Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, Manchester, M13 9PT, UK.
Human Physiology, College of Health, Massey University, North Shore, Auckland, 0630, New Zealand.
Mol Cell Biochem. 2018 Jul;444(1-2):1-13. doi: 10.1007/s11010-017-3222-7. Epub 2017 Nov 20.
The JNK-interacting protein 3 (JIP3) is a molecular scaffold, expressed predominantly in neurons, that serves to coordinate the activation of the c-Jun N-terminal kinase (JNK) by binding to JNK and the upstream kinases involved in its activation. The JNK pathway is involved in the regulation of many cellular processes including the control of cell survival, cell death and differentiation. JIP3 also associates with microtubule motor proteins such as kinesin and dynein and is likely an adapter protein involved in the tethering of vesicular cargoes to the motors involved in axonal transport in neurons. We have used immunofluorescence microscopy and biochemical fractionation to investigate the subcellular distribution of JIP3 in relation to JNK and to vesicular and organelle markers in rat pheochromocytoma cells (PC12) differentiating in response to nerve growth factor. In differentiated PC12 cells, JIP3 was seen to accumulate in growth cones at the tips of developing neurites where it co-localised with both JNK and the JNK substrate paxillin. Cellular fractionation of PC12 cells showed that JIP3 was associated with a subpopulation of vesicles in the microsomal fraction, distinct from synaptic vesicles, likely to be an anterograde-directed exocytic vesicle pool. In differentiated PC12 cells, JIP3 did not appear to associate with retrograde endosomal vesicles thought to be involved in signalling axonal injury. Together, these observations indicate that JIP3 may be involved in transporting vesicular cargoes to the growth cones of PC12 cells, possibly targeting JNK to its substrate paxillin, and thus facilitating neurite outgrowth.
JNK 相互作用蛋白 3(JIP3)是一种分子支架,主要在神经元中表达,通过与 JNK 及其上游激活激酶结合,协调 c-Jun N 端激酶(JNK)的激活。JNK 途径参与许多细胞过程的调节,包括细胞存活、细胞死亡和分化的控制。JIP3 还与微管马达蛋白如驱动蛋白和动力蛋白结合,可能是一种衔接蛋白,参与将囊泡货物与神经元轴突运输中涉及的马达连接。我们使用免疫荧光显微镜和生化分级分离技术,研究了 JIP3 与 JNK 以及囊泡和细胞器标记物在对神经生长因子有反应的大鼠嗜铬细胞瘤细胞(PC12)分化过程中的亚细胞分布。在分化的 PC12 细胞中,JIP3 被发现在发育中的神经突尖端的生长锥中积累,与 JNK 和 JNK 底物桩蛋白共定位。PC12 细胞的细胞分级分离显示,JIP3 与微粒体部分中的囊泡亚群相关,与突触囊泡不同,可能是正向分泌的囊泡池。在分化的 PC12 细胞中,JIP3 似乎不与被认为参与信号转导轴突损伤的逆行内体囊泡相关。总之,这些观察结果表明,JIP3 可能参与将囊泡货物运输到 PC12 细胞的生长锥,可能将 JNK 靶向其底物桩蛋白,从而促进神经突生长。