PDZ-scaffold protein, Tamalin promotes dendritic outgrowth and arborization in rat hippocampal neuron
- Authors
- Mo, Jiwon; Choi, Sukwoo; Ahn, Poong Gi; Sun, Woong; Lee, Hyun Woo; Kim, Hyun
- Issue Date
- 1-6월-2012
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Tamalin; Dendritic development; EFA6A; Arf6; F-actin; MAP2
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.422, no.2, pp.250 - 255
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 422
- Number
- 2
- Start Page
- 250
- End Page
- 255
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/108181
- DOI
- 10.1016/j.bbrc.2012.04.136
- ISSN
- 0006-291X
- Abstract
- Tamalin is a scaffold protein known to regulate membrane trafficking through its interaction with cytohesin-2/ARNO, guanine nucleotide exchange factor (GEF) on ADP-ribosylation factor (Arf) 1/6, and induces actin reorganization. However, the neuronal function of Tamalin is not well understood. Here, we report that Tamalin participates in neurite development through the association with exchange factor for Arf6 (EFA6A)/Arf6 signaling. In immature hippocampal neuron, Tamalin knockdown markedly reduced the dendritic outgrowth, the number of dendritic tips and the levels of filamentous actin (F-actin) and microtubule-associated protein 2 (MAP2) in dendrites. In addition, Tamalin colocalized with EFA6A and Arf6 in the dendritic shaft. Tamalin knockdown reduced the number, size, and intensity of endogenous EFA6A cluster, whereas overexpression of Tamalin showed opposite effects compared with those of knockdown. These results suggest that Tamalin is responsible for neuronal dendritic development via regulation of EFA6A/Arf6-mediated cytoskeleton dynamics. (C) 2012 Elsevier Inc. All rights reserved.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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