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* Department of Clinical Molecular Biology, In response to low ambient temperature,
mammalian cells as well as microorganisms change various physiological functions, but the molecular mechanisms underlying these adaptations are just beginning
to be understood. We report here the isolation of a
mouse cold-inducible RNA-binding protein (cirp)
cDNA and investigation of its role in cold-stress response of mammalian cells. The cirp cDNA encoded an
18-kD protein consisting of an amino-terminal RNAbinding domain and a carboxyl-terminal glycine-rich domain and exhibited structural similarity to a class of
stress-induced RNA-binding proteins found in plants.
Immunofluorescence microscopy showed that CIRP
was localized in the nucleoplasm of BALB/3T3 mouse
fibroblasts. When the culture temperature was lowered
from 37 to 32°C, expression of CIRP was induced and
growth of BALB/3T3 cells was impaired as compared
with that at 37°C. By suppressing the induction of CIRP
with antisense oligodeoxynucleotides, this impairment
was alleviated, while overexpression of CIRP resulted in impaired growth at 37°C with prolongation of G1
phase of the cell cycle. These results indicate that CIRP
plays an essential role in cold-induced growth suppression of mouse fibroblasts. Identification of CIRP may
provide a clue to the regulatory mechanisms of cold responses in mammalian cells.
Department of Urology, Faculty of Medicine, Kyoto University, Kyoto 606, Japan
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