Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
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G-protein-coupled receptor kinases in inflammation and diseaseAtomic Structure of GRK5 Reveals Distinct Structural Features Novel for G Protein-coupled Receptor KinasesGRK3 suppresses L-DOPA-induced dyskinesia in the rat model of Parkinson's disease via its RGS homology domainRegulation of amygdalar PKA by beta-arrestin-2/phosphodiesterase-4 complex is critical for fear conditioningParkinson's disease-implicated kinases in the brain; insights into disease pathogenesis.Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology.Lentiviral overexpression of GRK6 alleviates L-dopa-induced dyskinesia in experimental Parkinson's disease.Increased G protein-coupled receptor kinase (GRK) expression in the anterior cingulate cortex in schizophreniaDistinct cellular and subcellular distributions of G protein-coupled receptor kinase and arrestin isoforms in the striatum.Multiple scaffolding functions of {beta}-arrestins in the degradation of G protein-coupled receptor kinase 2Reduced expression of G protein-coupled receptor kinases in schizophrenia but not in schizoaffective disorderG Protein-coupled Receptor Kinases of the GRK4 Protein Subfamily Phosphorylate Inactive G Protein-coupled Receptors (GPCRs).G protein-coupled receptor kinases: more than just kinases and not only for GPCRsThe evolving impact of g protein-coupled receptor kinases in cardiac health and diseaseG protein-coupled receptor kinase 5 phosphorylates nucleophosmin and regulates cell sensitivity to polo-like kinase 1 inhibition.Glucocorticoids regulate arrestin gene expression and redirect the signaling profile of G protein-coupled receptorsCognitive effects of dopamine depletion in the context of diminished acetylcholine signaling capacity in mice.Therapeutic potential of β-arrestin- and G protein-biased agonists.Altered expression and subcellular distribution of GRK subtypes in the dopamine-depleted rat basal ganglia is not normalized by l-DOPA treatment.G protein-coupled receptor kinase 2 (GRK2) is localized to centrosomes and mediates epidermal growth factor-promoted centrosomal separation.Constitutively active rhodopsin mutants causing night blindness are effectively phosphorylated by GRKs but differ in arrestin-1 bindingRich tapestry of G protein-coupled receptor signaling and regulatory mechanisms.Arrestin-2 and arrestin-3 differentially modulate locomotor responses and sensitization to amphetamine.G protein-coupled receptor kinases as regulators of dopamine receptor functions.Pro-inflammatory cytokines mediate GPCR dysfunction.Overexpression of GRK6 rescues L-DOPA-induced signaling abnormalities in the dopamine-depleted striatum of hemiparkinsonian rats.G Protein-Coupled Receptor Kinases in the Inflammatory Response and Signaling.The Role of G Protein-coupled Receptor Kinases in Cancer.Loss of GPR3 reduces the amyloid plaque burden and improves memory in Alzheimer's disease mouse models.Utilizing a structure-based docking approach to develop potent G protein-coupled receptor kinase (GRK) 2 and 5 inhibitors.
P2860
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P2860
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@ast
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@en
type
label
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@ast
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@en
prefLabel
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@ast
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@en
P2093
P2860
P1476
Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia.
@en
P2093
E R Bychkov
E V Gurevich
J L Benovic
V V Gurevich
P2860
P304
P356
10.1016/J.NEUROBIOLAGING.2006.10.012
P577
2006-11-27T00:00:00Z