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the GRIK4 polymorphisms genotypes were distributed as follows: rs79526501: CC696: 16, CG302: 274, GG31: 35; rs11218016: CC455: 483, CT473: 436, TT101: 108; and rs6589847: AA32: 29, AG307: 314, GG690: 686. However, there was no significant difference in allelic or genotypic frequency distributions between patients and controls. We did not find any significant association between GRIK4 polymorphisms and schizophrenia.
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Results firstly indicated that rs56275759 of GRIK4 gene might be associated with major depressive disorder in Chinese Han population.
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This study showed the lower GluK4 mRNA levels in pregnant women.
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Data suggest the involvement of glutamate receptor, ionotropic, kainate 4 protein (GRIK4) in treatment-resistant depression (TRD) and in the risk of developing psychotic symptoms during depressive episodes.
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Subjects possessing the C allele or CC genotype of the GRIK4 polymorphism rs1954787 are more likely to respond to antidepressant treatment.
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The deletion allele affords protection against bipolar disorder through increased KA1 protein abundance in neuronal cells.
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Activation of kainate receptors could serve as a novel mechanism for enhancing B cell activation and immunoglobulin production.
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The GRIK4 single nucleotide polymorphism (rs12800734) shows a strong association with disease remission in antidepressant treatment.
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Cytogenetic and genetic findings provide molecular evidence for common etiologies for schizophrenia and and bipolar disorder and further support the 'glutamate hypothesis' of psychotic illness.
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An insertion/deletion (indel) variant in the 3' untranslated region (3'UTR) of the GRIK4 gene in subjects carrying the protective bipolar disorder haplotype was found.
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This report provides the first evidence that genetic variation in the GRIK4 gene modulates hippocampal function.