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Blood, Vol. 92 No. 5 (September 1), 1998:
pp. 1668-1676
A Janus Kinase Inhibitor, JAB, Is an
Interferon- -Inducible Gene and Confers Resistance to
Interferons
Hiroshi Sakamoto,
Hideo Yasukawa,
Masaaki Masuhara,
Shyu Tanimura,
Atsuo Sasaki,
Kentaro Yuge,
Motoaki Ohtsubo,
Akira Ohtsuka,
Takasi Fujita,
Tsunetaka Ohta,
Yusuke Furukawa,
Satsuki Iwase,
Hisashi Yamada, and
Akihiko Yoshimura
From the Institute of Life Science, Kurume University, Aikawamachi,
Kurume; the Department of Tumor Cell Biology, Tokyo Metropolitan
Institute of Medical Science, Bunkyoku, Tokyo; the Fujisaki Institute,
Hayashibara Biochemical Laboratories, Inc, Okayama; the Division of
Hemopoiesis, Institute of Hematology, Jichi Medical School, Tochigi;
and the Departments of Internal Medicine (IV) and Molecular Genetics,
Institute of DNA Medicine, Jikei University School of Medicine, Tokyo,
Japan.
It has been shown that interferons (IFNs) exert their signals
through receptor-associated Janus kinases (JAKs) and signal transducers and activators of transcription (STATs). However, molecular
mechanism of regulation of IFN signaling has not been fully understood.
We have reported novel cytokine-inducible SH2 protein (CIS) and JAK
binding protein (JAB) family genes that can potentially modulate
cytokine signaling. Here we report that JAB is strongly induced
by IFN- but not by IFN- in mouse myeloid leukemia M1
cells and NIH-3T3 fibroblasts. NIH-3T3 cells ectopically expressing JAB
but not CIS3 lost responsiveness to the antiviral effect of IFN- and
IFN-. M1 leukemic cells stably expressing JAB were also resistant to
IFN- and IFN--induced growth arrest. In both NIH-3T3 and M1
transformants expressing JAB, IFN- did not induce tyrosine
phosphorylation and DNA binding activity of STAT1. Moreover,
IFN--induced activation of JAK1 and JAK2 and IFN--induced JAK1
and Tyk2 activation were inhibited in NIH-3T3 JAB transformants. These
results suggest that JAB inhibits IFN signaling by blocking JAK
activity. We also found that IFN-resistant clones derived from LoVo
cells and Daudi cells expressed high levels of JAB without stimulation.
In IFN-resistant Daudi cells, IFN-induced STAT1 and JAK phosphorylation
was partially reduced. Therefore, overexpression of JAB could be, at
least in part, a mechanism of IFN resistance.
© 1998 by The American Society of Hematology.
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