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FAM150A and FAM150B are activating ligands for Anaplastic Lymphoma Kinase.

Journal article
Authors Jikui Guan
Ganesh Umapathy
Yasuo Yamazaki
Georg Wolfstetter
Patricia Mendoza
Kathrin Pfeifer
Ateequrrahman Mohammed
Fredrik Hugosson
Hongbing Zhang
Amy W Hsu
Robert Halenbeck
Bengt Hallberg
Ruth H. Palmer
Published in eLife
Pages article no. e09811
ISSN 2050-084X
Publication year 2015
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages article no. e09811
Language en
Links dx.doi.org/10.7554/eLife.09811
Subject categories Biological Sciences, Molecular biology, Molecular biology, Cell Biology, Developmental Biology

Abstract

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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