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The present results provide novel cause-effect evidence supporting a role for CEA Homer2 in the regulation of both basal anxiety and the time-dependent intensification of negative affective states in individuals with a history of binge-drinking during adolescence.
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detected an additional 15 novel Homer2-interacting proteins, most of which are part of the N-methyl-D-aspartate receptor signaling pathway. These results corroborate the central role Homer2 plays in glutamatergic transmission and expand the network of proteins potentially contributing to the behavioral abnormalities associated with altered Homer2 expression
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stress-alcohol locomotor cross-sensitization was regulated by Homer2.
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NMDA receptor function, but not ethanol sensitivity, is reduced in hippocampal neurons lacking the Homer2 gene
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mouse mutants homozygous for the targeted deletion of Homer2 present with early-onset rapidly progressive hearing loss.
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Findings indicate an important regulation of plasma membrane Ca(2+)-ATPase (PMCA) by Homer2 protein that has a central role on PMCA-mediated Ca(2+) signaling in parotid acinar cells.
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This study deministrated that PFC Homer2 overexpression enhances cocaine-conditioned reward in mice.
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Homer 1b/c isoform is identical irrespective of the muscle; Homer 2a/b is instead characteristic of the slow-twitch phenotype.
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These data support the over-arching hypothesis that augmented accumbens Homer2-mediated glutamate signaling may be an endophenotype related to genetic variance in alcohol consumption
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Homer2 tunes G protein-coupled receptors stimulus intensity by regulating RGS proteins and PLCbeta GAP activities.
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In the developing olfactory bulb, Cupidin/Homer 2a/b is up-regulated in the granular, external plexiform, and glomerular layers
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Homer2 KO mice demonstrate enhanced locomotor stimulant and conditioned place preference responses to cocaine
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necessary and active role for accumbens Homer2 expression in regulating EtOH-induced behavioral and cellular neuroplasticity
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Expression of HOMER2 enhanced the ability of MYO18B to suppress anchorage-independent growth. These results indicate that HOMER2 and MYO18B cooperate together in tumor suppression.
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Accumbens Homer2 overexpression facilitates alcohol-induced neuroplasticity in C57BL/6J mice.
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study found that Homer2 and Homer3 are negative regulators of T cell activation; this is achieved through binding of nuclear factor of activated T cells (NFAT) and by competing with calcineurin
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Homer2 and Homer3 proteins interact specifically with amyloid precursor protein (APP) by inhibiting APP processing and reducing secretion of Abeta peptides.
