Glucose is one of the most important nutrients for yeast growth,which induces cell death of S.cerevisiae in the absence of other nutrients to support growth.In the present study,we reported that the S.cerevisiae ste20...Glucose is one of the most important nutrients for yeast growth,which induces cell death of S.cerevisiae in the absence of other nutrients to support growth.In the present study,we reported that the S.cerevisiae ste20 mutant was resistant to glucose-induced cell death.Cells of ste20 mutant that were treated with glucose maintained intact membrane and nuclei.Ste20 kinase phosphorylates histone H2B at serine 10(S10)during hydrogen peroxide(H2O2)-induced cell death.Therefore,glucose-induced cell death(GICD)may be regulated via a similar pathway of H2O2-induced apoptosis.展开更多
目的探讨哺乳动物ste20样激酶1(mammalian sterile20-like 1,MST1)基因的miRNAs对肝脏内脂质堆积的影响。方法利用高脂诱导非酒精性脂肪性肝病(NAFLD)模型小鼠与低脂对照组小鼠的肝脏及脂肪组织进行miRNAsequence分析,选取表达上调的miR...目的探讨哺乳动物ste20样激酶1(mammalian sterile20-like 1,MST1)基因的miRNAs对肝脏内脂质堆积的影响。方法利用高脂诱导非酒精性脂肪性肝病(NAFLD)模型小鼠与低脂对照组小鼠的肝脏及脂肪组织进行miRNAsequence分析,选取表达上调的miRNAs,通过数据库miRDB、starBase筛选出可能靶向MST1靶基因3’UTR区的miRNAs进行研究,利用Western blot及双荧光素酶报告基因实验检测miRNAs对MST1的靶向效应。并在NAFLD细胞模型内进行MST1过表达或干扰,进一步验证miRNAs对MST1的表达调控作用。结果 Western blot实验显示得到mmu miR 149-5p和mmu miR 499-5p抑制鼠MST1基因蛋白水平的表达,Luciferases实验证明mmu miR 149-5p和mmu miR 499-5p靶向MST1能够增加AML-12细胞内的脂质堆积。结论mmu miR 149-5p、mmu miR 499-5p能够调控小鼠肝脏MST1表达并影响肝脏内脂质堆积。展开更多
Recently, inflammatory bowel disease （IBD） has been the subject of considerable research, with increasing attention being paid to the loss of intestinal epithelial cell barrier function as a mechanism of pathogenesi...Recently, inflammatory bowel disease （IBD） has been the subject of considerable research, with increasing attention being paid to the loss of intestinal epithelial cell barrier function as a mechanism of pathogenesis. Ste20-related proline/alanine-rich kinase （SPAK） is involved in regulating barrier function. SPAK is known to interact with inflammation-related kinases （such as p38, JNK, NKCC1, PKCS, WNK and MLCK）, and with transcription factor AP-1, resulting in diverse biological phenomena, including cell differentiation, cell transformation and proliferation, cytoskeleton rearrangement, and regulation of chloride transport. This review examines the involvement of Ste20-1ike kinases and downstream mitogen-activated protein kinases （MAPKs） pathways in the pathogenesis and control of intestinal inflammation. The primary focus will be on the molecular features of intestinal inflammation, with an emphasis on the interaction between SPAK and other molecules, and the effect of these interactions on homeostatic maintenance, cell volume regulation and increased cell permeability in intestinal inflammation.展开更多
[目的]研究MST4对非小细胞肺癌A549细胞增殖和转移的影响。[方法]采用蛋白免疫印迹实验检测MST4在不同细胞、组织中的表达水平;将非小细胞肺癌A549细胞分为4个实验组:阴性对照组、MST4敲低组(si MST4组)、JAK2/STAT3通路抑制剂组(SD-102...[目的]研究MST4对非小细胞肺癌A549细胞增殖和转移的影响。[方法]采用蛋白免疫印迹实验检测MST4在不同细胞、组织中的表达水平;将非小细胞肺癌A549细胞分为4个实验组:阴性对照组、MST4敲低组(si MST4组)、JAK2/STAT3通路抑制剂组(SD-1029组)、JAK2/STAT3通路激动剂组(SC-39100组)。以CCK-8实验检测A549细胞的增殖能力;划痕实验检测A549细胞的迁移能力;Transwell实验检测A549细胞的侵袭能力;蛋白免疫印迹实验分析A549细胞中JAK2、STAT3蛋白的表达量。[结果]MST4在非小细胞肺癌组织中表达增加(0.39±0.03 vs 0.83±0.05,P<0.05),非小细胞肺癌细胞(H358、A549和H1299)细胞株中的MST4表达水平增加(0.11±0.03 vs 0.89±0.05 vs 0.88±0.02 vs 0.91±0.09,P<0.05)。与阴性对照组相比,si MST4以及SD-1029组的A549细胞增殖能力下降,SC-39100组的A549细胞增殖能力增加;si MST4以及SD-1029组的A549细胞迁移能力下降,SC-39100组的A549细胞迁移能力增加;si MST4以及SD-1029组的A549细胞的侵袭能力下降,SC-39100组的A549细胞侵袭能力增加;si MST4以及SD-1029组的A549细胞JAK2、STAT3蛋白表达减少(0.85±0.07 vs 0.19±0.05 vs 0.80±0.02 vs 0.81±0.08,P<0.05;0.61±0.03 vs 0.26±0.09 vs 0.28±0.02 vs 0.89±0.05,P<0.05;0.63±0.03 vs 0.29±0.07 vs 0.31±0.01 vs 0.88±0.03,P<0.05),SC-39100组的A549细胞JAK2、STAT3蛋白表达增加。[结论]MST4在非小细胞肺癌细胞以及组织中表达上调。抑制MST4表达后,A549细胞的增殖活性、迁移与侵袭能力降低,该作用与MST4调节JAK2/STAT3信号通路相关。展开更多
文摘Glucose is one of the most important nutrients for yeast growth,which induces cell death of S.cerevisiae in the absence of other nutrients to support growth.In the present study,we reported that the S.cerevisiae ste20 mutant was resistant to glucose-induced cell death.Cells of ste20 mutant that were treated with glucose maintained intact membrane and nuclei.Ste20 kinase phosphorylates histone H2B at serine 10(S10)during hydrogen peroxide(H2O2)-induced cell death.Therefore,glucose-induced cell death(GICD)may be regulated via a similar pathway of H2O2-induced apoptosis.
文摘目的探讨哺乳动物ste20样激酶1(mammalian sterile20-like 1,MST1)基因的miRNAs对肝脏内脂质堆积的影响。方法利用高脂诱导非酒精性脂肪性肝病(NAFLD)模型小鼠与低脂对照组小鼠的肝脏及脂肪组织进行miRNAsequence分析,选取表达上调的miRNAs,通过数据库miRDB、starBase筛选出可能靶向MST1靶基因3’UTR区的miRNAs进行研究,利用Western blot及双荧光素酶报告基因实验检测miRNAs对MST1的靶向效应。并在NAFLD细胞模型内进行MST1过表达或干扰,进一步验证miRNAs对MST1的表达调控作用。结果 Western blot实验显示得到mmu miR 149-5p和mmu miR 499-5p抑制鼠MST1基因蛋白水平的表达,Luciferases实验证明mmu miR 149-5p和mmu miR 499-5p靶向MST1能够增加AML-12细胞内的脂质堆积。结论mmu miR 149-5p、mmu miR 499-5p能够调控小鼠肝脏MST1表达并影响肝脏内脂质堆积。
文摘Recently, inflammatory bowel disease （IBD） has been the subject of considerable research, with increasing attention being paid to the loss of intestinal epithelial cell barrier function as a mechanism of pathogenesis. Ste20-related proline/alanine-rich kinase （SPAK） is involved in regulating barrier function. SPAK is known to interact with inflammation-related kinases （such as p38, JNK, NKCC1, PKCS, WNK and MLCK）, and with transcription factor AP-1, resulting in diverse biological phenomena, including cell differentiation, cell transformation and proliferation, cytoskeleton rearrangement, and regulation of chloride transport. This review examines the involvement of Ste20-1ike kinases and downstream mitogen-activated protein kinases （MAPKs） pathways in the pathogenesis and control of intestinal inflammation. The primary focus will be on the molecular features of intestinal inflammation, with an emphasis on the interaction between SPAK and other molecules, and the effect of these interactions on homeostatic maintenance, cell volume regulation and increased cell permeability in intestinal inflammation.
文摘[目的]研究MST4对非小细胞肺癌A549细胞增殖和转移的影响。[方法]采用蛋白免疫印迹实验检测MST4在不同细胞、组织中的表达水平;将非小细胞肺癌A549细胞分为4个实验组:阴性对照组、MST4敲低组(si MST4组)、JAK2/STAT3通路抑制剂组(SD-1029组)、JAK2/STAT3通路激动剂组(SC-39100组)。以CCK-8实验检测A549细胞的增殖能力;划痕实验检测A549细胞的迁移能力;Transwell实验检测A549细胞的侵袭能力;蛋白免疫印迹实验分析A549细胞中JAK2、STAT3蛋白的表达量。[结果]MST4在非小细胞肺癌组织中表达增加(0.39±0.03 vs 0.83±0.05,P<0.05),非小细胞肺癌细胞(H358、A549和H1299)细胞株中的MST4表达水平增加(0.11±0.03 vs 0.89±0.05 vs 0.88±0.02 vs 0.91±0.09,P<0.05)。与阴性对照组相比,si MST4以及SD-1029组的A549细胞增殖能力下降,SC-39100组的A549细胞增殖能力增加;si MST4以及SD-1029组的A549细胞迁移能力下降,SC-39100组的A549细胞迁移能力增加;si MST4以及SD-1029组的A549细胞的侵袭能力下降,SC-39100组的A549细胞侵袭能力增加;si MST4以及SD-1029组的A549细胞JAK2、STAT3蛋白表达减少(0.85±0.07 vs 0.19±0.05 vs 0.80±0.02 vs 0.81±0.08,P<0.05;0.61±0.03 vs 0.26±0.09 vs 0.28±0.02 vs 0.89±0.05,P<0.05;0.63±0.03 vs 0.29±0.07 vs 0.31±0.01 vs 0.88±0.03,P<0.05),SC-39100组的A549细胞JAK2、STAT3蛋白表达增加。[结论]MST4在非小细胞肺癌细胞以及组织中表达上调。抑制MST4表达后,A549细胞的增殖活性、迁移与侵袭能力降低,该作用与MST4调节JAK2/STAT3信号通路相关。
