Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

DRD2/AKT1 interaction on D2 c-AMP independent signaling, attentional processing, and response to olanzapine treatment in schizophrenia.

Proceedings of the National Academy of Sciences of the United States of America - 18 Jan 2011

Blasi Giuseppe, Napolitano Francesco, Ursini Gianluca, Taurisano Paolo, Romano Raffaella, Caforio Grazia, Fazio Leonardo, Gelao Barbara, Di Giorgio Annabella, Iacovelli Luisa, Sinibaldi Lorenzo, Popolizio Teresa, Usiello Alessandro, Bertolino Alessandro

Abstract excerpt

The D2/AKT1/GSK-3β signaling pathway has been involved in the downstream intracellular effects of dopamine, in the pathophysiology of cognitive deficits and related brain activity in schizophrenia, as well as in response to treatment with antipsychotics. Polymorphisms in the D2 (DRD2 rs1076560) and AKT1 (AKT1 rs1130233) genes have been associated with their respective protein expression and with higher-order...

Read the complete abstract on PubMed

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antipsychotic Agents
Share to Attention
Share to Benzodiazepines
Share to Glycogen Synthase Kinase 3
Share to Glycogen Synthase Kinase 3 beta
Share to Olanzapine
Share to Psychomotor Performance
Share to Receptors, Dopamine D2

Source

Open in PubMed Open full text

Identifiers

PMID: 21187413
DOI: 10.1073/pnas.1013535108
PMCID: PMC3024671

Genes

AKT1
DRD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

DRD2/AKT1 interaction on D2 c-AMP independent signaling, attentional processing, and response to olanzapine treatment in schizophrenia.PMID 21187413Read ↗

New Repeat Polymorphism in the AKT1 Gene Predicts Striatal Dopamine D2/D3 Receptor Availability and Stimulant-Induced Dopamine Release in the Healthy Human Brain.Semantic proximity Read ↗

Identification of AKT1 3'UTR variants in two Indian schizophrenia patients with poor executive functioning.Semantic proximity Read ↗

Genetic variation in AKT1 is linked to dopamine-associated prefrontal cortical structure and function in humans.Semantic proximity Read ↗

Genetic study of eight AKT1 gene polymorphisms and their interaction with DRD2 gene polymorphisms in tardive dyskinesia.Semantic proximity Read ↗

Decreased VEGFR2 expression and increased phosphorylated Akt1 in the prefrontal cortex of individuals with schizophrenia.Semantic proximity Read ↗

Biological validation of increased schizophrenia risk with NRG1, ERBB4, and AKT1 epistasis via functional neuroimaging in healthy controls.Semantic proximity Read ↗

A signaling pathway AKTing up in schizophrenia.Semantic proximity Read ↗

Epistatic interactions of AKT1 on human medial temporal lobe biology and pharmacogenetic implications.Semantic proximity Read ↗

The effect of the AKT1 gene and cannabis use on cognitive performance in healthy subjects.Semantic proximity Read ↗

Marked reduction of AKT1 expression and deregulation of AKT1-associated pathways in peripheral blood mononuclear cells of schizophrenia patients.Semantic proximity Read ↗

Gene expression profiling in treatment-naive schizophrenia patients identifies abnormalities in biological pathways involving AKT1 that are corrected by antipsychotic medicationSemantic proximity Read ↗

The AKT1 gene is associated with attention and brain morphology in schizophrenia.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.