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- 저자 : Li Jieying (검색결과 4 건)
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Epigenetic silencing of UBXN8 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
Yang Erna,Guan Wei,Gong Desheng,Li Jieying,Han Caixia,Zhang Juan,Wang Hong,Kang Synat,Gao Xuefeng,Li Yonghui,Yu Li 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
The formation of the RUNX1-RUNX1T1 fusion protein, resulting from the t(8;21) translocation, is considered to be one of the initiating events of t(8;21) acute myeloid leukemia (AML). However, the mechanisms of the oncogenic mechanism of RUNX1- RUNX1T1 remain unclear. In this study, we found that RUNX1-RUNX1T1 triggers the heterochromatic silencing of UBXN8 by recognizing the RUNX1-binding sites and recruiting chromatin-remodeling enzymes to the UBXN8 promoter region. Decitabine, a specific inhibitor of DNA methylation, upregulated the expression of UBXN8 in RUNX1-RUNX1T1+ AML cell lines. Overexpression of UBXN8 inhibited the proliferation and colony-forming ability of and promoted cell cycle arrest in t(8;21) AML cell lines. Enhancing UBXN8 levels can significantly inhibit tumor proliferation and promote the differentiation of RUNX1-RUNX1T1+ cells in vivo. In conclusion, our results indicated that epigenetic silencing of UBXN8 via methylation of its promoter region mediated by the RUNX1- RUNX1T1 fusion protein contributes to the leukemogenesis of t(8;21) AML and that UBXN8 targeting may be a potential therapeutic strategy for t(8;21) AML. The formation of the RUNX1-RUNX1T1 fusion protein, resulting from the t(8;21) translocation, is considered to be one of the initiating events of t(8;21) acute myeloid leukemia (AML). However, the mechanisms of the oncogenic mechanism of RUNX1-RUNX1T1 remain unclear. In this study, we found that RUNX1-RUNX1T1 triggers the heterochromatic silencing of UBXN8 by recognizing the RUNX1-binding sites and recruiting chromatin-remodeling enzymes to the UBXN8 promoter region. Decitabine, a specific inhibitor of DNA methylation, upregulated the expression of UBXN8 in RUNX1-RUNX1T1 + AML cell lines. Overexpression of UBXN8 inhibited the proliferation and colony-forming ability of and promoted cell cycle arrest in t(8;21) AML cell lines. Enhancing UBXN8 levels can significantly inhibit tumor proliferation and promote the differentiation of RUNX1-RUNX1T1 + cells in vivo. In conclusion, our results indicated that epigenetic silencing of UBXN8 via methylation of its promoter region mediated by the RUNX1-RUNX1T1 fusion protein contributes to the leukemogenesis of t(8;21) AML and that UBXN8 targeting may be a potential therapeutic strategy for t(8;21) AML.
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Jieying Wang,Taomin Bai,Nana Wang,Hongyan Li,Xiangyang Guo 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.1
The present study was aimed to explore the neuroprotective role of imatinib in global ischemia-reperfusion-induced cerebral injury along with possible mechanisms. Global ischemia was induced in mice by bilateral carotid artery occlusion for 20 min, which was followed by reperfusion for 24 h by restoring the blood flow to the brain. The extent of cerebral injury was assessed after 24 h of global ischemia by measuring the locomotor activity (actophotometer test), motor coordination (inclined beam walking test), neurological severity score, learning and memory (object recognition test) and cerebral infarction (triphenyl tetrazolium chloride stain). Ischemia-reperfusion injury produced significant cerebral infarction, impaired the behavioral parameters and decreased the expression of connexin 43 and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in the brain. A single dose administration of imatinib (20 and 40 mg/kg) attenuated ischemia-reperfusioninduced behavioral deficits and the extent of cerebral infarction along with the restoration of connexin 43 and p-STAT3 levels. However, administration of AG490, a selective Janus-activated kinase 2 (JAK2)/STAT3 inhibitor, abolished the neuroprotective actions of imatinib and decreased the expression of connexin 43 and p-STAT3. It is concluded that imatinib has the potential of attenuating global ischemia-reperfusion- induced cerebral injury, which may be possibly attributed to activation of JAK2/ STAT3 signaling pathway along with the increase in the expression of connexin 43.
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Removal of COD from coking-plant wastewater in the moving-bed biofilm sequencing batch reactor
JieYing Jing,Jie Feng,Ying Xu,WenYing Li 한국화학공학회 2009 Korean Journal of Chemical Engineering Vol.26 No.2
The objective of this paper is to investigate COD removal efficiency of the coking-plant wastewater by applying the moving-bed biofilm sequencing batch reactor (MBBSBR). The operation is simple and 30% WD-F10-4 BioMTM were packed as carrier materials. It was found that the coking-plant wastewater could be effectively treated with 92.9% of COD removal efficiency at a low organic loading rate (OLR) of 0.449 kgCOD·m−3·d−1. The removal efficiency decreased gradually down to 70.9% when OLR increased to 2.628 kgCOD·m−3·d−1. The system has strong tolerance to organic shock loading in this experiment. The COD removal results in the blank experiments of biofilm and sludge showed that the attached biofilm has higher activity than suspended sludge and contributes about 60% to the COD removal.
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