FAM150A and FAM150B are activating ligands for anaplastic lymphoma kinase

被引：116

作者：

Guan, Jikui ^{[1
]}

Umapathy, Ganesh ^{[1
]}

Yamazaki, Yasuo ^{[1
]}

Wolfstetter, Georg ^{[1
]}

Mendoza, Patricia ^{[1
]}

Pfeifer, Kathrin ^{[1
]}

Mohammed, Ateequrrahman ^{[1
]}

Hugosson, Fredrik ^{[1
]}

Zhang, Hongbing ^{[2
]}

Hsu, Amy W. ^{[2
]}

Halenbeck, Robert ^{[2
]}

Hallberg, Bengt ^{[1
]}

Palmer, Ruth H. ^{[1
]}

机构：

[1] Univ Gothenburg, Sahlgrenska Acad, Dept Med Biochem & Cell Biol, Inst Biomed, Gothenburg, Sweden

[2] Five Prime Therapeut Inc, San Francisco, CA USA

来源：

ELIFE | 2015年 / 4卷

关键词：

RECEPTOR TYROSINE KINASE; MONOCLONAL-ANTIBODIES; GROWTH-FACTOR; ALK KINASE; NEUROBLASTOMA; MUTATIONS; PLEIOTROPHIN; GENE; EXPRESSION; PROTEIN;

D O I：

10.7554/eLife.09811

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Aberrant activation of anaplastic lymphoma kinase (ALK) has been described in a range of human cancers, including non-small cell lung cancer and neuroblastoma (Hallberg and Palmer, 2013). Vertebrate ALK has been considered to be an orphan receptor and the identity of the ALK ligand(s) is a critical issue. Here we show that FAM150A and FAM150B are potent ligands for human ALK that bind to the extracellular domain of ALK and in addition to activation of wild-type ALK are able to drive 'superactivation' of activated ALK mutants from neuroblastoma. In conclusion, our data show that ALK is robustly activated by the FAM150A/B ligands and provide an opportunity to develop ALK-targeted therapies in situations where ALK is overexpressed/activated or mutated in the context of the full length receptor.

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页数：16

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