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. 2015 Mar 2;208(5):613–627. doi: 10.1083/jcb.201408026

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© 2015 Chung et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 8. — A model depicting the significance of K17- and hnRNP K–dependent expression of CXCR3 ligands. K17 binds to hnRNP K and is required for its cytoplasmic localization. hnRNP K binds to and regulates mRNA transcripts for the CXCR3 ligands CXCL9, CXCL10, and CXCL11 in a K17-dependent manner. The K17–hnRNP K interaction and expression of CXCR3 ligands are both regulated by RSK activity. CXCR3 ligand secretion and CXCR3 signaling are required for K17- and hnRNP K–dependent enhancement of tumor cell growth and invasion.