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1.
目的:探讨RNA干扰RelB基因对鼠RM-1前列腺癌细胞株放射敏感性的影响及其机制。方法:利用靶向RelB基因的慢病毒载体(pLentilox-sh-RelB),脂质体介导转染RM-1细胞后进行放射(2,4,6,和8Gy剂量)处理培养,分别采用RT-PCR、Western印迹法及流式细胞术等方法检测RelB的mRNA和蛋白表达,锰超氧化物歧化酶(Mn-SOD)活力及细胞放射敏感性的变化。结果:转染后放射处理培养,siRelB-RM-1组RelB的mRNA和蛋白表达水平明显低于siVector-RM-1组和nontrans-RM-1组(P<0.05);放射处理培养后siRelB-RM-1组细胞凋亡百分率明显高于siVector-RM-1组和nontrans-RM-1组(P<0.05);培养后siRelB-RM-1组细胞Mn-SOD活力下降,放射增敏比为5.13。结论:RNA干扰RelB基因可增强鼠RM-1前列腺癌细胞株放射后的放射敏感性,其机制可能与RNA干扰RelB基因,抑制细胞增殖,降低Mn-SOD活力和诱导凋亡有关。  相似文献   
2.
目的:以往研究显示,宫颈癌发生可能与体内ApoE、 CLU、 RelB和mTOR等血浆蛋白质表达水平变化存在一定的关系。此研究探讨宫颈癌发生与肿瘤组织中上述蛋白质的表达水平的关系,为建立宫颈癌早期预警指标提供依据。方法收集维吾尔族和汉族妇女宫颈鳞癌( cervical squamous cell carcinoma, CSCC)组织标本36例和正常对照组织25例。设计与合成ApoE、 CLU、 RelB和mTOR的mRNA序列特异性引物,采用定量RT?PCR方法,对宫颈癌和正常对照组织RNA进行mRNA表达水平鉴定。结果肿瘤组织中ApoE、 CLU和RelB 3种基因的转录水平上调,与正常对照组比较有显著差异(P<0.05),但是mTOR表达水平无统计学差异(P>0.05),其中ApoE、 CLU和RelB表达水平变化与以往研究报道的血浆水平变化一致。结论宫颈癌的发生与肿瘤组织内ApoE、 CLU和RelB表达水平上调存在密切关系,与血浆水平变化一致,证明这些基因可能成为宫颈癌早期预警的组织和血浆检测指标。  相似文献   
3.
目的 探讨DC2.4表面分子表达水平与RelB基因表达间的关系.方法 用RPMI 1640完全培养液培养DC2.4细胞系,光学显微镜观察培养细胞的形态特征;透射电镜观察DC2.4的细胞结构;流式细胞术分析DC2.4的表面标记(MHC-Ⅱ、CD86和CD40);RT-PCR检测DC2.4的RelB表达水平.结果 光镜观察DC2.4细胞表面有明显的树突状突起,形态极不规则;透射电镜显示DC2.4细胞内含许多质地均匀的脂滴,可见吞噬小泡样的结构.流式细胞术显示MHC-Ⅱ类分子和CD40呈低水平表达,而CD86分子却呈高水平表达;RT-PCR结果显示RelB呈低水平表达,与骨髓源性DC中的未成熟状态DC的RelB表达水平接近.结论 DC2.4具有强吞噬功能,其表面CD40分子和细胞内RelB基因均呈低水平表达,提示DC2.4是一种未成熟状态的细胞系.  相似文献   
4.

Background

High-grade gliomas are one of the most invasive and therapy-resistant cancers. We have recently shown that noncanonical NF-κB/RelB signaling is a potent driver of tumorigenesis and invasion in the aggressive, mesenchymal subtype of glioma. However, the relevant signals that induce activation of noncanonical NF-κB signaling in glioma and its function relative to the canonical NF-κB pathway remain elusive.

Methods

The ability of tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) to regulate NF-κB signaling and promote tumor progression was investigated in both established and primary high-grade glioma tumor lines using a three-dimensional (3-D) collagen invasion assay. The roles of specific NF-κB proteins in regulating glioma cell invasion and expression of Matrix Metalloproteinase 9 (MMP9) in response to TWEAK were evaluated using shRNA-mediated loss-of-function studies. The ability of NF-κB-inducing kinase (NIK) to promote glioma growth in vivo was investigated using an orthotopic xenograft mouse model.

Results

In glioma cells that display elevated noncanonical NF-κB signaling, loss of RelB attenuates invasion without affecting RelA expression or phosphorylation and RelB is sufficient to promote invasion in the absence of RelA. The cytokine TWEAK preferentially activates the noncanonical NF-κB pathway through induction of p100 processing to p52 and nuclear accumulation of both RelB and p52 without activating the canonical NF-κB pathway. Moreover, TWEAK, but not TNFα, significantly increases NIK mRNA levels. TWEAK also promotes noncanonical NFκB-dependent MMP9 expression and glioma cell invasion. Finally, expression of NIK is sufficient to increase gliomagenesis in vivo.

Conclusions

Our data establish a key role for NIK and noncanonical NF-κB in mediating TWEAK-induced, MMP-dependent glioma cell invasion. The findings also demonstrate that TWEAK induces noncanonical NF-κB signaling and signal-specific regulation of NIK mRNA expression. Together, these studies reveal the important role of noncanonical NF-κB signaling in regulating glioma invasiveness and highlight the therapeutic potential of targeting activation of NIK in this deadly disease.

Electronic supplementary material

The online version of this article (doi:10.1186/s12943-014-0273-1) contains supplementary material, which is available to authorized users.  相似文献   
5.
Multiple receptors that control cell growth and inflammation activate the NFκB pathway that comprises of two pathways. Dysfunction of the classical pathway leads to impaired adaptive and innate immunity in humans. In contrast the exact role of the alternative NFκB pathway mediated by RelB in humans remains largely elusive. We have recently identified deleterious mutations in RelB in patients with combined immunodeficiency and autoimmunity.We studied here the biological effects of RelB deficiency on the immune system. We show that the thymus in this patient is dysplastic and consequently new thymus emigrants are rare and there is an accumulation of CD45 RO+ T cells with an increase in CD62L+ central memory cells. The TCR repertoire of these cells appears skewed with selective clonal expansion. In vitro responses to T cell mitogens were markedly depressed and so were PHA induced IL2 and IFNγ production. In addition, the TH1 promoting T bet and STAT1 were reduced. In contrast, hyper-activation was seen in response to anti-CD3 and CD28. T cell dependent antibody responses were low to absent in all patients. We found that BAFF-R was reduced and CD40 signaling aberrant. Critically, CD27+ memory cells were absent.We have shown here for the first time the role of RelB on lymphocyte development in humans. In the absence of RelB, B cells development is arrested, resulting in poor production of immunoglobulins and specific antibodies. T cell maturation in the thymus appears altered with reduced output and production of a skewed T cell repertoire with expansion of clones which are likely the cause of the autoimmune features observed in these patients.  相似文献   
6.
目的:通过模拟人阻塞性睡眠呼吸暂停综合征(OSAS)间歇性低氧(IH)环境,观察其对人外周血来源树突状细胞(DCs)迁徙能力的影响,并通过干预RelB、p38的表达探讨IH致DCs迁徙能力改变的可能通路机制。方法培养前将DCs分为RelB、p38干扰及非干扰质粒组。利用间歇低氧舱设置低氧环境,其中,给氧浓度为0.5%、1.5%、5.0%、10.0%,低氧/再氧合时间比为1∶1、1∶3、1∶5、1∶9,常氧对照组予以持续21.0%氧浓度供应。体外培养结束后蛋白质印迹法检测RelB、p38的表达,侵袭小室检测DCs的迁徙能力。结果相对于常氧,体外IH下DCs整体迁徙能力下降,且DCs迁徙能力与IH环境下平均氧分压水平呈正相关(r=0.867,P<0.05),IH可促进DCs胞内RelB、p38表达,而干预二者表达均未逆转IH下迁徙能力的改变。结论体外IH可导致DCs迁徙能力下降,且可能与RelB、p38激活无关。  相似文献   
7.
目的:探讨胁坍基因沉默的髓源树突状细胞(BMDC)负载电鳗乙酰胆碱受体(TAChR)优势肽段Tα146~162在TAChR预致敏C57BL/6小鼠中能否诱导免疫耐受。方法:制备产生RelBsiRNA分子的重组慢病毒和对照病毒。慢病毒感染BMDC后,给予LPS刺激,相应的DC命名为DC—siRelB和DC—control。应用实时定量PCR和Western印迹分析细胞中RelB表达,流式细胞仪检测细胞表型,ELISA检测上清白细胞介素(IL)-12水平。36只C57BL/6小鼠随机分为A1,A2,A3,K1,K2,K3共6组。实验前1天,A1-A3组用TAChR+完全福氏佐剂(CFA)致敏;K1~K3组用钥孔戚血清蛋白(KLH)4-CFA致敏。第7天,A2和K2组注射Tα146-162脉冲的DC-siRelB;A3和K3组注射Tα146-162脉冲的DC—control;A1和K1组给予PBS。第14天,^3H-TdR掺入法检测淋巴细胞增殖反应。结果:成功构建了含RelB^shRNA基因的重组慢病毒,RelBsiRNA可显著下调DC中RelB的表达。与DC—control相比,DC—siRelB中CD80,CD86,MHCII表达及IL-12水平显著降低。与A1和A3组相比,A2组TAChR刺激下淋巴细胞增殖反应显著降低(P〈0.05),ConA和KLH刺激下淋巴细胞增殖反应差异无统计学意义(P〉0.05)。K1,K2和K3组在KLH刺激下淋巴细胞增殖反应差异均无统计学意义(P〉0.05)。结论:慢病毒介导的RelB基因沉默的BMDC可抵制成熟诱导反应并能在TAChR预致敏的C57BL/6小鼠中诱导抗原特异性免疫耐受,为研究其用于治疗重症肌无力奠定了基础。  相似文献   
8.
目的:探讨核转录因子NF-кB/RelB基凶沉默的树突状细胞(RNAi RelB dendritic cell,RNAi helB DC)诱导异基因CD4+CD25+双阳性T细胞牛成的生物效应.方法:实验分为Control-DC组、LPS-DC组、RNAi RelB DC组和LPS-RNAiRelB DC组,各组DC均与同种异基因T淋巴细胞混合反应后,采用流式细胞术(FCM)分析各组CD4+CD25+双阳性T细胞牛成比例.结果:Control-Dc组DC较LPS-Dc组DC诱导CD4+CD25+双阳性T细胞的增高幅度更显著,两者差异具有统计学意义(P<0.01).RNAi RelB DC组和LPS-RNAiRelB DC组DC诱导CD4+CD25+双阳性T细胞牛成比例与LPS-DC组相比均存在显著差异(P<0.01),RNAi RelB DC组DC诱导CD4+CD25+双阳性T细胞牛成能力较Control-DC组强,差异具有统计学意义(P<0.05).结论:RelB基凶被沉默后DC具有较强的诱导CD4+CD25+双阳性T细胞生成的能力,表现出未成熟DC的特点,这种RNAi RelB DC有望成为一种新型的致耐受DC用于免疫耐受的诱导研究.  相似文献   
9.
The discovery of the new crosstalk between the aryl hydrocarbon receptor (AhR) and the NF-κB subunit RelB may extend our understanding of the biological functions of the AhR and at the same time raises a number of questions, which will be addressed in this review. The characteristics of this interaction differ from that of AhR with RelA in that the latter appears to be mostly negative unlike the collaborative interactions of AhR/RelB. The AhR/RelB dimer is capable of binding to DNA response elements including the dioxin response element (DRE) as well as NF-κB binding sites supporting the activation of target genes of the AhR as well as NF-κB pathway. Further studies show that AhR/RelB complexes can be found not only in lymphoid cells but also in a human hepatoma cell line (HepG2) or breast cancer cell line (MDA-MB-231). RelB has been implicated in carcinogenesis of breast cancer for instance and RelB is known to be a critical factor for the function and differentiation of dendritic cells; interestingly the participation of AhR in both processes has been suggested recently, which offers the great potential to expand the scope of the physiological roles of the AhR. There is evidence indicating that RelB may serve as a pro-survival factor, including its ability to promote “inflammation resolution” besides the association of RelB with inflammatory disorders. Based on such information, a hypothesis has been proposed in this review that AhR together with RelB functions as a coordinator of inflammatory responses.  相似文献   
10.
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