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The Nrxn1beta-LRRTM2 interface involves Ca(2+)-mediated interactions and overlaps with the Nrxn-neuroligin interface.
CTNNA1 and CTNNA2 contain alternative 5' exons linked to bidirectional promoters that are shared with the antisense oriented LRRTM2 and LRRTM1 genes, respectively.
Genetic deletion of LRRTM1,2 in vivo in CA1 neurons using Cre recombinase-expressing lentiviruses dramatically impaired long-term potentiation (LTP), an impairment that was rescued by simultaneous expression of LRRTM2, but not LRRTM4.
The crystal structure of a thermostabilized LRRTM2 protein was determined.
Data indicate that neural Cell Adhesion Molecules Lrrtm1 and Lrrtm2 mRNA expression is controlled by synaptic activity and nuclear calcium signaling.
This study demonistrated that LRRTM2 is essential for maintenance of long-term potentiation in mice hippocampus.
The LRRTM2 acts redundantly to maintain excitatory synapses and that synapse elimination caused by the absence of LRRTM2 is promoted by synaptic activity and mediated by a postsynaptic Ca(2+)/CaM-dependent signaling pathway.
Involved in the development and maintenance of excitatory synapse in the vertebrate nervous system. Regulates surface expression of AMPA receptors. Acts as a ligand for the presynaptic receptors NRXN1-A and NRXN1-B.
leucine rich repeat transmembrane neuronal 2
, leucine-rich repeat neuronal 2 protein
, leucine-rich repeat transmembrane neuronal 2 protein
, leucine-rich repeat transmembrane neuronal protein 2