http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Qiuning Yu (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
-
( Qiuning He ),( Zhibin Feng ),( Yanhua Wang ),( Kewen Wang ),( Kailu Zhang ),( Le Kai ),( Xiuying Hao ),( Zhifen Yu ),( Lijuan Chen ),( Yihe Ge ) 한국미생물생명공학회(구 한국산업미생물학회) 2019 Journal of microbiology and biotechnology Vol.29 No.8
As an opportunistic bacterial pathogen, Pseudomonas aeruginosa PAO1 contains two phenazineproducing gene operons, phzA1B1C1D1E1F1G1 (phz1) and phzA2B2C2D2E2F2G2 (phz2), each of which is independently capable of encoding all enzymes for biosynthesizing phenazines, including phenazine-1-carboxylic acid and its derivatives. Other previous study reported that the RpoS-deficient mutant SS24 overproduced pyocyanin, a derivative of phenazine-1- carboxylic acid. However, it is not known how RpoS mediates the expression of two phz operons and regulates pyocyanin biosynthesis in detail. In this study, with deletion of the rpoS gene in the PAΔphz1 mutant and the PAΔphz2 mutant respectively, we demonstrated that RpoS exerted opposite regulatory roles on the expression of the phz1and phz2 operons. We also confirmed that the phz1 operon played a critical role and especially biosynthesized much more phenazines than the phz2 operon when the rpoS gene was knocked out in P. aeruginosa. By constructing the translational reporter fusion vector lasR’-’lacZ and the chromosomal fusion mutant PAΔlasR::lacZ, we verified that RpoS deficiency caused increased expression of lasR, a transcription regulator gene in a first quorum sensing system (las) that activates overexpression of the phz1 operon, suggesting that in the absence of RpoS, LasR might act as an intermediate in overproduction of phenazine biosynthesis mediated by the phz1 operon in P. aeruginosa.
-
Xiaodan Zhu,Fanglei Ye,Shaojuan Hao,Qiuning Yu,Yang Wang,Weihua Lou,Kun Zhao,Hongmin Li 한국생물공학회 2022 Biotechnology and Bioprocess Engineering Vol.27 No.1
Cholesteatoma is a pathologically benign but clinically destructive middle ear disease characterized by hyperproliferative keratinocytes. B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) has been reported to be upregulated in cholesteatoma tissues. This study aimed to explore the biological role and underlying mechanisms of BMI1 in the progression of cholesteatoma. The expression levels of microRNA (miR)-1297, miR-26a- 5p, and BMI1 in cholesteatoma tissues and cells were examined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Functional experiments were performed by CCK-8 assay for cell proliferation viability, 5-ethynyl-2'deoxyuridine (EdU) incorporation assay for DNA biosynthesis, colony formation assay for cloning forming ability analysis, transwell assay and wound healing assay for cell metastasis, flow cytometry for cell cycle distribution and cell apoptosis. The protein expression of apoptosis-associated proteins was investigated by western blot. Dual-luciferase reporter assay was conducted to verify the interaction between miR-1297 or miR-26a-5p and BMI1. BMI1 was highly expressed in cholesteatoma tumor tissues. Functional analyses showed that BMI1 knockdown could inhibit the proliferation, colony formation, migration, invasion, cell cycle progression and promoted the apoptosis of keratinocytes. Mechanically, BMI1 was a target of miR-1297 and miR-26a-5p. Moreover, the rescue experiments presented that BMI1 addition could abolish the suppressive effects of miR-1297 or miR-26a-5p overexpression on cell malignant behaviors in keratinocytes. BMI1 could exert an oncogenic role in the malignant development of cholesteatoma through serving as the targets of miR-1297 and miR-26a-5p, which might provide novel strategies for cholesteatoma treatment.
ScienceON
KISS연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
