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Search Results: 1 - 10 of 22227 matches for " c-Jun "
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Cucurbitacin-I (JSI-124) activates the JNK/c-Jun signaling pathway independent of apoptosis and cell cycle arrest in B Leukemic Cells
Ganchimeg Ishdorj, James B Johnston, Spencer B Gibson
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-268
Abstract: BJAB, I-83, NALM-6 and primary CLL cells were treated with JSI-124 as indicated. Apoptosis was measured using flow cytometry for accumulation of sub-G1 phase cells (indicator of apoptosis) and Annexin V/PI staining. Cell cycle was analyzed by FACS for DNA content of G1 and G2 phases. Changes in phosphorylation and protein expression of p38, Erk1/2, JNK, c-Jun, and XIAP were detected by Western blot analysis. STAT3 and c-Jun genes were knocked out using siRNA transfection. VEGF expression was determined by mRNA and protein levels by RT-PCR and western blotting. Streptavidin Pull-Down Assay was used to determine c-Jun binding to the AP-1 DNA binding site.Herein, we show that JSI-124 activates c-Jun N-terminal kinase (JNK) and increases both the expression and serine phosphorylation of c-Jun protein in the B leukemic cell lines BJAB, I-83 and NALM-6. JSI-124 also activated MAPK p38 and MAPK Erk1/2 albeit at lower levels than JNK activation. Inhibition of the JNK signaling pathway failed to effect cell cycle arrest or apoptosis induced by JSI-124 but repressed JSI-124 induced c-Jun expression in these leukemia cells. The JNK pathway activation c-Jun leads to transcriptional activation of many genes. Treatment of BJAB, I-83, and NALM-6 cells with JSI-124 lead to an increase of Vascular Endothelial Growth Factor (VEGF) at both the mRNA and protein level. Knockdown of c-Jun expression and inhibition of JNK activation significantly blocked JSI-124 induced VEGF expression. Pretreatment with recombinant VEGF reduced JSI-124 induced apoptosis.Taken together, our data demonstrates that JSI-124 activates the JNK signaling pathway independent of apoptosis and cell cycle arrest, leading to increased VEGF expression.Cucurbitacin-I (JSI-124) can be found in a variety of plants that have been used for centuries as folk medicines in Asia [1-3]. However, the molecular mechanisms responsible for the various biological effects of JSI-124 have not been fully investigated. JSI-124 is a sel
Model based design of inhibitors for c-jun
Pallavi Chauhan 1,Madhvi Shakya
Bioinformation , 2009,
Abstract: Literature shows that various molecular cascades are activated by stress, UV rays and pollutants leading to wrinkle formation of the skin. These cascades start from five types of receptors (EGFR, PDGFR, PAFR, IL1R, TNFRB) and terminate with the production of matrix metalloproteinase’s, which degrades collagen leading to wrinkle formation. Signaling pathway leading to wrinkle formation showed that c-jun is involved in these cascades. Therefore, c-jun is the preferential choice for inhibition to reduce the intensity of collagen degradation. Hence, the 3D structure of c-jun was modeled using segment based homology modeling by MODELLER 9v5. Evaluation of the constructed model was done by PROCHECK, WHAT CHECK and through RMSD/RMSF calculations. Ligands for the inhibitory sites were designed using LIGANDSCOUT. The interaction study of ligand and receptor was performed by AUTODOCK. A library of analogues was constructed for three known inhibitory sites. The receptor-analogue study was performed using the software MOLEGRO Virtual Docker. The analogues constructed from the designed novel reference ligands showed good binding with the receptor binding sites. It should be noted that these predicted data should be validated using suitable assays for further consideration.
中国公共卫生 , 2005, DOI: 10.11847/zgggws2005-21-02-30
Abstract: ?目的观察铅对小鼠学习记忆功能及海马区cjun表达的影响。方法5~6周龄小白鼠交配后,通过饮水饲以不同浓度醋酸铅2.4,4.8,9.6mmol/L。小鼠子代自胚胎期始即暴露于醋酸铅。幼鼠出生后,先通过哺乳接触铅,断乳后则自行饮用与母鼠饮用浓度相同的含铅水。6周后用跳台学习试验测试小鼠学习记忆能力;最后处死小鼠,用RTPCR法观察各组小鼠海马区cjunmRNA的表达状况。结果3个染铅组小鼠跳台学习成绩显著低于对照组(P<0.01);3个染铅组小鼠cjunmRNA水平均明显降低,并具有剂量效应关系。结论cjun基因表达水平的下降可能是铅致小鼠学习记忆功能损害的分子机制之一。
第三军医大学学报 , 2012,
Abstract: 目的探讨XIAP及c-jun在原发性肺癌组织中的表达水平及其临床意义。方法选用组织芯片应用免疫组化S-P法检测XIAP、c-jun蛋白在正常肺组织、肺良性病变、肺癌旁组织和原发性肺癌组织中的表达。结果XIAP、c-jun在肺癌组织中的阳性表达率均明显升高,恶性组显著高于正常组、良性组和癌旁组(P<0.05),XIAP、c-jun在肺癌临床晚期(Ⅲ期和Ⅳ期)组的阳性表达水平(MOD值)均明显高于临床早期(Ⅰ期和Ⅱ期)组(P<0.05),XIAP、c-jun的阳性表达水平在有淋巴结转移组均高于无淋巴结转移组(P<0.05),XIAP与c-jun在肺癌组织中阳性表达呈正相关(r=0.232,P<0.05),术后生存期小于1年患者的XIAP、c-jun阳性表达率均明显高于生存期超过1年患者(P<0.05)。XIAP、c-jun的MOD值与患者性别、年龄、肿块直径和组织学类型均无关(P>0.05)。结论XIAP、c-jun蛋白阳性水平的高表达提示患者预后较差,联合检测XIAP、c-jun蛋白阳性表达水平可作为临床诊断及患者预后预测的参考指标。
Effect of Chlorimethylmercury on the Expression of c-fos and c-jun Genes in Rat Brain

Cheng Jinping,Wang Wenhua,Jia Jinping,

环境科学 , 2003,
Abstract: To study the role of immediate early genes (IEG) c-fos and c-jun in the neurotoxic mechanism of methylmercury chloride(MMC), expression of FOS and JUN in rat brains was observed by using immuohistochemical methods. In the test group MMC (5.0mg/kg and 0.1mg/kg ) was injected into rats while in the control group normal saline was injected. The results showed that after rats exposed for 3 hours, the expression of FOS and JUN in brains was higher than those of the control rats, the results indicated that IEG could participate in the neurological toxicity induced by chlorimethylmercury.
- , 2018, DOI: 10.16781/j.0258-879x.2018.06.0633
Abstract: 目的 研究银杏内酯A、B混合物(GKAB)对永久性大脑中动脉栓塞(pMCAO)大鼠神经元的保护作用及相关分子机制。方法 取雄性SD大鼠60只,随机分为假手术组、pMCAO模型组和GKAB处理低、中、高剂量组。除假手术组(仅分离动脉而不阻断)外,其余4组均采用阻断右侧大脑中动脉的方法制备大鼠pMCAO模型。GKAB处理低、中、高剂量组于术后10 min分别经舌下静脉注射GKAB 12.5、25、50 mg/kg,假手术组、pMCAO模型组给予中剂量组药物等容量的生理盐水。用药12 h后,采用TUNEL法检测各组大鼠脑组织神经细胞凋亡率,免疫组织化学法检测神经细胞磷酸化JNK(p-JNK)表达,蛋白质印迹法检测脑组织中p-JNK、Bcl-2、Bax、细胞色素C(Cyt C)、caspase-9、caspase-3以及cleaved caspase-9、cleaved caspase-3蛋白的表达。结果 与假手术组相比,pMCAO模型组大鼠神经细胞凋亡率和p-JNK表达水平均增加(P<0.01),凋亡相关蛋白Bax、cleaved caspase-9、cleaved caspase-3的表达均升高(P<0.01),Bcl-2、caspase-9、caspase-3的表达均降低(P<0.01);给予GKAB处理后,与pMCAO模型组比较,GKAB处理低、中、高剂量组大鼠神经细胞凋亡率和p-JNK水平均降低(P<0.01),凋亡相关蛋白Bax、cleaved caspase-9、cleaved caspase-3的表达也呈下降趋势(P<0.01),而Bcl-2、caspase-9、caspase-3的表达呈升高趋势(P<0.01),并表现出一定的剂量依赖性。与假手术组相比,pMCAO模型组神经细胞胞质Cyt C表达升高,线粒体Cyt C表达降低(P<0.01);与pMCAO模型组比较,GKAB低、中、高剂量组神经细胞胞质Cyt C表达逐渐降低,线粒体Cyt C表达逐渐升高(P<0.05,P<0.01)。结论 GKAB可抑制pMCAO大鼠脑神经细胞凋亡,其机制可能与其抑制JNK磷酸化、抑制JNK信号通路的激活、阻断线粒体凋亡途径有关。
Objective To investigate the protective effect of ginkgolide A and ginkgolide B (GKAB) mixture on neurons of rats with permanent middle cerebral artery occlusion (pMCAO) and related molecular mechanisms. Methods Sixty male Sprague-Dawley rats were randomly divided into sham group, pMCAO permanent focal cerebral ischemia group and GKAB-treated low-, medium- and high-dose groups. In addition to the sham group (only isolated without interruption of the arteries), the rats in the remaining four groups were induced pMCAO by blocking the right middle cerebral artery. Rats in the GKAB-treated low-, medium- and high-dose groups were injected with GKAB 12.5, 25, and 50 mg/kg through sublingual vein at 10 min after pMCAO, while the sham and pMCAO groups were injected with saline of the same volume as the medium-dose group. After 12 h of treatment, the neuronal apoptosis was determined by TUNEL method, the level of phosphorylated c-Jun N-terminal kinase (p-JNK) was determined by immunohistochemistry, the expressions of p-JNK, Bcl-2, Bax, cytochrome C (Cyt C), caspase-9, caspase-3, cleaved caspase-9, and cleaved caspase-3 in brain tissues were detected by Western blotting. Results Compared with the sham group, the apoptosis rate and p-JNK expression of neurons in the pMCAO group were significantly increased (P<0.01), and the expressions of apoptosis-related proteins Bax, cleaved caspase-9 and cleaved caspase-3 in brain tissues were significantly increased (P<0.01), while the expressions of Bcl-2, caspase-9 and caspase-3 in brain tissues were significantly decreased (P<0.01). Compared with the pMCAO group, the
c-Jun N-末端激酶信号转导通路调节细胞迁移的机制
Mechanisms of c-Jun N-terminal kinase signal transduction pathway regulating cell migration

- , 2015, DOI: 10.7518/gjkq.2015.05.025
Abstract: 摘要: c-Jun N-末端激酶(JNK)是促丝裂原激活蛋白激酶家族成员,转导细胞外信号为细胞内反应。JNK信号通路主要被细胞因子和应激刺激激活,调节细胞迁移,参与细胞增殖、分化、炎症和程序性死亡。细胞迁移机制与细胞骨架、黏着斑、黏着斑激酶、整联蛋白、鼠肉瘤病毒同源癌基因家族蛋白、G-蛋白和水通道蛋白等紧密相关,但其调控机制尚不清楚。目前JNK通路调节细胞迁移的研究显示:在上皮和成纤维细胞,JNK信号通路被活化,可促进细胞迁移,增强伤口愈合、组织修复;在肿瘤细胞,JNK信号通路被抑制可降低肿瘤细胞的迁移能力;在炎症环境下,JNK的作用与机制表现出差异性,有待进一步研究。诠释JNK信号转导通路参与调节细胞迁移的具体机制可为组织修复、炎症控制和肿瘤治疗提供新的思路。
Effects of Ambroxol on JNK Signaling Pathway in Gastric Aspiration Induced Lung Injury in Rats

- , 2015, DOI: 10.7507/1671-6205.2015091
Abstract: 目的探讨氨溴索对大鼠胃内容物吸入后损伤肺组织中c-Jun氨基末端激酶(JNK)信号通路的影响。 方法40只健康SD雄性大鼠随机分为对照组、损伤组、SP600125组和氨溴索组, 每组10只。复制大鼠胃内容物吸入性肺损伤动物模型, SP600125组术前给予尾静脉注射JNK特异性抑制剂SP600125(3 mg/100 g), 氨溴索组于损伤发生后2 h给予尾静脉注射氨溴索(50 mg/kg)。检测各组大鼠支气管肺泡灌洗液(BALF)中性粒细胞计数与丙二醛(MDA)活性、肺组织湿/干重比值(W/D)、髓过氧化物酶(MPO)活性变化。蛋白免疫印迹法(Western blot)检测肺组织中JNK、磷酸化JNK (p-JNK)及诱导型一氧化氮合酶(iNOS)的蛋白表达。光镜下观察肺组织结构变化。 结果与对照组比较, 损伤组BALF中性粒细胞计数与丙二醛(MDA)活性、肺组织W/D及MPO活性显著增加(均P<0.05);p-JNK与iNOS蛋白表达均显著增高(均P<0.05);肺组织出现明显病理组织学损伤。与损伤组比较, SP600125组和氨溴索组BALF中性粒细胞计数与MDA活性、肺组织W/D及MPO活性显著下降(均P<0.05);p-JNK与iNOS蛋白表达显著下降(均P<0.05);肺组织病理学损伤减轻。Western blot结果显示各组大鼠肺组织中JNK蛋白表达差异无统计学意义。 结论JNK参与胃内容物吸入性肺损伤炎症反应。氨溴索可能通过抑制JNK信号通路、抑制iNOS表达发挥抗炎、抗氧化保护作用。
ObjectiveTo investigate the effect of ambroxol hydrochloride on c-Jun N-terminal kinase (JNK) signal pathway in gastric aspiration lung injury. MethodsForty healthy male Sprague Dawley rats were randomly divided into a control group, an injury group, a SP600125 (JNK specific inhibitor) group and an ambroxol group. The model of gastric aspiration lung injury was established by aspiration of gastric contents. The rats in the SP600125 group preoperatively received intravenous injection of JNK specific inhibitor SP600125 (3 mg/100 g). The rats in the ambroxol group received intravenous injection of ambroxol hydrochloride (50 mg/kg) 2 hours after the damage occurred. The neutrophil count and malondialdehyde (MDA) activity in bronchoalveolar lavage fluid (BALF), the lung wet weight/dry weight ratio (W/D), and myeloperoxidase (MPO) activity were measured. The protein expressions of JNK and phosphorylated JNK (p-JNK) and inducible nitric oxide synthase (iNOS) in lung tissue were detected by Western blot method. The changes of lung tissue structure were observed under light microscope. ResultsIn the injury group, the neutrophil counts and MDA activity in BALF, W/D, MPO activity, p-JNK and iNOS protein expression increased significantly, lung tissue appeared obvious histopathological injury compared with the control group. In the SP600125 group and the ambroxol group, neutrophil count and MDA activity in BALF, lung W/D, MPO activity, p-JNK and iNOS protein expression were significantly decreased compared with the injury group (P < 0.05), and the damage of the lung tissue pathology was reduced. The expression of JNK protein in lung tissue was not different in all groups (P > 0.05). ConclusionsJNK is involved in inflammatory reaction of gastric aspiration lung injury. The protective effect of ambroxol may be related to the inhibition of JNK signaling pathway and the inhibition of iNOS expression.
Localization of the mRNA of early genes along cytoskeleton
Wenjun Ju,Duanshun Wang
Chinese Science Bulletin , 1997, DOI: 10.1007/BF02882580
中国公共卫生 , 2014, DOI: 10.11847/zgggws2014-30-11-07
Abstract: ?目的观察砷对大鼠脑海马区c-fos、c-jun蛋白表达和细胞凋亡影响,探索砷对大脑神经毒性机制。方法将56只SD大鼠随机分成4组,即低、中、高剂量染砷组(亚砷酸钠:5、10、20mg/kg)和对照组,染砷组灌胃染毒,对照组给予蒸馏水,连续15d,处死大鼠;免疫组化法和DNA断裂原位末端标记法(TUNEL)法分别测定大鼠脑海马区c-fos、c-jun蛋白表达和细胞凋亡指数。结果低、中、高剂量组大鼠脑海马区c-fos、c-jun蛋白表达阳性率分别为(54.86±10.35)%、(64.18±6.23)%、(73.69±5.52)%和(0.434±0.044)%、(0.620±0.067)%、(0.711±0.026)%,细胞凋亡指数分别为(37.80±5.28)%、(48.49±5.25)%、(72.30±4.81)%,与对照组比较差异有统计学意义(P<0.01),且呈剂量-反应关系;经相关性分析显示,大鼠海马区c-fos、c-jun蛋白表达阳性率与细胞凋亡指数均呈正相关,c-fos与c-jun蛋白表达阳性率也呈正相关。结论砷可诱导大鼠脑海马区c-fos、c-jun蛋白表达,促使细胞凋亡增加;过度的c-fos、c-jun表达可能是砷致大脑神经毒性的原因之一。
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