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- 저자 : Lusha Zhang (검색결과 2 건)
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Lusha Ji,Cheng-Chao Zheng,Rui Xu,Longtao Lu,Jiedao Zhang,Guodong Yang,Jinguang Huang,Changai Wu 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.2
Nuclear matrix attachment regions (MARs) regulate the higher-order organization of chromatin and affect the expression of their flanking genes. In this study, a tobacco MAR, TM6, was isolated and demonstrated to remarkably increase the expression of four different promoters that drive gusA gene and adjacent nptII gene. In turn, this expression enhanced the transformation frequency of transgenic tobacco. Deletion analysis of topoisomerase II-binding site, AT-rich element, and MAR recognition signature (MRS) showed that MRS has the highest contribution (61.7%) to the TM6 sequence-mediated transcription activation. Micrococcal nuclease (MNase) accessibility assay showed that 35S and NOS promoter regions with TM6 are more sensitive than those without TM6. The analysis also revealed that TM6 reduces promoter DNA methylation which can affect the gusA expression. In addition, two to-bacco chromatin-associated proteins, NtMBP1 and NtHMGB, isolated using a yeast one-hybrid system, specifically bound to the TM6II-1 region (761 bp to 870 bp) and to the MRS element in the TM6II-2 (934 bp to 1,021 bp) region, respectively. We thus suggested that TM6 mediated its chromatin opening and chromatin accessibility of its flanking promoters with consequent enhancement of transcription.
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Chunxiao Li,Lu Chen,Min Song,Zhirui Fang,Lusha Zhang,Joel Wake Coffie,Liyuan Zhang,Lulu Ma,Qianyi Wang,Wenjie Yang,Leyu Fang,Shaoxia Wang,Xiumei Gao,Hong Wang 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.8
Acute myocardial infarction (AMI) resultsin irreversible cardiac cell damage or death because ofdecreased blood fl ow to the heart. Apoptosis plays an importantrole in the process of tissue damage after myocardialinfarction (MI), which has pathological and therapeuticimplications. Ferulic acid (FA) is a phenolic acid endowedwith strong antioxidative and cytoprotective activities. Thepresent study aimed to investigate whether FA protectscardiomyocytes from apoptosis by regulating autophagy,which is a cellular self-digestion process, and one of thefi rst lines of defense against oxidative stress. Apoptosis wasinduced by TNF-α (10 ng/mL) and cycloheximide (CHX,5 μg/mL) in rat H9c2 cardiomyocytes. FA-inhibited TNF-α/CHX-induced apoptosis was determined by the quantifi cationof TUNEL-positive cells, and the eff ect was associatedwith decreased ROS production and inhibited caspase3activation. FA treatment enhanced autophagy and increasedautophagy-associated protein expression, leading to an inhibitionof mTOR signaling. When co-treated with 3-methyladenine(3-MA), an autophagy inhibitor, the anti-apoptoticeff ect of FA was attenuated. In an in vivo mouse MI model,FA treatment decreased the apoptotic cell number, reducedinfarct size, and improved cardiac performance, as determinedby histological and echocardiographic assessments. Taken collectively, these results suggest that FA could protectcardiomyocytes from apoptosis by enhancing autophagy.
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