Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 4087K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jang, C. Articles by Chung, J. Search for Related Content PubMed PubMed Citation Articles by Jang, C. Articles by Chung, J. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH Hazardous Substances DB LACTIC ACID Related Collections Related Article Social Bookmarking                            What's this?

LKB1 induces apical trafficking of Silnoon, a monocarboxylate transporter, in Drosophila melanogaster

¹ National Creative Research Initiatives Center for Cell Growth Regulation and ² Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Yusong-gu, Taejon 305-701, Korea

Correspondence to Jongkyeong Chung: jchung{at}kaist.ac.kr

Silnoon (Sln) is a monocarboxylate transporter (MCT) that mediates active transport of metabolic monocarboxylates such as butyrate and lactate. Here, we identify Sln as a novel LKB1-interacting protein using Drosophila melanogaster genetic modifier screening. Sln expression does not affect cell cycle progression or cell size but specifically enhances LKB1-dependent apoptosis and tissue size reduction. Conversely, down-regulation of Sln suppresses LKB1-dependent apoptosis, implicating Sln as a downstream mediator of LKB1. The kinase activity of LKB1 induces apical trafficking of Sln in polarized cells, and LKB1-dependent Sln trafficking is crucial for triggering apoptosis induced by extracellular butyrate. Given that LKB1 functions to control both epithelial polarity and cell death, we propose Sln is an important downstream target of LKB1.

© 2008 Jang 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.jcb.org/misc/terms.shtml). 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/).

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

Related Article

Novel role for the LKB1 pathway in controlling monocarboxylate fuel transporters

Beatrice Maria Filippi and Dario R. Alessi
J. Cell Biol. 2008 183: 7-9. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

• Jansen, M., ten Klooster, J. P., Offerhaus, G. J., Clevers, H. (2009). LKB1 and AMPK Family Signaling: The Intimate Link Between Cell Polarity and Energy Metabolism. Physiol. Rev. 89: 777-798 [Abstract] [Full Text]  
• Filippi, B. M., Alessi, D. R. (2008). Novel role for the LKB1 pathway in controlling monocarboxylate fuel transporters. JCB 183: 7-9 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents