期刊
NATURE
卷 519, 期 7541, 页码 57-U107出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nature14228
关键词
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资金
- Japan Society for the Promotion of Science
- Uehara Memorial Foundation Fellowship
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Kanae Foundation for the Promotion of Medical Science
- National Science Council of Taiwan [NSC-101-2918-I-006-005, NSC-103-2320-B-006-032]
- NIH [R00DK088589, EY022611, CA132809, CA118165-09]
- FCCC-Temple University Nodal grant
- AACR-Landon Innovator Award in Tumor Microenvironment
- Pew Scholar in Biomedical Sciences Program
- CCFA [RFA2927]
- Croucher Foundation
- China Postdoctoral Science Foundation
- Research Service of the Department of Veterans Affairs
- UCSD Digestive Disease Research Center
- Grants-in-Aid for Scientific Research [24390321, 25670234] Funding Source: KAKEN
Inflammation promotes regeneration of injured tissues through poorly understood mechanisms, some of which involve interleukin (IL)-6 family members, the expression of which is elevated in many diseases including inflammatory bowel diseases and colorectal cancer. Here we show in mice and human cells that 0130, a co-receptor for IL-6 cytokines, triggers activation of YAP and Notch, transcriptional regulators that control tissue growth and regeneration, independently of the gp130 effector STAT3. Through YAP and Notch, intestinal gp130 signalling stimulates epithelial cell proliferation, causes aberrant differentiation and confers resistance to mucosal erosion. gp130 associates with the related tyrosine kinases Src and Yes, which are activated on receptor engagement to phosphorylate YAP and induce its stabilization and nuclear translocation. This signalling module is strongly activated upon mucosal injury to promote healing and maintain barrier function.
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