CDK5R1

Last update 08 May 2025

Basic Info

Synonyms

CDK5 activator 1, CDK5R, CDK5R1

+ [12]

Introduction

p35 is a neuron specific activator of CDK5. The complex p35/CDK5 is required for neurite outgrowth and cortical lamination. Involved in dendritic spine morphogenesis by mediating the EFNA1-EPHA4 signaling. Activator of TPKII. The complex p35/CDK5 participates in the regulation of the circadian clock by modulating the function of CLOCK protein: phosphorylates CLOCK at 'Thr-451' and 'Thr-461' and regulates the transcriptional activity of the CLOCK-BMAL1 heterodimer in association with altered stability and subcellular distribution.

100 Clinical Results associated with CDK5R1

100 Translational Medicine associated with CDK5R1

0 Patents (Medical) associated with CDK5R1

124

Literatures (Medical) associated with CDK5R1

01 Feb 2025·Molecular Diversity

Network pharmacology combined with molecular docking and dynamics to assess the synergism of esculetin and phloretin against acute kidney injury-diabetes comorbidity

Article

Author: Gaikwad, Anil Bhanudas ; Dagar, Neha ; Jadhav, Hemant R

Acute kidney injury (AKI) is a global health concern with high incidence and mortality, where diabetes further worsens the condition. The available treatment options are not uniformly effective against the complex pathogenesis of AKI-diabetes comorbidity. Hence, combination therapies based on the multicomponent, multitarget approach can tackle more than one pathomechanism and can aid in AKI-diabetes comorbidity management. This study aimed to investigate the therapeutic potential of esculetin and phloretin combination against AKI-diabetes comorbidity by network pharmacology followed by validation by molecular docking and dynamics. The curative targets for diabetes, AKI, esculetin, and phloretin were obtained from DisGeNET, GeneCards, SwissTargetPrediction database. Further, the protein-protein interaction of the potential targets of esculetin and phloretin against AKI-diabetes comorbidity was investigated using the STRING database. Gene ontology and pathway enrichment analysis were performed with the help of the DAVID and KEGG databases, followed by network construction and analysis via Cytoscape. Molecular docking and dynamic simulations were performed to validate the targets of esculetin and phloretin against AKI-diabetes comorbidity. We obtained 6341 targets for AKI-diabetes comorbidity. Further, a total of 54 and 44 targets of esculetin and phloretin against AKI-diabetes comorbidity were retrieved. The top 10 targets for esculetin selected based on the degree value were AKR1B1, DAO, ESR1, PLK1, CA3, CA2, CCNE1, PRKN, HDAC2, and MAOA. Similarly, phloretin's 10 key targets were ACHE, CDK1, MAPK14, APP, CDK5R1, CCNE1, MAOA, MAOB, HDAC6, and PRKN. These targets were enriched in 58 pathways involved in the pathophysiology of AKI-diabetes comorbidity. Further, esculetin and phloretin showed an excellent binding affinity for these critical targets. The findings of this study suggest that esculetin and phloretin combination as a multicomponent multitarget therapy has the potential to prevent AKI-diabetes comorbidity.

01 Jan 2025·Journal of Alzheimer's Disease Reports

Identifying Alzheimer's disease genes in apolipoprotein E ^−/− mice brains with confirmed Porphyromonas gingivalis entry

Article

Author: Consoli, Claudia ; Singhrao, Sim K

BackgroundThe apolipoprotein E allele ε4 is the most well-known predisposing genetic risk factor for Alzheimer's disease (AD).Objective To identify AD genes in apolipoprotein E −/− (ApoE −/− ) mice brains with confirmed entry of Porphyromonas gingivalis . Methods TaqMan™ Mouse AD arrays were performed on orally infected ApoE −/− mice with confirmed P. gingivalis entry and compared with sham infected mice brains (N = 4) at 12- and 24-weeks post infection. Results Gene expression by qPCR demonstrated that in the P. gingivalis 12-weeks post oral infection, two genes were statistically significantly changed in their expression. These were cyclin dependent kinase 5 regulatory subunit 1 (Cdk5r1, 0.15 logfold change, p = 0.05) and Interleukin 1 alpha, (IL1a, −0.10 log fold change, p = 0.012). In the P. gingivalis 24-weeks post oral infection, three genes were statistically significantly changed in their expression. These were cholinergic receptor nicotinic alpha 7 subunit or Chrna7 (0.10 log fold change, p = 0.02), mitogen-activated protein kinase 1 or Mapk1 (0.10 log fold change, p = 0.05) and visinin like 1 or Vnsl1 (0.01 log fold change, p = 0.04). 87 out of 92 AD target genes demonstrated no difference between infected and sham mice brains. Conclusions Five genes, from a recognized AD panel had statistically significantly altered expression in the ApoE −/− mouse AD model following P. gingivalis entry into the brain. This suggests the ApoE −/− genetic variation may control the biological activity of specific genes relevant to inflammation and neuronal plasticity following P. gingivalis infection.

01 Jan 2025·Open Veterinary Journal

Expression profiles of the Tau-associated genes GSk3β, CAPN1, and CDK5R1 in the brain cortex of aged female cynomolgus monkeys with cognitive impairment

Article

Author: Yuliana, Yuliana ; Hau, Jann ; Mariya, Sela S ; Saepuloh, Uus ; Darusman, Huda S ; Rosmanah, Lis

Background: Alzheimer's disease (AD) is characterized by the buildup and aggregation of misfolded proteins in the brain, including amyloid-β (Aβ) and hyperphosphorylated tau. The hyperphosphorylation state of Tau protein plays an important role in the development of AD. Our previous studies developed and characterized the cynomolgus monkey as a spontaneous animal model of AD. Aim: We demonstrated the validity of the model through experimental investigations of the relationships between cognitive decline and the neuro-pathy of AD. There is, however, little information about the expression actvity of hyperphosphorylated tau related genes in various brain areas in the in cynomolgus monkey spontaneous AD model. Methods: In the present study, total RNA was extracted from archived cortex and hippocampus tissues from the brains of two groups of cynomolgus monkeys, adult (10-12 years old, n=5) and aged (> 20 years old, n=4). The expression of the tau-protein-associated genes GSK3β, CAPN1, and CDK5R1 was evaluated using RT-qPCR technique Results: The expression of all three genes was increased up to five fold in the brain cortical area of the aged subjects compared to the adults Conclusion: The results add weight to the utility of cynomolgus macaques as a valid spontaneous model in translational preclinical research involving studies of the effect of aging on the formation of hyperphosphorylated tau protein, which causes AD-related lesions in the brain.

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CDK5R1

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