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Prepublished online as a Blood First Edition Paper on September 19, 2002; DOI 10.1182/blood-2002-06-1881.
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Blood, 1 February 2003, Vol. 101, No. 3, pp. 1185-1187
PHAGOCYTES
Brief report
LSSIG is a novel murine leukocyte-specific GPCR that is
induced by the activation of STAT3
Takeshi Senga,
Shotaro Iwamoto,
Tsunehiko Yoshida,
Takashi Yokota,
Koichi Adachi,
Eiichi Azuma,
Michinari Hamaguchi, and
Takashi Iwamoto
From the Department of Molecular Pathogenesis,
Department of Ophthalmology, Radioisotope Research Center Medical
Division, Nagoya University School of Medicine, Showa-ku, Nagoya,
Japan; Department of Pediatrics and Clinical Immunology,
Mie University School of Medicine, Tsu, Japan; Division of
Stem Cell Biology, Graduate School of Medical Science, Kanazawa
University, Kanazawa, Japan.
G-protein-coupled receptors (GPCRs) transduce the signal of a wide
variety of chemokines, cytokines, neurotransmitters, hormones, odorants, and others to regulate the biologic homeostasis,
including hematopoiesis and immunity. Here we report the molecular
cloning of leukocyte-specific STAT-induced GPCR (LSSIG), which
is a novel murine orphan GPCR with the highest homology to human GPR43.
The mRNA expression of LSSIG was clearly induced in M1 leukemia cells during the leukemia inhibitory factor (LIF)-induced differentiation to
macrophages, and the induction was evidently signal transducers and
activators of transcription 3 (STAT3)-dependent. GPR43
expression was also strongly induced in HL-60 and U937 leukemia cells
during the differentiation to monocytes. Further analysis showed that the expression of both LSSIG and GPR43 is highly restricted in hematopoietic tissues. Cytokine-stimulation induced LSSIG and GPR43 in
bone marrow cells, and monocytes and neutrophils, respectively. These
results suggest that LSSIG and GPR43 might play pivotal roles in
differentiation and immune response of monocytes and granulocytes.
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