The Noncanonical Role of ULK/ATG1 in ER-to-Golgi Trafficking Is Essential for Cellular Homeostasis
详细信息 查看全文
- 作者：Joung Hyuck Joo1 ; 13 ; Bo Wang1 ; 2 ; 13 ; Elisa Frankel3 ; Liang Ge4 ; Lu Xu5 ; Rekha Iyengar1 ; XiuJie Li-Harms1 ; Christopher Wright1 ; Timothy I. Shaw6 ; 7 ; Tullia Lindsten8 ; Douglas R. Green9 ; Junmin Peng6 ; 10 ; Linda M. Hendershot11 ; Fusun Kilic12 ; Ji Ying Sze5 ; Anjon Audhya3 ; Mondira Kundu1 ; mondira.kundu@stjude.org" class="auth_mail" title="E-mail the corresponding author
- 刊名：Molecular Cell
- 出版年：2016
- 出版时间：19 May 2016
- 年：2016
- 卷：62
- 期：4
- 页码：491-506
- 全文大小：6342 K
文摘
- •
ULK1 and ULK2 mediate phosphorylation of the COPII scaffold protein SEC16A at S846
- •
ULKs (not ATG13) regulate SEC16A-dependent ER-to-Golgi trafficking of specific cargo
- •
ULK1/2 deficiency causes ER stress and selective loss of hippocampal neurons.
- •
Restoring ER-to-Golgi trafficking in ULK-deficient cells quells the ER stress response