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RNA synthesis inhibition stabilises urokinase mRNA in macrophages
Author(s) -
Stacey Katryn J.,
Nagamine Yoshikuni,
Hume David A.
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)01294-6
Subject(s) - messenger rna , rna , urokinase , plasminogen activator , microbiology and biotechnology , chemistry , urokinase receptor , protein biosynthesis , biology , biochemistry , gene , endocrinology , genetics
Urokinase‐type plasminogen activator (uPA) mRNA is induced in macrophages by the lineage specific growth factor CSF‐1. Upon removal of CSF‐1 from bone marrow‐derived macrophages (BMM), uPA mRNA decayed with a half‐life of 2 h. If RNA synthesis inhibitors actinomycin D, 5,6‐dichloro‐1‐β‐ribofuranosyl benzimidazole (DRB) or α‐amanitin were added at the time as CSF‐1 removal, the uPA message was stabilised. This was not a general effect on CSF‐1 responsive mRNAs, as c‐ myc mRNA decayed with normal kinetics in the presence of inhibitors. The requirement for ongoing RNA synthesis for the degradation of uPA mRNA in BMM suggests that a component of the degradative pathway may be induced following removal of CSF‐1.