کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8478535 | 1551138 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
ZDHHC17 promotes axon outgrowth by regulating TrkA-tubulin complex formation
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کلمات کلیدی
DPFNSCDHHChpftrkAJnkSMNERK1/2 - ERK1 / 2MAPK - MAPKtubulin - توبولینTyrosine kinase - تیروزین کینازAxon outgrowth - رشد آکسونdays post-fertilization - روز پس از لقاحhours post-fertilization - ساعت پس از لقاحNeural stem cell - سلول های بنیادی عصبیSpinal motor neuron - نورون حرکتی نخاعیpat - پاتPalmitoyltransferase - پالمیتویل ترانسفرازmitogen-activated protein kinase - پروتئین کیناز فعال با mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Correct axonal growth during nervous system development is critical for synaptic transduction and nervous system function. Proper axon outgrowth relies on a suitable growing environment and the expression of a series of endogenous neuronal factors. However, the mechanisms of these neuronal proteins involved in neuronal development remain unknown. ZDHHC17 is a member of the DHHC (Asp-His-His-Cys)-containing family, a family of highly homologous proteins. Here, we show that loss of function of ZDHHC17 in zebrafish leads to motor dysfunction in 3-day post-fertilization (dpf) larvae. We performed immunolabeling analysis to reveal that mobility dysfunction was due to a significant defect in the axonal outgrowth of spinal motor neurons (SMNs) without affecting neuron generation. In addition, we found a similar phenotype in zdhhc17 siRNA-treated neural stem cells (NSCs) and PC12 cells. Inhibition of zdhhc17 limited neurite outgrowth and branching in both NSCs and PC12. Furthermore, we discovered that the level of phosphorylation of extracellular-regulated kinase (ERK) 1/2, a major downstream effector of tyrosine kinase (TrkA), was largely upregulated in ZDHHC17 overexpressing PC12 cells by a mechanism independent on its palmitoyltransferase (PAT) activity. Specifically, ZDHHC17 is necessary for proper TrkA-tubulin module formation in PC12 cells. These results strongly indicate that ZDHHC17 is essential for correct axon outgrowth in vivo and in vitro. Our findings identify ZDHHC17 as an important upstream factor of ERK1/2 to regulate the interaction between TrkA and tubulin during neuronal development.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 68, September 2015, Pages 194-202
Journal: Molecular and Cellular Neuroscience - Volume 68, September 2015, Pages 194-202
نویسندگان
Wei Shi, Fen Wang, Ming Gao, Yang Yang, Zhaoxia Du, Chen Wang, Yao Yao, Kun He, Xueran Chen, Aijun Hao,