The RNA binding protein Larp1 regulates cell division, apoptosis and cell migration

Burrows, C. et al. (2010) The RNA binding protein Larp1 regulates cell division, apoptosis and cell migration. Nucleic Acids Research, 38(16), pp. 5542-5553. (doi:10.1093/nar/gkq294) (PMID:20430826) (PMCID:PMC2938220)

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Abstract

The RNA binding protein Larp1 was originally shown to be involved in spermatogenesis, embryogenesis and cell-cycle progression in Drosophila. Our data show that mammalian Larp1 is found in a complex with poly A binding protein and eukaryote initiation factor 4E and is associated with 60S and 80S ribosomal subunits. A reduction in Larp1 expression by siRNA inhibits global protein synthesis rates and results in mitotic arrest and delayed cell migration. Consistent with these data we show that Larp1 protein is present at the leading edge of migrating cells and interacts directly with cytoskeletal components. Taken together, these data suggest a role for Larp1 in facilitating the synthesis of proteins required for cellular remodelling and migration.

Item Type:Articles
Additional Information:Funding: Biotechnology and Biological Sciences Research Council (BBSRC) (to K.S. studentship, to A.E.W. Professorial Fellowship); Cancer Research UK (to D.M.G.); Wellbeing of Women (to S.-J.L. Entry Level Scholarship) and Experimental Cancer Medicine Centre (ECMC) (to C.B.). Funding for open access charge: Charitable research fund.
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Bushell, Professor Martin
Authors: Burrows, C., Abd Latip, N., Lam, S.-J., Carpenter, L., Sawicka, K., Tzolovsky, G., Gabra, H., Bushell, M., Glover, D. M., Willis, A. E., and Blagden, S. P.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cancer Sciences
Journal Name:Nucleic Acids Research
Publisher:Oxford University Press
ISSN:0305-1048
ISSN (Online):1362-4962
Published Online:29 April 2010
Copyright Holders:Copyright © The Authors 2010
First Published:First published in Nucleic Acids Research 38(16):5542-5553
Publisher Policy:Reproduced under a Creative Commons license

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