搜索到685篇“ F-ACTIN“的相关文章
Plectin通过诱导F-actin聚合增强肝癌细胞的迁移能力
2024年
目的研究Plectin的表达与肝癌细胞迁移能力的关系,揭示Plectin表达影响肝癌细胞迁移行为的分子机理。方法首先,Western blot检测正常肝细胞和肝癌细胞中Plectin的表达。其次,构建Plectin下调的肝癌细胞株,设立对照组(shNC组)和shPLEC组,各组分别设溶剂对照组(shNC+DMSO组或shPLEC+DMSO组)和F-actin骨架聚合诱导剂Jasplakinolide组(shNC+Jasp组或shPLEC+Jasp组)。采用Western blot检测各组肝癌细胞中Plectin的表达及上皮-间质转化(epithelial-mesenchymal transition,EMT)相关分子(N-cadherin、vimentin和E-cadherin)的表达;采用Transwell小室法分析肝癌细胞的迁移能力;采用KEGG(Kyoto Encyclopedia of Genes and Genomes)分析与Plectin基因有关的信号通路;采用免疫荧光技术检测Plectin表达变化对细胞骨架F-actin聚合的影响。结果与正常肝细胞相比,Plectin在肝癌细胞中高表达。与shNC组相比,shPLEC组Plectin的表达降低(P<0.05),肝癌细胞的迁移能力减弱(P<0.05),EMT进程被抑制(N-cadherin和vimentin表达降低,E-cadherin表达升高)(P<0.05);KEGG分析发现细胞骨架F-actin调控与Plectin的联系最为密切,shPLEC组肝癌细胞骨架F-actin发生解聚。采用F-actin骨架聚合诱导剂Jasplakinolide处理后,与shPLEC+DMSO组相比,shPLEC+Jasp组肝癌细胞迁移能力增强(P<0.05),EMT进程有所恢复(N-cadherin和vimentin表达升高,E-cadherin表达降低)(P<0.05),同时肝癌细胞骨架F-actin聚合亦有所恢复。结论Plectin在肝癌细胞中高表达,肝癌细胞中Plectin通过诱导F-actin聚合促进肝癌细胞的迁移和EMT。
徐茹霜杨凌霄宋关斌
关键词:PLECTIN肝癌细胞上皮-间质转化细胞骨架F-ACTIN
一种抗F-Actin抗体检测试剂盒和方法
本发明涉及一种磁珠标记F‑Actin抗原的方法,包括:向磁珠中加入0.05‑0.1M PB和F‑Actin抗原,并于15‑37度混匀反应2‑3小时;去除上清液,加入磁珠封闭液,并于15‑37度混匀5‑18小时;去除上清液...
李雁飞张水平
ECT2/SERPINE1/F-actin促进胶质瘤侵袭迁移能力机制的研究
研究背景:胶质瘤是成年人常见的原发性脑恶性肿瘤之一,其中恶性程度最高的是胶质母细胞瘤(Glioblastoma,GBM),对人类健康危害极大,预后不良。GBM患者预后差很大程度上是由于其侵袭能力强,瘤细胞异质性大以及手术...
陈光樑
关键词:胶质瘤F-ACTIN
ISKNV介导Rac1-PAK1-LIMK-Cofilin信号通路调控F-actin重排促进自身复制增殖
传染性脾肾坏死病毒(Infectious spleen and kidney necrosis virus,ISKNV)可感染多种鱼类,是造成鳜发病的主要病原之一,严重危害鳜养殖业的健康发展。微丝(F-actin)是细胞...
谭有燕
关键词:F-ACTIN
CXCR5 Regulates Neuronal Polarity Development and Migration in the Embryonic Stage via F‑Actin Homeostasis and Results in Epilepsy‑Related Behavior
2023年
Epilepsy is a common,chronic neurological disorder that has been associated with impaired neurodevelopment and immunity.The chemokine receptor CXCR5 is involved in seizures via an unknown mechanism.Here,we first determined the expression pattern and distribution of the CXCR5 gene in the mouse brain during different stages of development and the brain tissue of patients with epilepsy.Subsequently,we found that the knockdown of CXCR5 increased the susceptibility of mice to pentylenetetrazol-and kainic acid-induced seizures,whereas CXCR5 overexpression had the opposite effect.CXCR5 knockdown in mouse embryos via viral vector electrotransfer negatively influenced the motility and multipolar-to-bipolar transition of migratory neurons.Using a human-derived induced an in vitro multipotential stem cell neurodevelopmental model,we determined that CXCR5 regulates neuronal migration and polarization by stabilizing the actin cytoskeleton during various stages of neurodevelopment.Electrophysiological experiments demonstrated that the knockdown of CXCR5 induced neuronal hyperexcitability,resulting in an increased number of seizures.Finally,our results suggested that CXCR5 deficiency triggers seizure-related electrical activity through a previously unknown mechanism,namely,the disruption of neuronal polarity.
Zhijuan ZhangHui ZhangAna Antonic‑BakerPatrick KwanYin YanYuanlin Ma
关键词:EPILEPSYCXCR5F-ACTIN
果蝇合胞体胚胎中微丝和微管的动态调控
2023年
果蝇胚胎的卵裂为不完全卵裂,经过十三次细胞核分裂,形成合胞体囊胚。从受精到形成合胞体囊胚,经历了雌雄原核融合、细胞核轴向延伸、皮质迁移、皮质有丝分裂等过程。微丝和微管广泛参与果蝇合胞体胚胎的发育过程。该文梳理了果蝇合胞体胚胎形态发生的细胞学基础以及细胞骨架动态特征,并探讨了果蝇合胞体胚胎的特殊属性对细胞骨架研究的潜在价值。
王国庆尹传淏吕志一
关键词:微丝微管
Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer Metastasis被引量:2
2023年
F-actin(filamentous actin)has been shown to be sensitive to mechanical stimuli and play critical roles in cell attachment,migration,and cancer metastasis,but there are very limited ways to perturb F-actin dynamics with low cell toxicity.Magnetic field is a noninvasive and reversible physical tool that can easily penetrate cells and human bodies.Here,we show that 0.1/0.4-T 4.2-Hz moderate-intensity low-frequency rotating magnetic field-induced electric field could directly decrease F-actin formation in vitro and in vivo,which results in decreased breast cancer cell migration,invasion,and attachment.Moreover,lowfrequency rotating magnetic fields generated significantly different effects on F-actin in breast cancer vs.noncancerous cells,including F-actin number and their recovery after magnetic field retrieval.Using an intermittent treatment modality,low-frequency rotating magnetic fields could significantly reduce mouse breast cancer metastasis,prolong mouse survival by 31.5 to 46.0%(P<0.0001),and improve their overall physical condition.Therefore,our work demonstrates that low-frequency rotating magnetic fields not only can be used as a research tool to perturb F-actin but also can inhibit breast cancer metastasis through F-actin modulation while having minimum effects on normal cells,which reveals their potential to be developed as temporal-controlled,noninvasive,and high-penetration physical treatments for metastatic cancer.
Xinmiao JiXiaofei TianShuang FengLei ZhangJunjun WangRuowen GuoYiming ZhuXin YuYongsen ZhangHaifeng DuVitalii ZablotskiiXin Zhang
关键词:METASTASISINVASION
TRPM7 Kinase Domain is Part of the Rac1-SSH2-cofilin Complex Regulating F-actin in the Mouse Nervous System
2023年
Dear Editor,The ion channel transient receptor potential melastatin-like 7(TRPM7)has a serine-threonineα-kinase domain(M7CK)on its intracellular C-terminal[1,2].In cell lines,M7CK is cleaved and translocated to the nucleus to regulate a variety of cellular processes including cell proliferation and survival[3].In neuroblastoma cells.
Junzhuang ChangCui ChenWei LiNashat Abumaria
关键词:RAC1SSH2NEUROBLASTOMA
Yes相关蛋白通过调控细胞骨架F-actin蛋白表达抑制肿瘤坏死因子-α引起的肠上皮屏障损伤被引量:2
2022年
目的探讨Yes相关蛋白(YAP)在肠上皮屏障损伤中的作用及分子机制。方法培养人结肠腺癌细胞株Caco-2细胞建立肠上皮屏障模型,分为4组:对照组,正常建好屏障的Caco-2细胞不做任何处理;重组人肿瘤坏死因子(rhTNF)-α组,建好屏障的Caco-2细胞加入rhTNF-α100μg/L刺激细胞;Vector+rhTNF-α组,建好屏障的Caco-2细胞先加入对照质粒pcDNA3.1-vector,24 h后加入rhTNF-α100μg/L刺激细胞;YAP+rhTNF-α组,建好屏障的Caco-2细胞先加入YAP质粒pcDNA3.1-YAP,24 h后加入rhTNF-α100μg/L刺激细胞。通过实时定量PCR和Western blot检测YAP mRNA和蛋白表达,应用跨膜电阻(TEER)和荧光黄透过率检测细胞膜通透性,免疫荧光染色观察细胞骨架蛋白F-actin分布情况。结果与对照组[(607.3±29.3)Ω·cm^(2)]相比,rhTNF-α组TEER[(265.3±32.7)Ω·cm^(2)]明显下降,而YAP+rhTNF-α组TEER[(387.0±18.7)Ω·cm^(2)]较rhTNF-α组明显升高,差异均有统计学意义(P<0.001)。荧光黄透过率结果显示,rhTNF-α组(22.7%±0.5%)较对照组(6.3%±0.9%)明显增加,而YAP+rhTNF-α组(12.2%±0.8%)较rhTNF-α组明显降低,差异均有统计学意义(P<0.001)。免疫荧光染色结果显示,与对照组相比,rhTNF-α组细胞骨架F-actin纤维致密斑减少,部分细胞出现明显横跨细胞的应力纤维结构,而YAP+rhTNF-α组周边肌动蛋白丝带较清晰,胞质内应力纤维减少。结论YAP可抑制TNF-α引起的Caco-2细胞TEER下降、荧光黄透过率增加和细胞骨架F-actin重排。YAP通过调控细胞骨架蛋白F-actin表达从而改善TNF-α介导的肠上皮屏障功能损伤。
叶晓琳吴捷曹培同王东伟
关键词:炎症性肠病肠上皮屏障肿瘤坏死因子-Α
细粒棘球蚴囊液通过WASP/Arp2/3/F-actin通路抑制小鼠腹腔巨噬细胞吞噬功能的初步研究
2022年
目的 探讨细粒棘球蚴囊液(EgCF)通过成核促进因子Wiskott-Aldrich综合征蛋白(WASP),肌动蛋白相关蛋白(Arp)2/3复合体和肌动蛋白丝(F-actin)对小鼠腹腔巨噬细胞吞噬能力的影响。方法 分离C57BL/6小鼠腹腔巨噬细胞体外培养,分为对照组(Control),囊液(2.0 mg·mL^(-1))处理24 h组,囊液处理48 h组,囊液处理96 h组。流式细胞术检测细粒棘球蚴囊液对小鼠巨噬细胞吞噬能力的影响,Western blot检测WASP,Arp2的蛋白表达水平;激光共聚焦观察Arp2和F-actin蛋白表达及Arp2与F-actin的共定位与细胞骨架变化。结果 与对照组相比,囊液处理48 h和96 h后巨噬细胞吞噬能力显著降低(P<0.01);WASP,Arp2蛋白表达水平显著降低(P<0.01);免疫荧光结果显示,Arp2,F-actin平均荧光强度下降,Arp2与F-actin共定位程度下降,细胞伪足伸出不明显。结论 细粒棘球蚴囊液诱导小鼠腹腔巨噬细胞吞噬能力降低,与WASP、Arp2/3复合体和F-actin共同参与的细胞骨架异常重排有关。
贺飞明董丹陈宇婷蔺珂廖原吴向未陈雪玲
关键词:细粒棘球蚴巨噬细胞

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