Abstract

A functional mooring sequence, known to be required for apolipoprotein B (apoB) mRNA editing, exists in the mRNA encoding the neurofibromatosis type I (NF1) tumor suppressor. Editing of NF1 mRNA modifies cytidine in an arginine codon (CGA) at nucleotide 2914 to a uridine (UGA), creating an in frame translation stop codon. NF1 editing occurs in normal tissue but was several-fold higher in tumors. In vitro editing and transfection assays demonstrated that apoB and NF1 RNA editing will take place in both neural tumor and hepatoma cells. Unlike apoB, NF1 editing did not demonstrate dependence on rate-limiting quantities of APOBEC-1 (the apoB editing catalytic subunit) suggesting that different trans-acting factors may be involved in the two editing processes.

Publication Date

2-1-1996

Comments

Article may be found at: http://nar.oxfordjournals.org/cgi/content/abstract/24/3/478 This work was supported in part by grants from the NIH (CA55173) and from Cancer Action, Inc. (to G.R.S.) and by the NIH (DK43739) and The Council for Tobacco Research (to H.C.S.). M.S. is supported through an American Heart Association (NY state affiliate) fellowship. L.J.M. and A.J.C. are supported in part by a predoctoral award from the Interdepartmental Training Grant in Genetics and Regulation (GM07102).ISSN:1362-4962 Note: imported from RIT’s Digital Media Library running on DSpace to RIT Scholar Works in February 2014.

Document Type

Article

Department, Program, or Center

Thomas H. Gosnell School of Life Sciences (COS)

Campus

RIT – Main Campus

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