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 : Quansheng Zhou (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
Trp-tRNA synthetase bridges DNA-PKcs to PARP-1 to link IFN-款 and p53 signaling
Sajish, Mathew,Zhou, Quansheng,Kishi, Shuji,Valdez Jr, Delgado M,Kapoor, Mili,Guo, Min,Lee, Sunhee,Kim, Sunghoon,Yang, Xiang-Lei,Schimmel, Paul Nature Publishing Group, a division of Macmillan P 2012 NATURE CHEMICAL BIOLOGY Vol.8 No.6
Interferon-款 (IFN-款) engenders strong antiproliferative responses, in part through activation of p53. However, the long-known IFN-款??dependent upregulation of human Trp-tRNA synthetase (TrpRS), a cytoplasmic enzyme that activates tryptophan to form Trp-AMP in the first step of protein synthesis, is unexplained. Here we report a nuclear complex of TrpRS with the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) and with poly(ADP-ribose) polymerase 1 (PARP-1), the major PARP in human cells. The IFN-款??dependent poly(ADP-ribosyl)ation of DNA-PKcs (which activates its kinase function) and concomitant activation of the tumor suppressor p53 were specifically prevented by Trp-SA, an analog of Trp-AMP that disrupted the TrpRS??DNA-PKcs??PARP-1 complex. The connection of TrpRS to p53 signaling in vivo was confirmed in a vertebrate system. These and further results suggest an unexpected evolutionary expansion of the protein synthesis apparatus to a nuclear role that links major signaling pathways.
-
Energy informatics: Fundamentals and standardization
Biyao Huang,Xiaomin Bai,Zhenyu Zhou,Quansheng Cui,Daohua Zhu,Ruwei Hu 한국통신학회 2017 ICT Express Vol.3 No.2
Based on international standardization and power utility practices, this paper presents a preliminary and systematic study on the field of energy informatics and analyzes boundary expansion of information and energy system, and the convergence of energy system and ICT. A comprehensive introduction of the fundamentals and standardization of energy informatics is provided, and several key open issues are identified.
-
Ping Yang,Yingnan Qiao,Huaidong Liao,Yizheng Huang,Mei Meng,Yu Chen,Quansheng Zhou 한국유방암학회 2023 Journal of breast cancer Vol.26 No.2
Purpose: Invasive breast carcinomas (BRCAs) are highly lethal. The molecular mechanisms underlying progression of invasive BRCAs are unclear, and effective therapies are highly desired. The cancer-testis antigen CT45A1 promotes overexpression of pro-metastatic sulfatase-2 (SULF2) and breast cancer metastasis to the lungs, but its mechanisms are largely unknown. In this study, we aimed to elucidate the mechanism of CT45A1-induced SULF2 overexpression and provide evidence for targeting CT45A1 and SULF2 for breast cancer therapy. Methods: The effect of CT45A1 on SULF2 expression was assessed using reverse transcription polymerase chain reaction and western blot. The mechanism of CT45A1-induced SULF2 gene transcription was studied using protein-DNA binding assay and a luciferase activity reporter system. The interaction between CT45A1 and SP1 proteins was assessed using immunoprecipitation and western blot. Additionally, the suppression of breast cancer cell motility by SP1 and SULF2 inhibitors was measured using cell migration and invasion assays. Results: CT45A1 and SULF2 are aberrantly overexpressed in patients with BRCA; importantly, overexpression of CT45A1 is closely associated with poor prognosis. Mechanistically, gene promoter demethylation results in overexpression of both CT45A1 and SULF2. CT45A1 binds directly to the core sequence GCCCCC in the promoter region of SULF2 gene and activates the promoter. Additionally, CT45A1 interacts with the oncogenic master transcription factor SP1 to drive SULF2 gene transcription. Interestingly, SP1 and SULF2 inhibitors suppress breast cancer cell migration, invasion, and tumorigenicity. Conclusion: Overexpression of CT45A1 is associated with poor prognosis in patients with BRCA. CT45A1 promotes SULF2 overexpression by activating the promoter and interacting with SP1. Additionally, SP1 and SULF2 inhibitors suppress breast cancer cell migration, invasion, and tumorigenesis. Our findings provide new insight into the mechanisms of breast cancer metastasis and highlight CT45A1 and SULF2 as sensible targets for developing novel therapeutics against metastatic breast cancer.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
