Expression of Inositol 1,4,5
医学常用试剂缩写
collagen induced thrombus formation collagen membranes学文献光盘数据库
细胞膜
细胞质膜
厘泊(黏度单位)
脑梗死
趋化吸引剂
α-趋化因子受体
氯化丙咪嗪
产色多肽基质法
carboxypeptidase B carcino-embryonic antigen(CEA)
cardiopulmonary bypass(CPB)
carotid artery catalytic triad cathepsin G(CG)
GCBMdisc cell membrane(CM)
activated partial thromboplastin time(APTT)
activated protein C(APC)
activated protein C receptor(APCR)
activated protein C resistance(APCR)
Cactivation receptor actomyosin
α-fetal protein (AFP) (血小板)黏附障碍
analytical process analytical variability angioplasty 黏附蛋白
annexin Ⅱ ADP受体
annexin Ⅴ α2肾上腺素能受体
anticoagulant protein anti-nuclear antibody(ANA) 肾上腺素
contact activation pathway contact product-forming activity(CPFA)
Akt在非小细胞肺癌中作用的研究现状
Akt在非小细胞肺癌中作用的研究现状陈勃江【摘要】肺癌是目前世界上最常见的恶性肿瘤之一,但其发病机制尚不完全清楚.Akt是一种重要的信号通路关键蛋白,广泛参与肿瘤细胞的生长、增殖、凋亡及侵袭等过程.本文就Akt及其重要的上下游调节分子之--PDK1、Raf-1和p70S6K 在非小细胞肺癌中的作用研究现状做一综述,以期为阐明非小细胞肺癌的发病机制提供新的依据.【期刊名称】《中国肺癌杂志》【年(卷),期】2010(013)011【总页数】5页(P1059-1063)【关键词】Akt;PDK1;Raf-1;肺肿瘤【作者】陈勃江【作者单位】610041成都,四川大学华西医院呼吸内科【正文语种】中文【中图分类】R734.2肺癌是目前对人类健康威胁最大的恶性肿瘤之一，全球每年约有135万人被确诊为肺癌，120万人死于肺癌[1]。
虽然医学技术有了长足发展，但肺癌患者的5年生存率并未得到明显改善，仅为15%左右[1]。
其根本原因在于肺癌的发病机制尚不清楚、临床缺乏有效的早期诊断和治疗手段。
病理学上，肺癌分为小细胞肺癌（small cell lung cancer, SCLC）和非小细胞肺癌（non-small cell lung cancer, NSCLC），后者约占80%-85%。
20世纪90年代以来，信号传导通路逐渐成为肿瘤学研究领域的热点。
丝氨酸/苏氨酸蛋白激酶B（protein kinase B, PKB/Akt）因其处于多条信号通路的交叉点而受到广泛关注。
1 Akt 的研究现状Akt是存在于人类染色体基因组中鼠类胸腺淋巴瘤病毒（T-8 strain from AKR/J mouse, AKT8）致癌基因（v-Akt）的同源物，其编码的蛋白质Akt是一种丝氨酸/苏氨酸蛋白激酶，因与蛋白激酶A、C高度同源，又名蛋白激酶B（protein kinase B, PKB）[2]。
Akt经磷脂酰肌醇3-激酶（phosphatidylinositol 3-kinase, PI3K）活化后，磷酸化其下游多种底物，参与细胞生物学功能的调节，影响细胞生物学行为，主要表现为促进细胞增殖、抑制细胞凋亡、提高细胞的乏氧耐受性、促进肿瘤细胞侵袭转移和组织血管生成等，从而参与多种肿瘤的发生[3]。
未折叠蛋白反应英语
未折叠蛋白反应英语The Unfolded Protein Response.The unfolded protein response (UPR) is a cellular signaling pathway that is activated when the endoplasmic reticulum (ER) experiences a buildup of unfolded or misfolded proteins. This response is crucial for maintaining cellular homeostasis and preventing the accumulation of potentially harmful proteins. The UPR serves to restore ER function by enhancing protein folding capacity, reducing protein translation, and promoting the degradation of damaged proteins.The ER is a crucial organelle responsible for protein synthesis, folding, and trafficking. When the ER is unable to cope with the demand for protein folding, it triggers the UPR to address the imbalance. This imbalance can be caused by various factors such as changes in cellular metabolism, environmental stress, or mutations that affect protein folding.The UPR is initiated by three ER-resident transmembrane proteins: protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6 (ATF6). Under normal conditions, these proteins are bound to the ER chaperone BiP/GRP78, which inhibits their activation. However, when unfolded proteins accumulate in the ER, BiP/GRP78 dissociates from these sensors, allowing them to initiate the UPR.PERK activation leads to the phosphorylation of the eukaryotic translation initiation factor 2α (eIF2α), which attenuates global protein synthesis. This reductionin protein synthesis reduces the load on the ER, allowingit to focus on folding the existing proteins. Additionally, phosphorylated eIF2α promotes the translation of specific mRNAs, including those encoding transcription factors such as ATF4, which induce the expression of genes involved in amino acid metabolism, oxidative stress resistance, and chaperone synthesis.IRE1α activation leads to its endonuclease activity, which splices the mRNA of the transcription factor XBP1. This splicing event converts XBP1 from an inactive form to an active form that can regulate the expression of genes involved in ER expansion, lipid metabolism, and protein degradation.ATF6 activation leads to its translocation to the Golgi apparatus, where it is cleaved to release its cytosolic domain. This cleaved ATF6 fragment then enters the nucleus and activates the expression of genes encoding chaperones, ER-associated degradation (ERAD) components, and other proteins that enhance ER function.Collectively, these UPR signaling branches aim to restore ER homeostasis by enhancing protein folding capacity, reducing protein synthesis, and promoting the degradation of damaged proteins. If the ER stress persists despite these adaptive responses, the UPR can also trigger apoptotic signaling, leading to cell death.The UPR plays a crucial role in maintaining cellularprotein homeostasis and preventing the accumulation of potentially harmful proteins. Its activation is a highly conserved mechanism across different cell types and organisms, indicating its importance in maintainingcellular function and survival.In summary, the unfolded protein response is a complex cellular signaling pathway that is activated in response to ER stress. It involves the activation of three ER-resident sensors, PERK, IRE1α, and ATF6, which trigger adaptive responses to restore ER homeostasis. These responses include enhancing protein folding capacity, reducing protein synthesis, and promoting the degradation of damaged proteins. The UPR is crucial for maintaining cellular protein homeostasis and preventing the accumulation of potentially harmful proteins.。
Hoechst33342染色液
2. Yao G, Ling L, Luan J, Ye D, Zhu P. Nonylphenol induces apoptosis of Jurkat cells by a caspase-8 dependent mechanism. Int Immunopharmacol. 2007 Apr;7(4):444-53.
17. Gao X, Zhang X, Yang X. Morphological apoptotic characteristics of the post-meiotic micronuclei in Paramecium caudatum. Eur J Protistol. 2010;46(3):243-50. Epub 2010 May 21.
3. Wang Q, Wang Y, Liang C, Song J, Chen X. Identification of a hydrophobic domain of HA2 essential to morphogenesis of Helicoverpa armigera nucleopolyhedrovirus. J Virol. 2008 Apr;82(8):4072-81. Epub 2008 Jan 30.
神曲消食口服液对功能性消化不良小鼠胃肠运动的影响及机制
其病 情 多 反 复、 迁 延, 严 重 影 响 患 儿 身 心 健 康
[2]
。
目前,临床治疗常以经验性治疗为主,西药治疗后
往往会出现口苦、咽干等不良反应,导致患儿依从
性较差,影响治疗效果
[3]
。 赵咏梅等
[4]
研究指出,
神曲消食口服液对儿童功能性消化有较好的临床
gastrointestinal motility in mice with functional dyspepsia ( FD) . Methods This study involved 50 KM mice. Ten mice
were randomly assigned to the normal group, and the remaining 40 mice were used to establish animal models of FD by
mice with FD, which may be related to down-regulation of the expression of the endoplasmic reticulum factors IR11 and
TRAF2.
【 Keywords】 Shenqu Xiaoshi oral liquid; routine blood testing; liver and kidney function; functional dyspepsia;
Effects and mechanism of Shenqu Xiaoshi oral liquid on gastrointestinal
motility in mice with functional dyspepsia
0003碧云天磷酸酯酶抑制剂试剂盒说明书
包装清单：
产品编号 S1873 —
产品名称 Sodium orthovanadate (磷酸酯酶抑制剂)
说明书
包装 2g 1份
保存条件：
室温本产品对人体有害，操作时请小心，并注意有效防护以避免直接接触人体或吸入体内。 为了您的安全和健康，请穿实验服并戴一次性手套操作。
Sodium orthovanadate (磷酸酯酶抑制剂)
产品编号 S1873
产品名称 Sodium orthovanadate (磷酸酯酶抑制剂)
包装 2g
产品简介：
Sodium orthovanadate ， 中 文 名 为 正 钒 酸 钠 ， 是 一 种 常 用 的 磷 酸 酯 酶 抑 制 剂 ， 可 以 抑 制 碱 性 磷 酸 酯 酶 (alkaline phosphatase) ， 酸 性 磷 酸 酯 酶 (acid phosphatase) ， 蛋 白 酪 氨 酸 磷 酸 酯 酶 (tyrosine phosphatase) 等 磷 酸 酯 酶 。 Sodium orthovanadate也可以抑制Na+/K+ ATPase等ATPase。常用于抑制蛋白去磷酸化或促进蛋白的磷酸化激活，在提取细胞或组 织蛋白时常用于保持蛋白的磷酸化状态。
6. Sun SQ, Jiang CG, Lin Y, Jin YL, Huang PL. Enhanced T cell immunity by B7-H4 downregulation in nonsmall-cell lung cancer cell lines.
J Int Med Res. 2012;40(2):497-506. 7. Zhou L, Xue H, Wang Z, Ni J, Yao T, Huang Y, Yu C, Lu L.
C1025 Hoechst33342染色液
9. Zeng X, Nan F, Liang C, Song J, Wang Q, Vlak JM, Chen X. Functional analysis of the Autographa californica nucleopolyhedrovirus IAP1 and IAP2. Sci China C Life Sci. 2009 Aug;52(8):761-70. Epub 2009 Aug 29.
1. Li HG, Liao AH, Ding XF, Zhou H, Xiong CL. The expression and significance of CATSPER1 in human testis and ejaculated spermatozoa. Asian J Androl. 2006 May;8(3):301-6.
350nm，最大发射波长为461nm。 ¾ 本Hoechst 33342染色液可直接用于固定细胞或组织的细胞核染色，也可直接用于活细胞或组织的细胞核染色。
包装清单：
产品编号
C1025 —
产品名称 Hoechst 33342 染色液
IP3R1调控CaMKII和VDAC1在海洛因致心肌细胞节律异常中的作用
IP3R1调控CaMKII 和VDAC1在海洛因致心肌细胞节律异常中的作用*管雅玲1， 肖锦玲1， 苏丽萍2， 庄梦婕1， 刘丽2， 季敏2， 朱森森1，刘静宇1， 戴晨璐1， 蒲红伟3△（1新疆医科大学基础医学院，新疆 乌鲁木齐 830017；2新疆医科大学第一附属医院病理科，新疆 乌鲁木齐830054；3新疆医科大学第一附属医院学科建设科，新疆 乌鲁木齐 830054）［摘要］ 目的：探讨1，4，5-三磷酸肌醇1型受体（inositol 1，4，5-trisphosphate receptor type 1， IP3R1）调控钙/钙调蛋白依赖性蛋白激酶II （calcium/calmodulin -dependent protein kinase II ， CaMKII ）和电压依赖性阴离子通道1（voltage -dependent anion channel 1， VDAC1）在海洛因（heroin ， HE ）致心肌细胞节律异常中的作用。
方法：联合蛋白组学和GEO （Gene Expression Omnibus ）数据库分析心律失常芯片数据，寻找关键调控因子。
构建IP3R1基因敲减慢病毒并感染原代乳大鼠心肌细胞（neonatal rat cardiomyocytes ， NRCMs ），实验分为对照（control ）组、HE 组和HE+shIP3R1组。
结晶紫染色观察心肌细胞形态；ELISA 法检测乳酸脱氢酶（lactate dehydrogenase ， LDH ）和天冬氨酸转氨酶（aspartate aminotransferase ， AST ）水平；透射电镜观察线粒体形态学变化；Fluo -4/AM 探针法检测细胞内Ca 2+浓度；DCFH -DA 荧光探针检测细胞内活性氧（reactive oxygen species ， ROS ）含量；JC -1染色法检测线粒体膜电位（mitochondrial membrane potential ， MMP ）水平；ATP 检测试剂盒检测细胞内ATP 水平；免疫共沉淀（co -immunopre‑cipitation ， Co -IP ）分析IP3R1与CaMKIIδ和VDAC1蛋白之间的相互作用；Western blot 检测IP3R1、CaMKIIδ、p -CaM‑KIIδ（T287）和VDAC1的蛋白水平。