Proteome and behavioral alterations in phosphorylation-deficient mutant Collapsin Response Mediator Protein2 knock-in mice

Neurochemistry International
Haruko NakamuraYoshio Goshima

Abstract

CRMP2, alternatively designated as DPYSL2, was the first CRMP family member to be identified as an intracellular molecule mediating the signaling of the axon guidance molecule Semaphorin 3A (Sema3A). In Sema3A signaling, cyclin-dependent kinase 5 (Cdk5) primarily phosphorylates CRMP2 at Ser522. Glycogen synthase kinase-3β (GSK-3β) subsequently phosphorylates the residues of Thr509 and Thr514 of CRMP2. Previous studies showed that CRMP2 is involved in pathogenesis of neurological disorders such as Alzheimer's disease. In Alzheimer's disease, hyper-phosphorylated forms of CRMP2 are accumulated in the paired helical filaments. To get insight into the possible involvement of the phosphorylation of CRMP2 in pathogenesis of neurological disorders, we previously created CRMP2 S522A knock-in (crmp2ki/ki) mice and demonstrated that the phosphorylation of CRMP2 at Ser522 is involved in normal dendrite patterning in cortical neurons. However, the behavioral impact and in vivo signaling network of the CRMP2 phosphorylation are not fully understood. In this study, we performed behavioral and proteomics analysis of crmp2ki/ki mice. The crmp2ki/ki mice appeared healthy and showed no obvious differences in physical characteristics compared to ...Continue Reading

Citations

May 30, 2019·International Journal of Molecular Sciences·Ritsuko Ohtani-Kaneko
Mar 12, 2019·Journal of Alzheimer's Disease : JAD·Nicole CortésRicardo B Maccioni
Aug 6, 2019·Frontiers in Immunology·Rut Mazón-CabreraVeerle Somers
Mar 14, 2020·Journal of Cardiovascular Pharmacology·Nikita MokhashiSatoru Eguchi
Mar 7, 2021·Molecular Neurobiology·Lei ZhangYu Deng
Jun 10, 2019·Journal of Neuroimmunology·Valentyna SavchenkoDouglas L Feinstein

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