High impact information on Lgals12

• Galectin-12 is required for adipogenic signaling and adipocyte differentiation [1].
• 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) [1].
• 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 [1].
• We conclude that galectin-12 is required for signal transduction that conveys hormone stimulation to the induction of adipogenic factors essential for adipocyte differentiation [1].
• The findings suggest that galectin-12 is a major regulator of adipose tissue development [1].

Biological context of Lgals12

• 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 [1].

Other interactions of Lgals12

• Galectin-12 is a member of the galectin family consisting of beta-galactoside-binding proteins with conserved carbohydrate recognition domains [1].

References