Open AccessInduction of a 26‐kDa‐protein mRNA in human cells treated with an interleukin‐1‐related, leukocyte‐derived factor
Author(s) -
CONTENT Jean,
WIT Lucas,
POUPART Pascale,
OPDENAKKER Ghislain,
DAMME Jo,
BILLIAU Alfons
Publication year - 1985
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1985.tb09191.x
Subject(s) - cycloheximide , messenger rna , microbiology and biotechnology , biology , protein biosynthesis , interferon , effector , inducer , beta (programming language) , gene expression , cytokine , gene , immunology , biochemistry , computer science , programming language
A human‐leukocyte‐derived antiviral protein (22‐kDa factor), known to be an inducer of interferon‐β (IFN‐β) in fibroblastoid cells, and to be closely related to interleukin‐1 (IL‐1), was shown to likewise act as inducer of the mRNA of a 26‐kDa secreted protein. This protein was first described as the gene product of an mRNA that is co‐induced with the mRNA of IFN‐β by superinduction of fibroblasts (treatment with dsRNA and cycloheximide). Subsequently it was shown to be induced by treatment with cycloheximide only. The 22‐kDa factor induced high levels of the 26‐kDa‐protein mRNA and low levels of IFN‐β mRNA. Addition of cycloheximide to the 22‐kDa‐factor resulted in further significant increases in mRNA levels for both the 26‐kDa‐protein and IFN‐β. These observations add to the evidence already available that transcription of the genes for IFN‐β and the 26‐kDa‐protein are differently regulated. The observation that a factor that belongs to the IL‐1 family induces the 26‐kDa‐protein suggest that the latter plays a role as an intermediary or effector molecule in inflammatory or immunoregulatory processes.