多聚腺苷酸结合蛋白相互作用蛋白1[Poly(A)-binding protein-interacting protein 1,Paip1]是哺乳动物特有的蛋白质,可有效参与真核生物基因表达及细胞周期调控,并与肿瘤演进及预后密切相关。近年来Paip1成为肿瘤研究热点,Paip1与肿瘤...多聚腺苷酸结合蛋白相互作用蛋白1[Poly(A)-binding protein-interacting protein 1,Paip1]是哺乳动物特有的蛋白质,可有效参与真核生物基因表达及细胞周期调控,并与肿瘤演进及预后密切相关。近年来Paip1成为肿瘤研究热点,Paip1与肿瘤细胞增殖、迁移、侵袭和上皮间质转化进程密切相关,可能是肿瘤进展及预后不良的潜在生物标志和新的治疗靶点。但其具体作用机制尚未阐明。本文就Paip1的结构、功能、泛素化和降解及其与肿瘤的关系等方面作一综述,为其在肿瘤中的研究提供新思路。展开更多
目的研究姜黄素与高脂饮食小鼠胆囊胆固醇性结石关系及可能参与调控过程的因子。方法将C57BL6小鼠50只随机分为5组,其中一组予普通饲料,其余四组予高脂饮食饲料,同时灌喂不同剂量姜黄素[0、200、500、1 000 mg/(kg·d)],共4周。计...目的研究姜黄素与高脂饮食小鼠胆囊胆固醇性结石关系及可能参与调控过程的因子。方法将C57BL6小鼠50只随机分为5组,其中一组予普通饲料,其余四组予高脂饮食饲料,同时灌喂不同剂量姜黄素[0、200、500、1 000 mg/(kg·d)],共4周。计算小鼠胆囊结石成石率,收集小鼠血液、胆囊胆汁、胆囊、肝脏以及小肠。计算胆囊容积,称量肝脏质量,检测血液及胆汁胆固醇、甘油三酯等生化指标。用Realtime PCR及Western blotting方法分别检测小鼠小肠上皮NPC1L1及SREBP2 m RNA及蛋白表达。结果姜黄素能够降低小鼠胆囊结石的发生,大剂量姜黄素可降低胆囊结石发生率达60%,同时降低肝脏脂肪变性程度,降低小鼠血液胆固醇饱和度。同时,姜黄素可以抑制高脂饮食所致的NPC1L1 m RNA表达上调[(2.65±0.04)vs(2.06±0.07),(1.69±0.06),(1.33±0.05),P<0.01],且呈现剂量依赖关系,降低高脂饮食所致的NPC1L1蛋白高表达。姜黄素还可以抑制高脂饮食所致的SREBP2 m RNA表达上调[(1.34±0.08)vs(1.39±0.03),(1.19±0.01),(1.06±0.03),P<0.05],且呈现剂量依赖关系,降低高脂饮食所致的SREBP2蛋白表达上调。结论姜黄素能够降低高脂饮食小鼠胆囊结石的形成,NPC1L1和SREBP2可能参与了这个过程。展开更多
CREB-binding protein （CBP） and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, ce...CREB-binding protein （CBP） and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentia- tion and apoptosis. Several studies have suggested that CBP and p300 might be considered as tumour suppressors, with their prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli. They exert their actions mainly via acetylation of histones and other regulatory proteins （e.g. p53）. A major paradox in CBP/ p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberrations. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimate converging point of these derangements, and CBP/p300 represents key participants in this interplay. Thus, illumination of their molecular actions and interactions could reveal new potential targets for pharmacological interventions in respiratory epithelium carcinogenesis.展开更多
文摘多聚腺苷酸结合蛋白相互作用蛋白1[Poly(A)-binding protein-interacting protein 1,Paip1]是哺乳动物特有的蛋白质,可有效参与真核生物基因表达及细胞周期调控,并与肿瘤演进及预后密切相关。近年来Paip1成为肿瘤研究热点,Paip1与肿瘤细胞增殖、迁移、侵袭和上皮间质转化进程密切相关,可能是肿瘤进展及预后不良的潜在生物标志和新的治疗靶点。但其具体作用机制尚未阐明。本文就Paip1的结构、功能、泛素化和降解及其与肿瘤的关系等方面作一综述,为其在肿瘤中的研究提供新思路。
文摘目的研究姜黄素与高脂饮食小鼠胆囊胆固醇性结石关系及可能参与调控过程的因子。方法将C57BL6小鼠50只随机分为5组,其中一组予普通饲料,其余四组予高脂饮食饲料,同时灌喂不同剂量姜黄素[0、200、500、1 000 mg/(kg·d)],共4周。计算小鼠胆囊结石成石率,收集小鼠血液、胆囊胆汁、胆囊、肝脏以及小肠。计算胆囊容积,称量肝脏质量,检测血液及胆汁胆固醇、甘油三酯等生化指标。用Realtime PCR及Western blotting方法分别检测小鼠小肠上皮NPC1L1及SREBP2 m RNA及蛋白表达。结果姜黄素能够降低小鼠胆囊结石的发生,大剂量姜黄素可降低胆囊结石发生率达60%,同时降低肝脏脂肪变性程度,降低小鼠血液胆固醇饱和度。同时,姜黄素可以抑制高脂饮食所致的NPC1L1 m RNA表达上调[(2.65±0.04)vs(2.06±0.07),(1.69±0.06),(1.33±0.05),P<0.01],且呈现剂量依赖关系,降低高脂饮食所致的NPC1L1蛋白高表达。姜黄素还可以抑制高脂饮食所致的SREBP2 m RNA表达上调[(1.34±0.08)vs(1.39±0.03),(1.19±0.01),(1.06±0.03),P<0.05],且呈现剂量依赖关系,降低高脂饮食所致的SREBP2蛋白表达上调。结论姜黄素能够降低高脂饮食小鼠胆囊结石的形成,NPC1L1和SREBP2可能参与了这个过程。
文摘CREB-binding protein （CBP） and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentia- tion and apoptosis. Several studies have suggested that CBP and p300 might be considered as tumour suppressors, with their prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli. They exert their actions mainly via acetylation of histones and other regulatory proteins （e.g. p53）. A major paradox in CBP/ p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberrations. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimate converging point of these derangements, and CBP/p300 represents key participants in this interplay. Thus, illumination of their molecular actions and interactions could reveal new potential targets for pharmacological interventions in respiratory epithelium carcinogenesis.
