Journal
BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume 32, Issue 1, Pages 129-131Publisher
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.32.129
Keywords
Candida albicans; propranolol; EFG1; agglutinin like sequence 3; agglutinin like sequence 8
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Candida albicans (C. albicans) is known as an opportunistic pathogen that changes from a yeast form to a hyphae form in response to various outside environmental signals. The addition of propranolol inhibited hyphae formation of C albicans. Propranolol inhibited the expression of agglutinin like sequence 3 (ALS3) and ALS8mRNA, which are regulated by the cAMP-EFG1 pathway in C albicans. Propranolol did not affect the expression of CST20, HST7 or CPH1mRNA, which are components of the mitogen-activated protein (MAP) kinase cascade in C albicans. The expression of CYR1mRNA, which encodes adenylate cyclase of C albicans, was not affected by propranolol. These findings indicated that the interruption of hyphae formation by propranolol is caused by inhibition of the cAMP-EFG1 pathway, but not effects on the MAP kinase cascade.
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