: 26961956
4. Studied the effect of reduced levels of p25 and p35, two proteins required for cdk5 activation, on striatal neurodegeneration using mice with targeted deletion of p35. PMID: 24353748
5. provide a mechanistic explanation that Sig-1Rs help maintain proper tau phosphorylation by potentially carrying and providing myristic acid to p35 for enhanced p35 degradation to circumvent the formation of overreactive cdk5/p25 PMID: 25964330
6. the effects of p25, although normally attributed to activate CDK5, may be mediated in part by elevated GSK3beta activity. PMID: 25331900
7. The SIK2-p35-PJA2 complex is essential for glucose homeostasis and provides a link between p35-CDK5 and the AMPK family in excitable cells. PMID: 24561619
8. there were some abnormalities in the morphology/distribution of inhibitory interneurons of the dentate gyrus, overall inhibition in the p35 knockout mouse appeared to be largely intact PMID: 22612821
9. This study demonistrated that lysophosphatidylcholine is a molecular signal released from neurons to mediate glial activation and the recruitment of inflammatory mediators in p25Tg mice contributing to AD-like neuropathology. PMID: 22262900
10. This study demonistrated that p35 Knockout mice showed no hilar cell death, but moderate mossy fiber sprouting and granule cell dispersion. PMID: 21635231
11. findings suggest that dysregulation of Cdk5/p35 activity during development may contribute to ADHD pathology. PMID: 20832057
12. detection of endogenous p10, the smaller proteolytic fragment of the Cdk5 activator p35 in treated primary cortical neurons that underwent significant apoptosis PMID: 20830735
13. p35 is required for efficient HSV-1 replication in mice. PMID: 20839922
14. A novel mechanism of actin cytoskeletal regulation of Cdk5/p35 activity is negatively correlated in the mouse brain. PMID: 20492361
15. These are the first quantitative and site-specific measurements of phosphorylation of p35 PMID: 20097924
16. p35 deficiency is critically involved in the expression of a hyperactive behavioral phenotype with hyper-functioning of the dopaminergic system. PMID: 20403084
17. Increased expression of GSK-3beta and p25 acted by decreasing the frequency of mitochondrial movements driven by molecular motors and GSK-3beta and p25 might regulate these transports by controlling the time that mitochondria spend pausing. PMID: 20211702
18. Data show that crosslinking Fas on primary sensory neurons induces neurite growth through sustained activation of the extracellular-signal regulated kinase (ERK) pathway and the consequent upregulation of p35, a mediator of neurite outgrowth. PMID: 12545171
19. Partial rescue of the p35-/- brain phenotype by low expression of the p25 transgene. PMID: 12684463
20. Neither the CDK5 activator p25 immunoreactivity nor the p25/p35 ratio was elevated in Alzheimer disease brains or in other tauopathies (n = 34) compared with controls (n = 11) PMID: 12859671
21. Inside-out layering requires the distinct function of p35/Cdk5 signaling, which is essential for proper glia-guided migration. PMID: 14608361
22. P35 signaling can have both cell- and non cell-autonomous consequences on control of cortical neuron migration and layering. PMID: 14724258
23. Data show that both p35 and p39 are expressed in insulin-secreting beta cells, where they exhibit individual subcellular distributions and associate with membranous organelles of different densities. PMID: 15123626
24. These studies suggest that dentate granule cells in p35 knock-out mice contribute to epileptic seizure activity by forming an abnormal excitatory feedback circuit. PMID: 15483119
25. More oligodendrocytes and less demyelination were observed after SCI in p35 transgenic mice than in controls which did not carry the p35 transgene. Motor function recovered more in the cre/p35 transgenic mice than in the control cre mice. PMID: 15846791
26. These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses. PMID: 15908038
27. Low-level p25 expression had different consequences in male and female mutants. In the two genetic backgrounds LTP was severely impaired in male, but not in female, p25 mutants. PMID: 15978013
28. p35-dependent Cdk5 activity is important to learning and synaptic plasticity. Deletion of p35 may shift the substrate specificity of Cdk5 due to compensatory expression of p39. PMID: 15992381
29. Knockouts showed delayed responses to painful thermal stimulation compared with WT controls. PMID: 16407116
30. identify p35 as the first target gene for HSF2 in cortical development PMID: 16600913
31. We now report that aberrant dentate development can be recognized in the organotypic hippocampal slice culture preparation generated from p35-/- mouse pups. PMID: 17148953
32. The guidance of successive generations of daughter neurons to their proper locations requires the activation of Reelin and p35. PMID: 18494254
33. The differential nuclear accumulation of p39 and p35 suggests their segregated functions, p35-Cdk5 in the cytoplasm and p39-Cdk5 in the nucleus. PMID: 18507738
34. MEK inhibitor, which inhibits ERK activation, decreased p35 promoter activity, whereas the inhibitors of p38 MAPK, JNK, and NF-kappaB increased p35 promoter activity, indicating that these pathways regulate p35 expression differently PMID: 19049962
35. findings suggest synergistic effects of p35 over-expression and Abeta treatment in the apoptosis of neuronal cells PMID: 19362124
36. a role for Cdk5-p35 as a survival factor in countering MPP+-induced neuronal cell death. PMID: 19638632

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KEGG: mmu:12569

STRING: 10090.ENSMUSP00000099514

UniGene: Mm.142275