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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 (show MLXIP Proteins)-15/107 family might have a role in the pathogenesis of AD by increasing the levels of CDK5R1/p35 and consequently enhancing CDK5 (show CDK5 Proteins) activity.
It is shown that p5 binds the kinase at the same CDK5 (show CDK5 Proteins)/p25 (show LCN2 Proteins) and CDK5 (show CDK5 Proteins)/p35 (show ANXA1 Proteins) 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 (show CDK5 Proteins) and CDK5R1 genes may contribute to the onset of the NS-ID phenotype
Under cell-free in vitro conditions, p35 (show ANXA1 Proteins) is covalently modified by SUMO1 (show SUMO1 Proteins). SUMO2 (show SUMO2 Proteins) is conjugated to p35 (show ANXA1 Proteins) in cells. The 2 major SUMO acceptor lysines in p35 (show ANXA1 Proteins) are K246 and K290. Different degrees of oxidative stress resulted in differential p35 (show ANXA1 Proteins) sumoylation.
Cdk5 (show CDK5 Proteins)/p35 (show ANXA1 Proteins) is required for motor learning and involved in long-term synaptic plasticity.
Expression of p35 (show ANXA1 Proteins) is upregulated in human pituitary adenomas.
These results reveal a physiological role of p25 (show LCN2 Proteins) production in synaptic plasticity and memory and provide new insights into the function of p25 (show LCN2 Proteins) in Abeta (show APP Proteins)-associated neurotoxicity and Alzheimer's disease-like pathology.
Structural basis for the different stability and activity between the Cdk5 (show CDK5 Proteins) complexes with p35 (show ANXA1 Proteins) and p39 (show JUN Proteins) activators.
Reduced p35 (show ANXA1 Proteins) basal content and down--regulation of CDK5 (show CDK5 Proteins)/p35/p25 by antipsychotics are demonstrated in postmortem prefrontal cortex of schizophrenic subjects.
p35 likely acts downstream of egr1 (show EGR1 Proteins) to control the differentiation of Parvalbumin (show PVALB Proteins)+ amacrine cells.
CDK5 (show CDK5 Proteins) 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 (show NOS3 Proteins))-deficient (eNOS (show NOS3 Proteins)-/-) mice display increased levels of p25, an aberrant activator of cyclin-dependent kinase 5 (show CDK5 Proteins), which is one of the primary kinases responsible for tau hyperphosphorylation, and a statistically higher p25/p35 ratio.
The transiently active CDK5 (show CDK5 Proteins)-p35 complexes limited the LPS (show TLR4 Proteins)-stimulated phosphorylation and activation of various mitogen-activated protein kinases (MAPKs), thereby preventing the premature production of SOCS3 (suppressor of cytokine signaling 3 (show SOCS3 Proteins))
Cdk5 (cyclin-dependent kinase 5 (show CDK5 Proteins)) requires p35 regulatory subunit (Cdk5r1) for activation; data suggest Cdk5r1 stability regulates Cdk5 (show CDK5 Proteins) activity in neurons; Cdk5r1 is rapidly degraded by 2 proteasome methods, ubiquitination-dependent and -independent.
These data suggest p35 and p39 (show ATP6V0D1 Proteins) have specific and overlapping roles in oligodendrocyte development, some of which may be independent of Cdk5 (show CDK5 Proteins) activation.
Studied the effect of reduced levels of p25 and p35, two proteins required for cdk5 (show CDK5 Proteins) 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 (show CDK5 Proteins)-dependent phosphorylation. ...reveal a new mechanism of p35 in transcriptional regulation that does not require the kinase activity of Cdk5 (show CDK5 Proteins)
Cdk5 (show CDK5 Proteins)/p35 regulates spatial learning and memory.
Our findings suggest that p35/Rac1 signaling is critical in the CDK5 (show CDK5 Proteins) silencing-induced neuroprotection against glutamate (show GRIN1 Proteins) neurotoxicity
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