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  • γδT细胞在病毒感染性疾病中的研究进展 相关:αβT细胞 病毒感染性疾病 RECEPTOR
  • 1、γ6T细胞的概述 在几乎所有哺乳动物中,18T细胞是最早发生的T细胞。人γ6T细胞发生于7~8周正常胎儿的胸腺髓质。16T细胞的发育与αβT细胞相似,要经历功能性T细胞抗原受体(Tcell receptor,TCR)的表达和阴性选择以获得自身免疫耐受,但是否要经历阳性选择尚不清楚。
  • 中国科学家破解埃博拉病毒入侵人体机制的秘密 相关:埃博拉病毒 权威学术期刊 激发机制
  • 北京时间15日,国际权威学术期刊《Cell》在线发表中国科学院微生物研究所、中国疾病预防控制中心副主任高福研究团队的文章"Ebola Viral Glycoprotein Bound to Its Endosomal Receptor Niemann-Pick C1(埃博拉病毒糖蛋白结合内吞体受体NPC1的分子机制)",
  • 盐皮质激素受体对糖皮质激素的影响及其在自身免疫性内耳疾病中的作用 免费阅读 下载全文 相关:糖皮质激素受体 盐皮质激素受体 自身免疫性内耳疾病
  • 糖皮质激素(glucocorticoid ,GC )按其作用时长可分为三种类型:短效的氢化可的松和可的松,中效的强的松、甲强龙及长效的地塞米松和倍他米松等。在用激素治疗炎性疾病时,不同个体对GC的反应并不完全一致:有些患者对GC治疗敏感,而有些患者表现为对 GC的敏感性下降,甚至抵抗。由于体内影响 GC 发挥作用的因素很多,因此,形成GC抵抗的具体机制至今仍未被完全阐明。GC主要通过与糖皮质激素受体(glucocorticoid receptor , GR)结合发挥作用。GR是核受体家族的一员,而与其同为核受体家族成员的盐皮质激素受体(min-eralocorticoid receptor ,MR)与其结构非常相似,能够在体内与GC相互作用。本文从GC的作用机制及GC抵抗、M R的分子生物学特性、M R与GR的关系、GC与内耳组织中 M R的相互影响四个方面,综述体内M R对GC作用的影响。
  • Toll 样受体4在慢性鼻-鼻窦炎伴鼻息肉组织中的研究进展 免费阅读 下载全文 相关:Toll样受体 慢性鼻-鼻窦炎 鼻息肉组织
  • 慢性鼻-鼻窦炎伴鼻息肉(chronic rhinosinusitis with nasal polyps)为耳鼻咽喉-头颈外科常见疾病,是以上皮细胞损害和组织水肿为特征的炎症性病变,其具体的发病机制尚存在许多不明之处.有学者认为鼻息肉的病因复杂,可能是由多个基因及多种环境因素共同作用的结果[1].病原体感染也是重要的致病因素,Toll样受体(toll-like receptor,TLR)属于模式识别受体能识别病原微生物细胞壁成分,其中TLR-4作为Toll样受体的重要组成部分,已有研究显示在鼻息肉组织中的表达明显高于健康对照组[2],说明其对鼻息肉的病因及发展有重要意义,为此本文对TLR-4在慢性鼻-鼻窦炎伴鼻息肉的相关研究进行综述.
  • 胃癌血清应答因子和血管内皮生长因子受体2的表达及其临床意义 相关:胃肿瘤 血清应答因子 血管内皮生长因子受体2
  • 目的:观察胃癌组织中血清应答因子(SRF)和血管内皮生长因子受体2(VEGFR2)的表达及其临床意义。方法采用免疫组织化学SABC法检测50例胃癌、50例配对的手术切缘黏膜组织和29例胃癌淋巴结转移标本中SRF、VEGFR2的表达。结果胃癌组SRF表达阳性率为52.00%(26/50),高于正常黏膜组的16.00%(8/50),差异具有统计学意义(P<0.05),与淋巴结转移组(65.52%,19/29)比较,差异无统计学意义(P>0.05)。胃癌组VEGFR2表达阳性率为60.00%(30/50),高于正常黏膜组(10.00%,5/50),差异具有统计学意义(P<0.05),与淋巴结转移组(72.41%,21/29)比较差异无统计学意义(P>0.05)。胃癌中SRF表达与浸润深度、淋巴结转移相关(P<0.05);VEGFR2阳性表达率与胃癌分化程度、侵及浆膜及浆膜外、淋巴结转移相关(P<0.05),而与患者性别、年龄、肿瘤大小无关(P>0.05)。胃癌组SRF和VEGFR2共表达23例,具有正相关性(r=0.594,P<0.05)。结论胃癌中SRF和VEGFR2的高表达提示患者可能有胃癌侵袭、转移以及预后不良,在胃癌发生、发展中起到重要作用。
  • Molecular cloning and functional identification of an apple flagellin receptor MdFLS2 gene 免费阅读 下载全文 相关:APPLE FLAGELLIN RECEPTOR
  • The leucine-rich repeat receptor kinase flagellin-sensing 2 gene(MdFLS2; Gene ID: MDP0000254112) was cloned from Royal Gala apple(Malus×domestica Borkh.). This gene contained a complete open reading frame of 3 474 bp that encoded 1 158 amino acids. The phylogenetic tree indicated that Prunus persica FLS2 exhibited the highest sequence similarity to MdFLS2. The PlantCare database suggests that the promoter sequence of MdFLS2 contains several typical cis-acting elements, including ethylene-, gibberellin-, salicylic acid-, and drought-responsive elements. Quantitative real-time PCR analysis showed that MdFLS2 was widely expressed in the different tissues of the apple and most highly expressed in the leaves. Furthermore, MdFLS2 was significantly induced by the flagellin elicitor peptide flg22. Treatment of the apple seedling leaves with flg22 resulted in an increase in leaf callose levels with increased treatment duration. An increase in the production of O2– along with the expression of disease-related genes was also observed. An oxidative burst was detected in the treated seedlings, but not in the control seedlings, indicating that flg22 had stimulated the expression of the MdFLS2 gene and its downstream target genes. Furthermore, the ectopic expression of MdFLS2 complemented the function of the Arabidopsis fls2 mutant and conferred enhanced flg22 tolerance to the transgenic Arabidopsis, suggesting that MdFLS2 acts as a positive regulator in the response to pathogens in apple.
  • 胡荣贵研究组发现泛素信号调节细胞自噬、感应泛素胁迫的新机制 相关:细胞自噬 UBIQUITIN 信号调节
  • 5月5日,学术期刊Cell Research正式发表了中国科学院生物化学与细胞生物学研究所胡荣贵研究组的最新研究成果"Ubiquitylation of p62/Sequestosome1 Activates Its Autophagy Receptor Function and Controls Selective Autophagy Upon Ubiquitin Stress"。
  • 抗N-甲基-D-天冬氨酸受体脑炎与单纯疱疹病毒脑炎的相关性 相关:N-甲基-D-天冬氨酸受体 单纯疱疹病毒脑炎 免疫相关性
  • 抗N-甲基-D-天冬氨酸受体(N-methyl-D-aspartate receptor,NMDAR)脑炎是由抗NMDAR抗体介导的自身免疫相关性脑炎,近10年逐渐被认识。该病临床表现多变,确诊需结合特征性临床表现、脑脊液和(或)血清抗NMDAR抗体阳性,其中脑脊液抗体检测的敏感度和特异度优于血清,早期免疫治疗效果较好。
  • Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells 免费阅读 下载全文 相关:MicroRNA-22 APOPTOSIS Pancreatic
  • AIM To elucidate the underlying mechanism that microRNA-22(miR-22)promotes the apoptosis of rat pancreatic acinar cells(AR42J)and the elements that regulate the expression of miR-22.METHODS One hundred nanomoles per liter of caerulein(Cae)was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis.An amylase assay kit was used to measure the amylase expression level in the supernatant.Quantitative real-time PCR(qRT-PCR)was adopted to measure miR-22 expression.We used online tools to predict the potential transcription promoter of miR-22 and the binding sites,which was further identified by using luciferase reporter analysis,chromatin immunoprecipitation(ChIP)and ChIPqPCR assays.Then,a mimic of miR-22,Nr3c1 plasmid encoding the glucocorticoid receptor(GR),and si-Nr3c1 were used to transfect AR42J cells,respectively.The mRNA expression of miR-22,Nr3c1,and Erb-b2 receptor tyrosine kinase 3(ErbB3)was confirmed by qRT-PCR and the apoptosis rate of AR42J cells was detected by flow cytometry analysis.Western blot was used to detect the expression of ErbB3,GR,PI3k,PI3kp85α,Akt,p-Akt,Bad,Bax,Bcl-xl,Bcl-2,and cleaved caspase3.RESULTS After inducing apoptosis of AR42J cells in vitro,the expression of miR-22 was significantly increased by 2.20±0.26 and 4.19±0.54 times,respectively,at 3 h and 6 h in comparison with the control group.As revealed by qRT-PCR assay,the expression of miR-22 was 78.25±6.61 times higher in the miR-22 mimic group relative to the miRNA control group,accompanied with an obviously increased acinar cell apoptosis rate(32.53±1.15 vs 18.07±0.89,P=0.0006).The upregulation of miR-22 could suppress its target gene,ErbB3,and the phosphorylation of PI3k and Akt.Furthermore,we predicted the potential transcription promoter of miR-22 and the binding sites using online tools.Luciferase reporter analysis and sitedirected mutagenesis indicated that the binding site(GACAGCCATGTACA)of the GR,which is encoded ...
  • 胃饥饿素在抗动脉粥样硬化中的研究进展 免费阅读 下载全文 相关:抗动脉粥样硬化 饥饿 RECEPTOR
  • 胃饥饿素(Ghrelin)是Kojima等1999年发现的具有28个氨基酸残基的脑肠肽。Ghrelin在体内主要活性形式是酰基化后的ghrelin,其与生长激素促分泌物受体(growth hormone secretagogue receptor,GHSR)受体的一种亚型,即GHSR-1a相结合,
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