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Cell Signal. 2019 Mar;55:100-108. doi: 10.1016/j.cellsig.2019.01.003. Epub 2019 Jan 9.

SGTb regulates a surface localization of a guidance receptor BOC to promote neurite outgrowth.

Author information

1
Department of Molecular Cell Biology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea.
2
Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women's University, Seoul 04310, Republic of Korea.
3
Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women's University, Seoul 04310, Republic of Korea. Electronic address: gbae@sookmyung.ac.kr.
4
Department of Molecular Cell Biology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea; Samsung Biomedical Research Institute, Samsung Medical Center, Seoul, Republic of Korea. Electronic address: kangj01@skku.edu.

Abstract

Neuritogenesis is a critical event for neuronal differentiation and neuronal circuitry formation during neuronal development and regeneration. Our previous study revealed a critical role of a guidance receptor BOC in a neuronal differentiation and neurite outgrowth. However, regulatory mechanisms for BOC signaling pathway remain largely unexplored. In the current study, we have identified Small glutamine-rich tetratricopeptide repeat (TPR)-containing b (SGTb) as a BOC interacting protein through yeast two-hybrid screening. Like BOC, SGTb is highly expressed in brain and P19 embryonal carcinoma (EC) cells differentiated into neuronal cells. BOC and SGTb proteins co-precipitate in mouse brain and differentiated P19 EC cells. Furthermore, BOC and SGTb co-localize in neurites and especially are concentrated at the tip of neurites in various neuronal cells. SGTb depletion attenuates neuronal differentiation of P19 cells through reduction of the surface level of BOC. Additionally, SGTb depletion causes BOC localization at neurite tip, coinciding with decreased p-JNK levels critical for actin cytoskeleton remodeling. The overexpression of SGTb or BOC restores JNK activation in BOC or SGTb-depleted cells, respectively. Finally, SGTb elevates the level of surface-resident BOC in BOC-depleted cells, restoring JNK activation. Taken together, our data suggest that SGTb interacts with BOC and regulates its surface level and consequent JNK activation, thereby promoting neuronal differentiation and neurite outgrowth.

KEYWORDS:

BOC; JNK; Neurite outgrowth; Neuronal differentiation; SGTb; Surface localization

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