期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 279, 期 28, 页码 29761-29766出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M401303200
关键词
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资金
- NIAID NIH HHS [R01 AI20958, R01 AI39620] Funding Source: Medline
Galectin-12 is a member of the galectin family consisting of beta-galactoside-binding proteins with conserved carbohydrate recognition domains. This protein is preferentially expressed in peripheral blood leukocytes and adipocytes. We previously showed that galectin-12 is induced by cell cycle block at the G(1) phase and causes G(1) arrest when overexpressed ( Yang, R.-Y., Hsu, D. K., Yu, L., Ni, J., and Liu, F.- T. ( 2001) J. Biol. Chem. 276, 20252 20260). Here, we show that the galectin-12 gene is expressed in mouse preadipocytes and is up-regulated when preadipocytes undergo cell cycle arrest, concomitant with acquisition of the competence to undergo differentiation in response to adipogenic hormone stimulation. Following a brief down-regulation 1 day after adipogenic treatment, its expression was once again markedly elevated when cells underwent terminal differentiation. Down-regulation of endogenous galectin-12 expression by RNA interference greatly reduced the expression of the adipogenic transcription factors CCAAT/enhancer-binding protein-beta and -alpha and peroxisome proliferator-activated receptor-gamma and severely suppressed adipocyte differentiation as a result of defective adipogenic signaling. We conclude that galectin-12 is required for signal transduction that conveys hormone stimulation to the induction of adipogenic factors essential for adipocyte differentiation. The findings suggest that galectin-12 is a major regulator of adipose tissue development.
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