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LRRTM3 polymorphisms may play a role in the pathogenesis of late-onset Alzheimer's disease (LOAD) in a Northern Han Chinese population.
protein interactions between LRRTM3, APP (show APP Antibodies) and BACE1 (show BACE Antibodies), as well as complex associations between mRNA levels of LRRTM3, CTNNA3 (show CTNNA3 Antibodies), APP (show APP Antibodies) and BACE1 (show BACE Antibodies) in humans might influence APP (show APP Antibodies) metabolism and ultimately risk of AD
LRRTM3 is not an essential regulator of amyloid-beta production in adult mice; there are no differences in genotype between levels of Abeta (show APP Antibodies) or Abeta (show APP Antibodies) protein precursor C-terminal fragments in vivo.
Apart from the complexity of its regulation, alterations in both CTNNA3 (show CTNNA3 Antibodies) and LRTMM3 are implicated in human disease.
Data suggest that LRRTM3 is a functional and positional candidate gene for Alzheimer disease, and, given its receptor-like structure and restricted expression, a potential therapeutic target.
An ancestral risk haplotype clade in ACE (show ACE Antibodies) and putative multilocus association between ACE (show ACE Antibodies), A2M (show A2M Antibodies), and LRRTM3 in Alzheimer disease.
LRRTM3 is required for dentate gyrus excitatory synapse development and regulates activity-dependent AMPAR surface expression.
May play a role in the development and maintenance of the vertebrate nervous system.
leucine rich repeat transmembrane neuronal 3
, leucine-rich repeat transmembrane neuronal protein 3