期刊
GENES & DEVELOPMENT
卷 18, 期 13, 页码 1533-1538出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1199104
关键词
LKB1; TSC2; Peutz-Jeghers syndrome; tuberous sclerosis complex; mTOR; AMPK
资金
- NICHD NIH HHS [5-T32-HD075005, R21 HD075005] Funding Source: Medline
- NIDDK NIH HHS [R01 DK124709] Funding Source: Medline
Tuberous sclerosis complex (TSC) and Peutz-Jeghers syndrome (PJS) are dominantly inherited benign tumor syndromes that share striking histopathological similarities. Here we show that LKB1, the gene mutated in PJS, acts as a tumor suppressor by activating TSC2, the gene mutated in TSC. Like TSC2, LKB1 inhibits the phosphorylation of the key translational regulators S6K and 4EBP1. Furthermore, we show that LKB1 activates TSC2 through the AMP-dependent protein kinase (AMPK), indicating that LRB1 plays a role in cell growth regulation in response to cellular energy levels. Our results suggest that PJS and other benign tumor syndromes could be caused by dysregulation of the TSC2/mTOR pathway.
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