期刊
MOLECULAR & CELLULAR ONCOLOGY
卷 5, 期 3, 页码 -出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/23723556.2018.1458015
关键词
beta-catenin; AXIN1; PGAM5; mitochondria; Wnt signaling
类别
资金
- Friedrich-Alexander University of Erlangen-Nuremberg Interdisciplinary Center for Clinical Research
- Johannes und Frieda Marohn-Stiftung
Cellular abundance of mitochondria is dynamically regulated. We could recently show that dysfunctional mitochondria release the phosphatase PGAM family member 5 (PGAM5) into the cytosol, where it interacts with the Wnt signaling-component AXIN1 and dephosphorylates AXIN1 -bound /J-catenin (CTNNB1) thereby activating Wnt/beta-catenin signaling. Because Wnt/beta-catenin signaling induces mitochondrial biogenesis dysfunctional mitochondria trigger their own replacement by releasing PGAM5.
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