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Metabolites from the Fungus Cephalosporium sp. AL031
Yun-Mei Bi,Xu-Bin Bi,Fang A,Qian-Rong Zhao 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.3
A new pyrone derivative, 7, 9-dihydroxy-10-methyl-2H, 4aH, 6H, 10bH-pyrano[5,6-c][2]benzopyran- 2,6-dione (1), was isolated from a culture broth of a strain of the fungus Cephalosporium sp. AL031, together with three known compounds, 3-acetyl-7-hydroxy-5-methoxyl-3Hisobenzofuran- 1-one (2), vermopyrone (3), and 5-methylmellein (4). Their structures were elucidated by spectroscopic analysis including MS and 2D-NMR. Compounds 2, 3, and 4 are reported for the first time from fermentation broth of this fungus through the present study.
( Yun Deng ),( Bi Sheng Liu ),( Xiong Wei Fan ),( Yue Qun Wang ),( Ming Tang ),( Xiao Yang Mo ),( Yong Qing Li ),( Zao Chu Ying ),( Yong Qi Wan ),( Na Luo ),( Jun Mei Zhou ),( Xiu Shan Wu ),( Wu Zhou 한국생화학분자생물학회 (구 한국생화학회) 2010 BMB Reports Vol.43 No.3
In this study, we report the identification and characterization of a novel C2H2 zinc finger protein, ZNF552, from a human embryonic heart cDNA library. ZNF552 is composed of three exons and two introns and maps to chromosome 19q13.43. The cDNA of ZNF552 is 2.3 kb, encoding 407 amino acids with an amino-terminal KRAB domain and seven carboxyl-terminal C2H2 zinc finger motifs in the nucleus and cytoplasm. Northern blotting analysis indicated that a 2.3 kb transcript specific for ZNF552 was expressed in liver, lung, spleen, testis and kidney, especially with a higher level in the lung and testis in human adult tissues. Reporter gene assays showed that ZNF552 was a transcriptional repressor, and overexpression of ZNF552 in the COS-7 cells inhibited the transcriptional activities of AP-1 and SRE, which could be relieved through RNAi analysis. Deletion studies showed that the KRAB domain of ZNF552 may be involved in this inhibition. [BMB reports 2010; 43(3): 193-198]
Zu-Guo Zhao,Yun Mei Yu,Bi Yu Xu,Shuang-Shuang Yan,Jun-Fa Xu,Fang Liu,Guo-Ming Li,Yuan Lin Ding,Shu Qing Wu 한국생물공학회 2013 Biotechnology and Bioprocess Engineering Vol.18 No.2
In Pseudomonas aeruginosa, a quorum sensing (QS) system regulates the expression of many virulence factors. N-acyl homoserine lactone (HSL) is the signal molecule of QS system. In order to find a novel HSL binder to interfere with QS signaling and to attenuate P. aeruginosa virulence, an amino lactam surrogate (ALS) of HSL was used as a target to screen HSL aptamers with the technique of systematic evolution of ligands by exponential enrichment (SELEX). Eight HSL aptamers with high affinities for 3O-C12-HSL (20 nM ≤ Kd < 35 nM) or C4-HSL (25 nM < Kd < 50 nM) were finally obtained. In vitro QS-inhibiting study of P. aeruginosa showed that HSL aptamers could inhibit virulence in a dose-dependent manner. ALSap-8 which bound C4-HSL primarily acted on the rhl system and inhibited the secretion of pyocyanin. ALSap-5 which bound 3O-C12-HSL not only showed strong inhibitory activity on biofilm formation as well as secretions of LasA protease and LasB elastase, but also reduced pyocyanin secretion. Since the las system is capable of activating the rhl system mildly, we speculated that ALSap-5 can simultaneously interfere with the las and rhl systems. High-affinity aptamers against HSL in this study are novel QS and virulence-inhibitors, and may have potential as drug candidates for the treatment of P. aeruginosa infection.