ArticleThe Journal of biological chemistry2015
Nuclear Translocation of Calcium/Calmodulin-dependent Protein Kinase IIδ3 Promoted by Protein Phosphatase-1 Enhances Brain-derived Neurotrophic Factor Expression in Dopaminergic Neurons.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- Myocardial Recovery With Mechanical Circulatory Support Is Linked to Alternative Splicing and Subcellular Localization of CAMK2D.Circulation · 2026Article
- Nuclear CaMKII Isoforms as Regulators of Transcription: From Developmental to Pathological Persistence.Medical sciences (Basel, Switzerland) · 2025Review
- Article
- PP1γ regulates neuronal insulin signaling and aggravates insulin resistance leading to AD-like phenotypes.Cell communication and signaling : CCS · 2023Article
- A comprehensive toxicological analysis of trans-fatty acids (TFAs) reveals a pro-apoptotic action specific to industrial TFAs counteracted by polyunsaturated FAs.Scientific reports · 2023Article
- Article
- Loss of CAMK2G affects intrinsic and motor behavior but has minimal impact on cognitive behavior.Frontiers in neuroscience · 2022Article
- Retracted: Allopregnanolone restores the tyrosine hydroxylase-positive neurons and motor performance in a 6-OHDA-injected mouse model.CNS neuroscience & therapeutics · 2020Article
- Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage.Frontiers in cellular neuroscience · 2019Article
- The intellectual disability-associated CAMK2G p.Arg292Pro mutation acts as a pathogenic gain-of-function.Human mutation · 2018Article
- CaMKII Isoforms in Learning and Memory: Localization and Function.Frontiers in molecular neuroscience · 2018Review
- Aripiprazole exerts a neuroprotective effect in mouse focal cerebral ischemia.Experimental and therapeutic medicine · 2018Article
- Physiological and Pathological Roles of CaMKII-PP1 Signaling in the Brain.International journal of molecular sciences · 2017Review
- Neuroprotection by aripiprazole against β-amyloid-induced toxicity by P-CK2α activation via inhibition of GSK-3β.Oncotarget · 2017Article
- Article
- Activation of the sigma-1 receptor by haloperidol metabolites facilitates brain-derived neurotrophic factor secretion from human astroglia.Neurochemistry international · 2017Article
- Antidepressant Effects of Aripiprazole Augmentation for Cilostazol-Treated Mice Exposed to Chronic Mild Stress after Ischemic Stroke.International journal of molecular sciences · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have reported previously that dopamine D2 receptor stimulation activates calcium/calmodulin-dependent protein kinase II (CaMKII) δ3, a CaMKII nuclear isoform, increasing BDNF gene expression. However, the mechanisms underlying that activity remained unclear. Here we report that CaMKIIδ3 is dephosphorylated at Ser(332) by protein phosphatase 1 (PP1), promoting CaMKIIδ3 nuclear translocation. Neuro-2a cells transfected with CaMKIIδ3 showed cytoplasmic and nuclear staining, but the staining was predominantly nuclear when CaMKIIδ3 was coexpressed with PP1. Indeed, PP1 and CaMKIIδ3 coexpression significantly increased nuclear CaMKII activity and enhanced BDNF expression. In support of this idea, chronic administration of the dopamine D2 receptor partial agonist aripiprazole increased PP1 activity and promoted nuclear CaMKIIδ3 translocation and BDNF expression in the rat brain substantia nigra. Moreover, aripiprazole treatment enhanced neurite extension and inhibited cell death in cultured dopaminergic neurons, effects blocked by PP1γ knockdown. Taken together, nuclear translocation of CaMKIIδ3 following dephosphorylation at Ser(332) by PP1 likely accounts for BDNF expression and subsequent neurite extension and survival of dopaminergic neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.