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Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology.
Mutations in the amyloid precursor protein (APP) gene cause early-onset familial Alzheimer disease (AD) by affecting the formation of the amyloid beta (A beta) peptide, the major constituent of ADExpand
Importance of AMPA receptors for hippocampal synaptic plasticity but not for spatial learning.
Gene-targeted mice lacking the L-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor subunit GluR-A exhibited normal development, life expectancy, and fine structure of neuronalExpand
A family of AMPA-selective glutamate receptors.
Four cloned cDNAs encoding 900-amino acid putative glutamate receptors with approximately 70 percent sequence identity were isolated from a rat brain cDNA library. In situ hybridization revealedExpand
RNA editing in brain controls a determinant of ion flow in glutamate-gated channels
L-glutamate, the principal excitatory transmitter in the brain, gates ion channels mediating fast neurotransmission. Subunit components of two related classes of glutamate receptor channels have beenExpand
Flip and flop: a cell-specific functional switch in glutamate-operated channels of the CNS.
In the central nervous system (CNS), the principal mediators of fast synaptic excitatory neurotransmission are L-glutamate-gated ion channels that are responsive to the glutamate agonistExpand
RNA editing of AMPA receptor subunit GluR-B: A base-paired intron-exon structure determines position and efficiency
A functionally critical position (Q/R site) of the AMPA receptor subunit GluR-B is controlled by RNA editing that operates in the nucleus, since in brain and clonal cell lines of neural origin,Expand
A glutamate receptor channel with high affinity for domoate and kainate.
The non‐NMDA family of glutamate receptors comprises a growing number of structurally related subunits (GluR‐A to ‐D or −1 to −4; GluR‐5, −6; KA‐1). GluR‐A to ‐D appear to constitute the major AMPAExpand
Destabilization of β-catenin by mutations in presenilin-1 potentiates neuronal apoptosis
Mutations of the presenilin-1 gene are a major cause of familial early-onset Alzheimer's disease. Presenilin-1 can associate with members of the catenin family of signalling proteins, but theExpand
Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid.
Transgenic mice that overexpress mutant human amyloid precursor protein (APP) exhibit one hallmark of Alzheimer's disease pathology, namely the extracellular deposition of amyloid plaques. Here, weExpand
The dopamine D2 receptor: two molecular forms generated by alternative splicing.
Cloned human dopamine D2 receptor cDNA was isolated from a pituitary cDNA library and found to encode an additional 29 amino acid residues in the predicted intracellular domain between transmembraneExpand
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