Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
p35 likely acts downstream of egr1 (show EGR1 ELISA Kits) to control the differentiation of Parvalbumin (show PVALB ELISA Kits)+ amacrine cells.
CDK5 (show CDK5 ELISA Kits) 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
It is shown that p5 binds the kinase at the same CDK5 (show CDK5 ELISA Kits)/p25 (show LCN2 ELISA Kits) and CDK5 (show CDK5 ELISA Kits)/p35 (show ANXA1 ELISA Kits) 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 (show UTS2R ELISA Kits) rs735555 polymorphism was associated with increased risk for NS-ID. In conclusion, our data suggest that mutations and polymorphisms in CDK5 (show CDK5 ELISA Kits) and CDK5R1 genes may contribute to the onset of the NS-ID phenotype
Under cell-free in vitro conditions, p35 (show ANXA1 ELISA Kits) is covalently modified by SUMO1 (show SUMO1 ELISA Kits). SUMO2 (show SUMO2 ELISA Kits) is conjugated to p35 (show ANXA1 ELISA Kits) in cells. The 2 major SUMO acceptor lysines in p35 (show ANXA1 ELISA Kits) are K246 and K290. Different degrees of oxidative stress resulted in differential p35 (show ANXA1 ELISA Kits) sumoylation.
Cdk5 (show CDK5 ELISA Kits)/p35 (show ANXA1 ELISA Kits) is required for motor learning and involved in long-term synaptic plasticity.
Expression of p35 (show ANXA1 ELISA Kits) is upregulated in human pituitary adenomas.
These results reveal a physiological role of p25 (show LCN2 ELISA Kits) production in synaptic plasticity and memory and provide new insights into the function of p25 (show LCN2 ELISA Kits) in Abeta (show APP ELISA Kits)-associated neurotoxicity and Alzheimer's disease-like pathology.
Structural basis for the different stability and activity between the Cdk5 (show CDK5 ELISA Kits) complexes with p35 (show ANXA1 ELISA Kits) and p39 (show JUN ELISA Kits) activators.
Reduced p35 (show ANXA1 ELISA Kits) basal content and down--regulation of CDK5 (show CDK5 ELISA Kits)/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 (show GSK3b ELISA Kits), 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.
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 ELISA Kits))-deficient (eNOS (show NOS3 ELISA Kits)-/-) mice display increased levels of p25, an aberrant activator of cyclin-dependent kinase 5 (show CDK5 ELISA Kits), which is one of the primary kinases responsible for tau hyperphosphorylation, and a statistically higher p25/p35 ratio.
The transiently active CDK5 (show CDK5 ELISA Kits)-p35 complexes limited the LPS (show TLR4 ELISA Kits)-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 ELISA Kits))
Cdk5 (cyclin-dependent kinase 5 (show CDK5 ELISA Kits)) requires p35 regulatory subunit (Cdk5r1) for activation; data suggest Cdk5r1 stability regulates Cdk5 (show CDK5 ELISA Kits) activity in neurons; Cdk5r1 is rapidly degraded by 2 proteasome methods, ubiquitination-dependent and -independent.
These data suggest p35 and p39 (show ATP6V0D1 ELISA Kits) have specific and overlapping roles in oligodendrocyte development, some of which may be independent of Cdk5 (show CDK5 ELISA Kits) activation.
Studied the effect of reduced levels of p25 and p35, two proteins required for cdk5 (show CDK5 ELISA Kits) activation, on striatal neurodegeneration using mice with targeted deletion of p35.
p35 interacts with NIF-1 (show ZNF335 ELISA Kits) and regulates the subcellular localization of the protein independent of Cdk5 (show CDK5 ELISA Kits)-dependent phosphorylation. ...reveal a new mechanism of p35 in transcriptional regulation that does not require the kinase activity of Cdk5 (show CDK5 ELISA Kits)
Cdk5 (show CDK5 ELISA Kits)/p35 regulates spatial learning and memory.
Our findings suggest that p35/Rac1 signaling is critical in the CDK5 (show CDK5 ELISA Kits) silencing-induced neuroprotection against glutamate (show GRIN1 ELISA Kits) 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
Data suggest that up-regulation of S100A8 (show S100A8 ELISA Kits) and S100A9 (show S100A9 ELISA Kits) is a key component of early endometrial response to uterine involution in the post-partum period and to prevent chronic endometritis/uterine inflammation; up-regulation can be influenced by diet.
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.
cyclin-dependent kinase 5, regulatory subunit 1 (p35)
, cyclin-dependent kinase 5 regulatory subunit
, cyclin-dependent kinase 5 activator 1
, cyclin-dependent kinase 5 regulatory subunit 1
, CDK5 activator 1
, TPKII regulatory subunit
, neuronal CDK5 activator
, regulatory partner for CDK5 kinase
, tau protein kinase II 23kDa subunit
, cyclin-dependent kinase 5, regulatory subunit (p35) 1
, tau protein kinase II 23 kDa subunit
, Harvey rat sarcoma oncogene, subgroup R
, Harvey rat sarcoma virus oncogene, subgroup R
, Ras-related protein R-RAS (P23)
, ras-related protein R-Ras
, S100 calcium-binding protein A9
, neutrophil cytosolic 23 kDa protein
, protein S100-A9
, 21 kDa transmembrane-trafficking protein
, p24 family protein delta-1
, transmembrane emp24 domain-containing protein 10
, transmembrane protein Tmp21
, transmembrane trafficking protein
, growth-related translationally controlled tumor protein
, growth-related translationally-controlled tumor protein
, translationally-controlled tumor protein homolog