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Continuity between schizophrenia and schizotypy exists with regard to the psychological effects of allelic variation in LRRTM1, and epigenetic variation in the imprinted gene mediates the development and expression of human handedness.
Hypomethylation of the paternally inherited LRRTM1 promoter is linked to schizophrenia.
CTNNA1 (show CTNNA1 Proteins) and CTNNA2 (show CTNNA2 Proteins) contain alternative 5' exons linked to bidirectional promoters that are shared with the antisense oriented LRRTM2 (show LRRTM2 Proteins) and LRRTM1 genes, respectively.
16 SNPs in 12 genes showed significant interaction at P < .05, 3 of which survived correction for multiple testing (P < .0003), situated in AKT1 (show AKT1 Proteins) (rs2494732 and rs1130233) and LRRTM1 (rs673871).
LRRTM1 on chromosome 2p12 is a maternally suppressed gene that is associated paternally with handedness and schizophrenia.
Whether or not LRRTM1 on chromosome 2p12 is indeed the genetic basis of handedness is still unclear, although the controversy of the claim seems indisputable.
While we agree (and indeed first proposed) that the variation underlying psychosis is intrinsically related to the cerebral torque, which we take to be the anatomical basis of language, we are unconvinced by the data for LRRTM1.
Recent study in which the first putative genetic effect on human handedness was identified (the imprinted locus LRRTM1 on human chromosome 2).
Results strengthen the evidence for an association of imprinted alleles of LRRTM1 with schizophrenia. Weaker supportive evidence was also obtained for a possible association of LRTTM1 with human brain asymmetry.
Data indicate that neural Cell Adhesion Molecules Lrrtm1 and Lrrtm2 (show LRRTM2 Proteins) mRNA expression is controlled by synaptic activity and nuclear calcium signaling.
This study demonistrated that LRRTM1 is essential for maintenance of long-term potentiation in mice hippocampus.
LRRTM1-knockout mice exhibit an extraordinary phenotype of avoiding small enclosures.
Lrrtm1 knockout mice were characterized behaviorally and morphologically.
The LRRTM1 acts redundantly to maintain excitatory synapses and that synapse elimination caused by the absence of LRRTM1 is promoted by synaptic activity and mediated by a postsynaptic Ca(2+)/CaM-dependent signaling pathway.
May play a role during the development of specific forebrain structures by influencing neuronal differentiation and connectivity, with a possible role in intracellular trafficking within axons (By similarity).
leucine-rich repeat transmembrane neuronal protein 1
, leucine-rich repeat transmembrane neuronal 1 protein
, leucine-rich repeat transmembrane neuronal 1