LRRTM1 leucine rich repeat transmembrane neuronal 1 [ (human)]. Gene ID: , updated on 7-Dec This gene is imprinted, being predominantly expressed from the paternal allele and showing a variable pattern of maternal down-regulation. May be associated . Leucine-rich repeat transmembrane neuronal protein 1. Gene. Lrrtm1. Organism. Mus musculus (Mouse). Status. Reviewed-Annotation score: Annotation.
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The Journal of Neuroscience.
LRRTM1 expression is downregulated maternally in humans. You can help Wikipedia by expanding it. Lay summary — BBC News. Developmental Gene Expression 7. When comparing expression between human and mouse, it seems that there is a striking absence of signal in caudate and putamen in mouse, at least at e15 and in adult.
Leucine-rich repeat transmembrane neuronal protein 1
LRRTM1 is not localized on the plasma membrane. Supplementary Figure S6 lrrtm1 1,K Click here to view. March 6, Last modified: Lack of this gene shows decreased performance in complex visual tasks.
UCSC genome browser More A ruler that provides location information. Replication validity of genetic association studies. Mice homozygous for a knock-out allele exhibit impaired cognitive function and altered hippocampal synapse morphology.
We also showed that LRRTM1 is expressed during the development of specific forebrain structures, and thus could influence neuronal differentiation and connectivity.
Since LRRTM1 appears to underlie the strongest linkage to schizophrenia in the genome, as identified by a meta-analysis of 20 genomewide linkage scans, 16 it is possible that LRRTM1 dysfunction causes a major, common subtype of schizophrenia. LRRTM1, leucine rich repeat transmembrane neuronal 1.
In the present study we have used genetic association mapping and gene-functional analysis to identify a novel imprinted gene on 2p12, LRRTM1, that we propose is responsible for causing the linkages of this chromosomal region to human handedness and schizophrenia.
Discussion Crow proposed that handedness, brain asymmetry and schizophrenia share an underlying genetic relationship. OMIM is intended for use primarily by physicians and other professionals concerned with genetic disorders, by genetics researchers, and by advanced students in science and medicine. Views Read Edit View history.
Q86UE6 Secondary accession number s: There was no significant paternal overtransmission of any other haplotype, nor was there maternal overtransmission of any haplotype.
Our data suggest that a subtype of schizophrenia, linked to misregulation of human LRRTM1, may have its origins in fetal neurodevelopment. PaxDb, a database of protein abundance averages across all three domains of life More Left—right asymmetrical function is a conserved feature of vertebrate central nervous systems.
Epigenetic heterogeneity at imprinted loci in normal populations. Highest levels were reached at postnatal day 1 and persisted into adulthood.
The molecular, developmental and evolutionary origins of human brain asymmetry are unknown. Conflicting reports of imprinting status of human GRB10 in developing brain: EMBL nucleotide sequence database More Pedigree tests of transmission disequilibrium.
Q86UE6 baseline and differential.
OMIM Entry – * – LEUCINE-RICH REPEAT TRANSMEMBRANE PROTEIN 1: LRRTM1
Localized morphological brain differences between English-speaking Caucasians and Chinese-speaking Asians: We genotyped the SNPs rs and either rs or rs the latter are equivalent tagging SNPs according to international HapMap data in four family samples of lrrtk1 European descent that included individuals with schizophrenia or poor-outcome schizoaffective disorder. Supplementary Information doc 86K Click here to view.
Genomewide scan in families with schizophrenia from the founder population of Afrikaners reveals evidence for linkage and uniparental disomy on chromosome 1.