| P25/CDK5-mediated Tau Hyperphosphorylation in Both Ipsilateral and Contralateral Cerebra Contributes to Cognitive Deficits in Post-stroke Mice. | P25/CDK5-mediated Tau Hyperphosphorylation in Both Ipsilateral and Contralateral Cerebra Contributes to Cognitive Deficits in Post-stroke Mice.
Yu J, Zhao Y, Gong XK, Liang Z, Zhao YN, Li X, Chen YJ, Yang YH, Wu MJ, Wang XC, Shu XJ, Bao J. | 01/4/2024 |
| p35 is a Crucial Player in NK-cell Cytotoxicity and TGFbeta-mediated NK-cell Dysfunction. | p35 is a Crucial Player in NK-cell Cytotoxicity and TGFβ-mediated NK-cell Dysfunction.
Wong DP, Fritz CE, Feinberg D, Huang AY, Parameswaran R., Free PMC Article | 07/3/2023 |
| Involvement of Cdk5 activating subunit p35 in synaptic plasticity in excitatory and inhibitory neurons. | Involvement of Cdk5 activating subunit p35 in synaptic plasticity in excitatory and inhibitory neurons.
Takahashi M, Nakabayashi T, Mita N, Jin X, Aikawa Y, Sasamoto K, Miyoshi G, Miyata M, Inoue T, Ohshima T., Free PMC Article | 05/7/2022 |
| RPS23RG1 modulates tau phosphorylation and axon outgrowth through regulating p35 proteasomal degradation. | RPS23RG1 modulates tau phosphorylation and axon outgrowth through regulating p35 proteasomal degradation.
Zhao D, Zhou Y, Huo Y, Meng J, Xiao X, Han L, Zhang X, Luo H, Can D, Sun H, Huang TY, Wang X, Zhang J, Liu FR, Xu H, Zhang YW., Free PMC Article | 12/25/2021 |
| AAV9-Mediated Cdk5 Inhibitory Peptide Reduces Hyperphosphorylated Tau and Inflammation and Ameliorates Behavioral Changes Caused by Overexpression of p25 in the Brain. | AAV9-Mediated Cdk5 Inhibitory Peptide Reduces Hyperphosphorylated Tau and Inflammation and Ameliorates Behavioral Changes Caused by Overexpression of p25 in the Brain.
Xu M, Huang Y, Song P, Huang Y, Huang W, Zhang HT, Hu Y. | 10/3/2020 |
| p35 Hemizygous Deletion in 5xFAD Mice Increases Abeta Plaque Load in Males but Not in Females. | p35 Hemizygous Deletion in 5xFAD Mice Increases Aβ Plaque Load in Males but Not in Females.
Barrett T, Marchalant Y, Park KHJ. | 09/26/2020 |
| Restoration of p35 expression in the hippocampus and cortex of Men1 conditional knockout mice rescues synaptic and cognitive deficits associated with Men1 deletion. | Neuron-Specific Menin Deletion Leads to Synaptic Dysfunction and Cognitive Impairment by Modulating p35 Expression.
Zhuang K, Huang C, Leng L, Zheng H, Gao Y, Chen G, Ji Z, Sun H, Hu Y, Wu D, Shi M, Li H, Zhao Y, Zhang Y, Xue M, Bu G, Huang TY, Xu H, Zhang J., Free PMC Article | 12/7/2019 |
| 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. | p35 hemizygosity activates Akt but does not improve motor function in the YAC128 mouse model of Huntington's disease.
Park KHJ, Franciosi S, Parrant K, Lu G, Leavitt BR. | 03/10/2018 |
| 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. | Increase of p25 associated with cortical neuronal death induced by hypoxia.
Huang T, Fang L, Lin Z, Huang E, Ye Q. | 05/20/2017 |
| 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. | Loss of Endothelial Nitric Oxide Synthase Promotes p25 Generation and Tau Phosphorylation in a Murine Model of Alzheimer's Disease.
Austin SA, Katusic ZS., Free PMC Article | 05/13/2017 |
| 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) | The early synthesis of p35 and activation of CDK5 in LPS-stimulated macrophages suppresses interleukin-10 production.
Na YR, Jung D, Gu GJ, Jang AR, Suh YH, Seok SH. | 09/10/2016 |
| 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. | Two Degradation Pathways of the p35 Cdk5 (Cyclin-dependent Kinase) Activation Subunit, Dependent and Independent of Ubiquitination.
Takasugi T, Minegishi S, Asada A, Saito T, Kawahara H, Hisanaga S., Free PMC Article | 08/6/2016 |
| These data suggest p35 and p39 have specific and overlapping roles in oligodendrocyte development, some of which may be independent of Cdk5 activation. | The Activators of Cyclin-Dependent Kinase 5 p35 and p39 Are Essential for Oligodendrocyte Maturation, Process Formation, and Myelination.
Luo F, Zhang J, Burke K, Miller RH, Yang Y., Free PMC Article | 07/30/2016 |
| 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. | Decreasing Levels of the cdk5 Activators, p25 and p35, Reduces Excitotoxicity in Striatal Neurons.
Park KH, Lu G, Fan J, Raymond LA, Leavitt BR., Free PMC Article | 05/14/2016 |
| 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 | p35 regulates the CRM1-dependent nucleocytoplasmic shuttling of nuclear hormone receptor coregulator-interacting factor 1 (NIF-1).
Zhao XS, Fu WY, Chien WW, Li Z, Fu AK, Ip NY., Free PMC Article | 12/19/2015 |
| Cdk5/p35 regulates spatial learning and memory. | Cdk5/p35 functions as a crucial regulator of spatial learning and memory.
Mishiba T, Tanaka M, Mita N, He X, Sasamoto K, Itohara S, Ohshima T., Free PMC Article | 11/14/2015 |
| Our findings suggest that p35/Rac1 signaling is critical in the CDK5 silencing-induced neuroprotection against glutamate neurotoxicity | p35 and Rac1 underlie the neuroprotection and cognitive improvement induced by CDK5 silencing.
Posada-Duque RA, López-Tobón A, Piedrahita D, González-Billault C, Cardona-Gomez GP., Free PMC Article | 09/26/2015 |
| 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 | Sigma-1 receptor regulates Tau phosphorylation and axon extension by shaping p35 turnover via myristic acid.
Tsai SY, Pokrass MJ, Klauer NR, Nohara H, Su TP., Free PMC Article | 08/29/2015 |
| 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. | Herpes simplex virus 1 upregulates p35, alters CDK-5 localization, and stimulates CDK-5 kinase activity during acute infection in neurons.
Mostafa HH, van Loben Sels JM, Davido DJ., Free PMC Article | 06/20/2015 |
| the effects of p25, although normally attributed to activate CDK5, may be mediated in part by elevated GSK3beta activity. | CDK5 activator protein p25 preferentially binds and activates GSK3β.
Chow HM, Guo D, Zhou JC, Zhang GY, Li HF, Herrup K, Zhang J., Free PMC Article | 04/18/2015 |
| Subcellular localization of Cdk5 is determined by its specific activators, cyclin I and p35. | Cyclin I and p35 determine the subcellular distribution of Cdk5.
Hagmann H, Taniguchi Y, Pippin JW, Kauerz HM, Benzing T, Shankland SJ, Brinkkoetter PT. | 04/11/2015 |
| 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. | Phosphorylation of cyclin-dependent kinase 5 (Cdk5) at Tyr-15 is inhibited by Cdk5 activators and does not contribute to the activation of Cdk5.
Kobayashi H, Saito T, Sato K, Furusawa K, Hosokawa T, Tsutsumi K, Asada A, Kamada S, Ohshima T, Hisanaga S., Free PMC Article | 10/4/2014 |
| The SIK2-p35-PJA2 complex is essential for glucose homeostasis and provides a link between p35-CDK5 and the AMPK family in excitable cells. | Role of the SIK2-p35-PJA2 complex in pancreatic β-cell functional compensation.
Sakamaki J, Fu A, Reeks C, Baird S, Depatie C, Al Azzabi M, Bardeesy N, Gingras AC, Yee SP, Screaton RA., Free PMC Article | 05/3/2014 |
| Structural basis for the different stability and activity between the Cdk5 complexes with p35 and p39 activators. | Structural basis for the different stability and activity between the Cdk5 complexes with p35 and p39 activators.
Saito T, Yano M, Kawai Y, Asada A, Wada M, Doi H, Hisanaga SI., Free PMC Article | 01/25/2014 |
| Both cyclin I and p35 are required for maximal survival benefit of cyclin-dependent kinase 5 in kidney podocytes. | Both cyclin I and p35 are required for maximal survival benefit of cyclin-dependent kinase 5 in kidney podocytes.
Taniguchi Y, Pippin JW, Hagmann H, Krofft RD, Chang AM, Zhang J, Terada Y, Brinkkoetter P, Shankland SJ., Free PMC Article | 07/21/2012 |