RNA synthesis inhibition stabilises urokinase mRNA in macrophages

K J Stacey, Y Nagamine, D A Hume

Research output: Contribution to journalArticlepeer-review

Abstract

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-beta-ribofuranosyl benzimidazole (DRB) or alpha-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.
Original languageEnglish
Pages (from-to)311-3
Number of pages3
JournalFEBS Letters
Volume356
Issue number2-3
Publication statusPublished - 19 Dec 1994

Keywords

  • Amanitins
  • Animals
  • Base Sequence
  • Bone Marrow
  • Cell Differentiation
  • Dactinomycin
  • Dichlororibofuranosylbenzimidazole
  • Enzyme Induction
  • Humans
  • Kinetics
  • Macrophage Colony-Stimulating Factor
  • Macrophages
  • Mice
  • Mice, Inbred BALB C
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides
  • RNA
  • RNA, Messenger
  • Recombinant Proteins
  • Urokinase-Type Plasminogen Activator

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