FAM150A and FAM150B are activating ligands for anaplastic lymphoma kinase.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 26418745.
- Also identified by DOI 10.7554/eLife.09811 and PMC identifier 4658194.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Cytokines
- Enzyme Activation
- Receptor Protein-Tyrosine Kinases