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Study demonstrated that NEAT1 and HOTAIR negatively regulate CDK5R1 mRNA levels, while MALAT1 has a positive effect.
the downregulation of the miR-15/107 family might have a role in the pathogenesis of AD by increasing the levels of CDK5R1/p35 and consequently enhancing CDK5 activity.
It is shown that p5 binds the kinase at the same CDK5/p25 and CDK5/p35 interfaces, and is thus a non-selective competitor of both activators, in agreement with available experimental data in vitro.
the minor allele of CDK5R1 3'-UTR rs735555 polymorphism was associated with increased risk for NS-ID. In conclusion, our data suggest that mutations and polymorphisms in CDK5 and CDK5R1 genes may contribute to the onset of the NS-ID phenotype
Under cell-free in vitro conditions, p35 is covalently modified by SUMO1. SUMO2 is conjugated to p35 in cells. The 2 major SUMO acceptor lysines in p35 are K246 and K290. Different degrees of oxidative stress resulted in differential p35 sumoylation.
Cdk5/p35 is required for motor learning and involved in long-term synaptic plasticity.
Expression of p35 is upregulated in human pituitary adenomas.
These results reveal a physiological role of p25 production in synaptic plasticity and memory and provide new insights into the function of p25 in Abeta-associated neurotoxicity and Alzheimer's disease-like pathology.
Structural basis for the different stability and activity between the Cdk5 complexes with p35 and p39 activators.
Reduced p35 basal content and down--regulation of CDK5/p35/p25 by antipsychotics are demonstrated in postmortem prefrontal cortex of schizophrenic subjects.
The present study dissects the role of 3 single nucleotide polymorphisms (rs334558 and rs6438552 of GSK3B, and rs735555 of CDK5R1) in Parkinson's disease pathogenesis among eastern Indians.
p10, the N-terminal domain of p35, protects against CDK5/p25-induced neurotoxicity.
The decrease in membrane-associated p35 in socially isolated transgenic mice reduces associated levels of p35, alpha-CaMKII, and GluR1 and leads to endocytosis of AMPA receptors.
CDK5/p35 may represent a biomarker for prognosis in patients with non-small cell lung cancer
findings indicate that miR-103 and miR-107 regulate CDK5R1 expression, allowing us to hypothesize that a miRNA-mediated mechanism may influence CDK5 activity and the associated molecular pathways
This study suggested that reduced p35 expression in schizophrenia has an impact on synaptic protein expression and cognition and that these deficits can be rescued, at least in part, by the inhibition of histone deacetylase 1.
Study reveals a unique role of Cdk5/p35 in activation of the major noncanonical function of EPRS, namely translational control of macrophage inflammatory gene expression.
These are the first quantitative and site-specific measurements of phosphorylation of p35
both proteasomal degradation and calpain cleavage of p35 and p39 are stimulated by membrane association, which is in turn mediated via myristoylation of their p10 regions.
Like p25, p29 was more stable than p39 and caused redistribution of Cdk5 in cortical neurons. Our data suggest that neurotoxic insults lead to calpain-mediated conversion of p39 to p29, which might contribute to deregulation of Cdk5.
p35 likely acts downstream of egr1 to control the differentiation of Parvalbumin+ amacrine cells.
CDK5 mRNA reaches the highest level in cerebral cortex at two months of age and in cerebellum and liver at 4 months of age, respectively, whereas the peak level of CDK5R1 was observed in both cerebral cortex and cerebellum at two months of age
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.
It suggests that ectopic increase of Cdk5 kinase activity through conversion of p35 to p25 is involved in the process of neuronal death induced by hypoxia.
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.
The transiently active CDK5-p35 complexes limited the LPS-stimulated phosphorylation and activation of various mitogen-activated protein kinases (MAPKs), thereby preventing the premature production of SOCS3 (suppressor of cytokine signaling 3)
Cdk5 (cyclin-dependent kinase 5) requires p35 regulatory subunit (Cdk5r1) for activation; data suggest Cdk5r1 stability regulates Cdk5 activity in neurons; Cdk5r1 is rapidly degraded by 2 proteasome methods, ubiquitination-dependent and -independent.
These data suggest p35 and p39 have specific and overlapping roles in oligodendrocyte development, some of which may be independent of Cdk5 activation.
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.
p35 interacts with NIF-1 and regulates the subcellular localization of the protein independent of Cdk5-dependent phosphorylation. ...reveal a new mechanism of p35 in transcriptional regulation that does not require the kinase activity of Cdk5
Cdk5/p35 regulates spatial learning and memory.
Our findings suggest that p35/Rac1 signaling is critical in the CDK5 silencing-induced neuroprotection against glutamate neurotoxicity
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
This report shows that herpes simplex virus 1 increases p35 levels, changes the primary localization of CDK-5 from the nucleus to the cytoplasm, and enhances CDK-5 activity during lytic or acute infection.
the effects of p25, although normally attributed to activate CDK5, may be mediated in part by elevated GSK3beta activity.
Subcellular localization of Cdk5 is determined by its specific activators, cyclin I and p35.
it was found that Tyr-15 phosphorylation occurred only on monomeric Cdk5, and the coexpression of activators, p35/p25, p39, or Cyclin I, inhibited the phosphorylation.
The SIK2-p35-PJA2 complex is essential for glucose homeostasis and provides a link between p35-CDK5 and the AMPK family in excitable cells.
Both cyclin I and p35 are required for maximal survival benefit of cyclin-dependent kinase 5 in kidney podocytes.
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
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.
The protein encoded by this gene (p35) is a neuron-specific activator of cyclin-dependent kinase 5 (CDK5)\; the activation of CDK5 is required for proper development of the central nervous system. The p35 form of this protein is proteolytically cleaved by calpain, generating a p25 form. The cleavage of p35 into p25 results in relocalization of the protein from the cell periphery to nuclear and perinuclear regions. P25 deregulates CDK5 activity by prolonging its activation and changing its cellular location. The p25 form accumulates in the brain neurons of patients with Alzheimer's disease. This accumulation correlates with an increase in CDK5 kinase activity, and may lead to aberrantly phosphorylated forms of the microtubule-associated protein tau, which contributes to Alzheimer's disease.
CDK5 activator 1
, TPKII regulatory subunit
, cyclin-dependent kinase 5 activator 1
, cyclin-dependent kinase 5 regulatory subunit 1
, neuronal CDK5 activator
, regulatory partner for CDK5 kinase
, tau protein kinase II 23kDa subunit
, cyclin-dependent kinase 5 regulatory subunit
, cyclin-dependent kinase 5, regulatory subunit 1 (p35)
, tau protein kinase II 23 kDa subunit
, cyclin-dependent kinase 5, regulatory subunit (p35) 1