论文部分内容阅读
Response of Soil Physicochemical Properties to Rocky Desertification Succession in South China Karst
【机 构】
：
Guizhou Normal University
【出 处】
：
第十五届中国生态学大会
【发表日期】
：
2016年4期
其他文献
目的：利用H2O2诱导的小鼠视网膜661w 细胞凋亡模型,研究17β-雌二醇(17β-Estradiol,βE2)通过雌激素受体(ER)与NF-E2 相关因子(nuclear factor erythroid 2-related factor 2,NRF2)的相互作用保护视网膜细胞的分子机制,为阐明βE2 保护视网膜作用的分子机制提供实验依据,也为视网膜退行性疾病的防治寻找新的靶点提供思路.方法：
目的：研究膜联蛋白ANXA11,miR-4521和FAM129A表达水平与慢性粒细胞白血病(CML)相关性,探讨三者间形成调控K562细胞恶性行为的新途径.方法：ANXA11干扰质粒稳转K562,获得ANXA11下调单克隆细胞株；CCK-8法和克隆形成实验检测ANXA11下调对K562增殖影响；Transwell法检测ANXA11下调对K562迁移及侵袭影响；检测ANXA11,miR-4521,F
在炎症反应发生时,白细胞粘附并穿过血管上的内皮细胞,在炎症部位发生募集。白细胞的粘附触发了内皮细胞上粘附分子P-选择素、E-选择素、细胞间粘附分子-1(ICAM-1)与微丝骨架的连接,在上述信号分子的调控下,导致微丝细胞骨架的快速、动态重组,并通过肌球蛋白轻链激酶调控白细胞的跨内皮迁移,但有关E-选择素调控微丝骨架、进而调控内皮细胞重组的现象、功能和信号转导机制目前鲜有报道。本文尝试从细胞骨架动力
Celastrol prevents cadmium-induced neuronal cell death by blocking mitochondrial ROS inactivation of
We have recently reported that celastrol prevents cadmium(Cd)-induced neuronal cell death by inhibiting Cd-activation of mammalian target of rapamycin(mTOR)pathway.Here we show that this was associate
GLI1 zinc finger protein is a transcription factor involved in the intracellular signal transduction controlled by the Hedgehog family of secreted molecules.Their abnormal regulation is implicated in
The function of the Nde1/Lis1/Dynein signaling pathway is evolutionarily conserved from fungi to mammals.Molecular and cellular studies demonstrate that Nde1/Lis1/Dynein signaling pathway is involved
Sweet state is a basic physiological sensation of humans and other mammals which is mediated by the broadly acting sweet taste receptor-the heterodimer of Tas1r2(taste receptor type 1 member 2)and Tas
Atherosclerosis(AS)is the primary cause leading to cardiovascular disease,the number of annual deaths due to AS-related diseases account for more than half of total global deaths.Exploring the pathoge
Ectodermal dysplasiais a group of syndromes that involves abnormalities of the ectodermal structures including hairs,glands,teeth and so on.Hypodontiabelongs to ectodermal dysplasia,X-linked hypohidro
目的：过表达CRKI/Ⅱ及低表达CRKII对Hca-P细胞体外增殖、克隆形成、迁移、侵袭、黏附影响；明确p130cas/CRK/Dock180/Rac1通路中起主导作用CRK成员；研究肿瘤潜在制剂去整合素rAdibitor通过该通路的作用机制.方法：1.构建pcDNA3.1/V5-HisB-CRKI过表达载体,稳转Hca-P,获得CRKI稳定上调细胞株,考察CRKI过表达Hca-P增殖、迁移、侵袭