目的:对大鼠GLUT3基因第一外显子5′侧翼转录调控区的碱基序列进行生物信息学分析,为后续的GLUT3基因的转录调控研究奠定基础。方法:通过搜索网络数据库,得到GLUT3基因现有的转录本序列以及翻译起始点上游6kb的序列。运用CpG island sea...目的:对大鼠GLUT3基因第一外显子5′侧翼转录调控区的碱基序列进行生物信息学分析,为后续的GLUT3基因的转录调控研究奠定基础。方法:通过搜索网络数据库,得到GLUT3基因现有的转录本序列以及翻译起始点上游6kb的序列。运用CpG island searcher,methprimer等软件对上述序列进行分析,预测出该段序列潜在的CpG岛,运用FirstEF、NNPP等软件分析可能的启动子区域以及运用Matlspector、TFSEARCH和TFBIND等软件分析潜在的转录因子结合位点。结果:GLUT3基因的启动子可能位于翻译起始点上游-795～-226bp(以翻译起始点ATG为+1),第一外显子位于-285～+15bp,在这段序列上存在包括SP1、CREBP、P300、AML1、NF1等约110多种转录因子的潜在结合位点。结论:对大鼠GLUT3基因第一外显子5′侧翼转录调控区序列进行了初步的生物信息学分析,为后续试验提供了研究基础。展开更多
Progesterone is an efficient candidate for treating stroke and traumatic brain damage. The current study was designed to investigate the effects of pro gesterone on glucose transporter proteins （GLUT1 and GLUT3） dur...Progesterone is an efficient candidate for treating stroke and traumatic brain damage. The current study was designed to investigate the effects of pro gesterone on glucose transporter proteins （GLUT1 and GLUT3） during hypoxicischemic injury in a neo natal rat model. We demonstrated strong staining for GLUT1 in the walls of blood vessels and GLUT3 im munoreactivity in hippocampal neurons after hypoxia ischemia. Hypoxiaischemia elevated GLUT1 and GLUT3 at both the mRNA and protein levels in the hippocampus, and pretreatment with progesterone （8 mg/kg） further enhanced their accumulation until 24 h after hypoxicischemic injury. These results showed that progesterone treatment induced the accumula tion of both GLUT1 and GLUT3 transporters, and an energycompensation mechanism may be involved in the neuroprotective effect of progesterone during hy poxicischemic injury after cerebral ischemic attacks.展开更多
目的:探讨急性淋巴细胞白血病患者葡萄糖转运蛋白-3(Glucose transporter 3,GLUT3)、肿瘤抑制物1(Tumor suppressor in lung cancer 1,TSLC1)的表达及临床意义。方法:选取2018年4月至2020年4月期间我院诊治的59例急性淋巴细胞白血病患...目的:探讨急性淋巴细胞白血病患者葡萄糖转运蛋白-3(Glucose transporter 3,GLUT3)、肿瘤抑制物1(Tumor suppressor in lung cancer 1,TSLC1)的表达及临床意义。方法:选取2018年4月至2020年4月期间我院诊治的59例急性淋巴细胞白血病患者作为研究对象的研究组,另选取53例同期非急性淋巴细胞白血病患者作为研究对象的对照组。比较两组患者骨髓单个核细胞中GLUT3、TSLC1的表达情况,以及患者的不同临床病理特征对骨髓单个核细胞中GLUT3、TSLC1表达的影响。结果:研究组GLUT3阳性表达率高于对照组、TSLC1阳性表达率低于对照组(P<0.05);血红蛋白(异常)、白细胞计数(异常)者GLUT3阳性率明显高于血红蛋白(正常)、白细胞计数(正常)者(P<0.05)。白细胞计数(异常)者TSLC1阳性率明显高于白细胞计数(正常)者(P<0.05)。结论:在急性淋巴细胞白血病患者骨髓单个核细胞中GLUT3阳性表达率高、TSLC1阴性表达率高。展开更多
Regulatory T cells(Tregs)establish dominant immune tolerance but obstruct tumor immune surveillance,warranting context-specific mechanistic insights into the functions of tumor-infiltrating Tregs(TIL-Tregs).We show th...Regulatory T cells(Tregs)establish dominant immune tolerance but obstruct tumor immune surveillance,warranting context-specific mechanistic insights into the functions of tumor-infiltrating Tregs(TIL-Tregs).We show that enhanced posttranslational O-linked N-acetylglucosamine modification(O-GlcNAcylation)of cellular factors is a molecular feature that promotes a tumor-specific gene expression signature and distinguishes TIL-Tregs from their systemic counterparts.We found that altered glucose utilization through the glucose transporter Glut3 is a major facilitator of this process.Treg-specific deletion of Glut3 abrogates tumor immune tolerance,while steady-state immune homeostasis remains largely unaffected in mice.Furthermore,by employing mouse tumor models and human clinical data,we identified the NF-κB subunit c-Rel as one such factor that,through Glut3-dependent O-GlcNAcylation,functionally orchestrates gene expression in Tregs at tumor sites.Together,these results not only identify immunometabolic alterations and molecular events contributing to fundamental aspects of Treg biology,specifically at tumor sites but also reveal tumor-specific cellular properties that can aid in the development of Treg-targeted cancer immunotherapies.展开更多
文摘目的:对大鼠GLUT3基因第一外显子5′侧翼转录调控区的碱基序列进行生物信息学分析,为后续的GLUT3基因的转录调控研究奠定基础。方法:通过搜索网络数据库,得到GLUT3基因现有的转录本序列以及翻译起始点上游6kb的序列。运用CpG island searcher,methprimer等软件对上述序列进行分析,预测出该段序列潜在的CpG岛,运用FirstEF、NNPP等软件分析可能的启动子区域以及运用Matlspector、TFSEARCH和TFBIND等软件分析潜在的转录因子结合位点。结果:GLUT3基因的启动子可能位于翻译起始点上游-795～-226bp(以翻译起始点ATG为+1),第一外显子位于-285～+15bp,在这段序列上存在包括SP1、CREBP、P300、AML1、NF1等约110多种转录因子的潜在结合位点。结论:对大鼠GLUT3基因第一外显子5′侧翼转录调控区序列进行了初步的生物信息学分析,为后续试验提供了研究基础。
基金supported by the National Natural Science Foundation of China (81100912)the Science Foundation of Xinxiang Medical University, China (CL and ZD 2009-63)the Science and Technology Project of Henan Province, China (092102310098)
文摘Progesterone is an efficient candidate for treating stroke and traumatic brain damage. The current study was designed to investigate the effects of pro gesterone on glucose transporter proteins （GLUT1 and GLUT3） during hypoxicischemic injury in a neo natal rat model. We demonstrated strong staining for GLUT1 in the walls of blood vessels and GLUT3 im munoreactivity in hippocampal neurons after hypoxia ischemia. Hypoxiaischemia elevated GLUT1 and GLUT3 at both the mRNA and protein levels in the hippocampus, and pretreatment with progesterone （8 mg/kg） further enhanced their accumulation until 24 h after hypoxicischemic injury. These results showed that progesterone treatment induced the accumula tion of both GLUT1 and GLUT3 transporters, and an energycompensation mechanism may be involved in the neuroprotective effect of progesterone during hy poxicischemic injury after cerebral ischemic attacks.
文摘目的:探讨急性淋巴细胞白血病患者葡萄糖转运蛋白-3(Glucose transporter 3,GLUT3)、肿瘤抑制物1(Tumor suppressor in lung cancer 1,TSLC1)的表达及临床意义。方法:选取2018年4月至2020年4月期间我院诊治的59例急性淋巴细胞白血病患者作为研究对象的研究组,另选取53例同期非急性淋巴细胞白血病患者作为研究对象的对照组。比较两组患者骨髓单个核细胞中GLUT3、TSLC1的表达情况,以及患者的不同临床病理特征对骨髓单个核细胞中GLUT3、TSLC1表达的影响。结果:研究组GLUT3阳性表达率高于对照组、TSLC1阳性表达率低于对照组(P<0.05);血红蛋白(异常)、白细胞计数(异常)者GLUT3阳性率明显高于血红蛋白(正常)、白细胞计数(正常)者(P<0.05)。白细胞计数(异常)者TSLC1阳性率明显高于白细胞计数(正常)者(P<0.05)。结论:在急性淋巴细胞白血病患者骨髓单个核细胞中GLUT3阳性表达率高、TSLC1阴性表达率高。
基金YC was financially supported by the Dissertation Completion Award of the University of Georgia and American Lebanese Syrian Associated Charities(ALSAC)at St.Jude Children’s Research HospitalAG acknowledges support by the High Performance and Cloud Computing Group at the Zentrum für Datenverarbeitung of the University of Tübingen,the state of Baden-Württemberg through bwHPC and the German Research Foundation(DFG)through grant no INST 37/935-1 FUGG,and the de.NBI Cloud within the German Network for Bioinformatics Infrastructure(de.NBI)and ELIXIR-DE(Forschungszentrum Jülich and W-de.NBI-001,W-de.NBI-004,W-de.NBI-008,W-de.NBI-010,W-de.NBI-013,W-de.NBI-014,W-de.NBI-016,W-de.NBI-022)for supporting the computational analysis carried out in this work.AS was supported by BrainKorea21 Plus scholarship from the National Research Foundation of Korea(NRF)+1 种基金This research,in part,was supported by the Basic Science Research Program(grant#4.24643.01)funded by the Ministry of Education,Korea,and NRF grants#RS-2023-00260454(AS)and RS-2024-00345575(SHI)funded by the Korea Ministry of Science and ICT(MSIT)DR is recipient of National Natural Science Foundation of China grant#32470980.
文摘Regulatory T cells(Tregs)establish dominant immune tolerance but obstruct tumor immune surveillance,warranting context-specific mechanistic insights into the functions of tumor-infiltrating Tregs(TIL-Tregs).We show that enhanced posttranslational O-linked N-acetylglucosamine modification(O-GlcNAcylation)of cellular factors is a molecular feature that promotes a tumor-specific gene expression signature and distinguishes TIL-Tregs from their systemic counterparts.We found that altered glucose utilization through the glucose transporter Glut3 is a major facilitator of this process.Treg-specific deletion of Glut3 abrogates tumor immune tolerance,while steady-state immune homeostasis remains largely unaffected in mice.Furthermore,by employing mouse tumor models and human clinical data,we identified the NF-κB subunit c-Rel as one such factor that,through Glut3-dependent O-GlcNAcylation,functionally orchestrates gene expression in Tregs at tumor sites.Together,these results not only identify immunometabolic alterations and molecular events contributing to fundamental aspects of Treg biology,specifically at tumor sites but also reveal tumor-specific cellular properties that can aid in the development of Treg-targeted cancer immunotherapies.
