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RISS 인기검색어
- 검색키워드
- 저자 : LANFORD, G. W. (검색결과 2 건)
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GLUTAMATE-INDUCED δ-CATENIN REDISTRIBUTION AND DISSOCIATION FRON POSTSYNAPTIC RECEPTOR COMPLEXES
JONES, S. B.,LANFORD, G. W.,CHEN, Y.-H.,MORIBITO, M.,KIM, K.,Lu, Q. 전남대학교 약품개발연구소 2002 약품개발연구지 Vol.11 No.-
δ-Catenin (or neural plakophilin-related arm-repeat protein/neurojngin) is primarily a brain specific member of the p120^ctm subfamily of armadillo/β-catenin proteins that play important roles in neuronal development. Our previous studies have shown that the ectopic expression of δ-catenin induces the formation of dendrite-like extension and that the overexpresssion of δ-catenin promotes dendritic branching and increases spine density. Here we demonstrate that δ-catenin displays a dendritic distribution pattern in the adult mouse brain and is co-enriched with postsynaptic density-95 (PSD-95) in the detergent insoluble postsynaptic scaffolds. δ-Catenin forms stable complexes with excitatory neurotransmitter receptors including ionotropic N-methyl-D-aspartic acid receptor 2A (NR2A), metabotropic glutamate receptor 1α (mGluR1α), as well as PSD-95 in vivo. In cultured primary embryonic neurons, δ-catenin clusters co-distribute with filamentous actin and resist detergent extraction. In dissociated hippocampal neurons overexpressing δ-catenin, glutamate stimulation leads to a rapid redistribution of δ-catenin that can be attenuated by 6-cyano-7-nitroquinoxaline-2,3-dione and dizocilpine, selective inhibitors of ionotropic glutamate receptors. Upon glutamate receptor activation, δ-catenin becomes down-regulated and its association with NR2A and mGluR1α in cultured neurons is diminished. These findings support a possible functional connection between δ-catenin and the glutamatergic excitatory synaptic signaling pathway during neuronal development.
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Dendrite-like Process Formation and Cytoskeletal Remodeling Regulated by δ-Catenin expression
Kim, Kwonseop,Sirota, Anna,Chen, Yan-hua,Jones, Shiloh B.,Dudek, Ronald,Lanford, George W.,Thakore, Chittam,Lu, Qun 전남대학교 약품개발연구소 2002 약품개발연구지 Vol.11 No.-
Actin- and microtubule-mediated changes in cell shape are essential for many cellular activities. However, the molecular mechanisms underlying the interplay between the two are complex and remain obscure. Here we show that the expression of δ-catenin (or NPRAP/Neurojungin), a member of p120^ctm subfamily of armadillo proteins can induce the branching of dendrite-like processes in 3T3 cells and enhance dendritic morphogenesis in primary hippocampal neurons. This induction of branching phenotype involves initially the disruption of filamentous actin, and requires the growth of microtubules. The carboxyl-terminal truncation mutant of δ-catenin can cluster and redistribute the full-length protein, and dominantly inhibit its branching effect. δ-Catenin forms protein complexes and can bind directly to actin in vitro. The carboxyl-terminal truncation of δ-catenin does not interfere with its actin-binding capability; therefore the actin interaction alone is not sufficient for the induction of dendrite-like processes. When δ-catenin-transformed cells establish elaborate dendrite-like branches, the main cellular processes become stabilized and resist the disruption od both actin filaments and microscopy and time-lapse recording analyses. We suggest that δ-catenin can effect a biphasic cytoskeletal remodeling event which differentially regulates actin and microtubules and promotes cellular morphogenesis.
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