Amyloid precursor like protein-1 promotes JNK-mediated cell migration in Drosophila
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Xingjun Wang1,*, Ying Sun1,*, Shilong Han1, Chenxi Wu2, Yeqing Ma1, Yu Zhao1, Yingyao Shao1, Yujun Chen1, Lingzhi Kong3, Wenzhe Li1, Fan Zhang3 and Lei Xue1
1Department of Interventional Radiology, Shanghai 10th People’s Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai 200092, China
2College of Chinese Medicine, North China University of Science and Technology, Tangshan 063210, China
3Clinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, China
*These authors have contributed equally to this work
Xingjun Wang, email: firstname.lastname@example.org
Lei Xue, email: email@example.com
Keywords: APLP1, cell migration, Drosophila, JNK
Received: May 18, 2015 Accepted: April 20, 2017 Published: May 08, 2017
The amyloid precursor like protein-1 (APLP1) is a member of the amyloid precursor protein (APP) family in mammals. While many studies have been focused on the pathologic role of APP in Alzheimer’s disease, the physiological functions of APLP1 have remained largely elusive. Here we report that ectopic expression of APLP1 in Drosophila induces cell migration, which is suppressed by the loss of JNK signaling and enhanced by the gain of JNK signaling. APLP1 activates JNK signaling through phosphorylation of JNK, which up-regulates the expression of matrix metalloproteinase MMP1 required for basement membranes degradation and promotes actin remodeling essential for cell migration. Our data thus provide the first in vivo evidence for a cell-autonomous role of APLP1 protein in migration.
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