为了进一步验证miR-423-3p是否介导GDEs对NHA转化的影响,从常氧条件下过表达miR-423-3p的P3#GBM细胞中提取GDEs来处理NHA。将含有抑制miR-423-3p的miRNA的H-GDEs添加到另一组中。MiR-423-3p显著增强了转化,而抑制RNA则挽救了H-GDE诱导的NHA转化(图4B,D-F,H,J)。总的来说,这些结果表明H-
miR-423-3p 诱导的自噬促进星形胶质细胞激活:转染 miR-423-3p mimics 的 NHAs 增殖、迁移能力增强,IL-6 和 IL-8 分泌增加,GFAP 表达上调,抑制自噬则会减弱这些作用。用过表达 miR-423-3p 的 P3#GBM 细胞来源的 GDEs 处理 NHAs,同样证实了 miR-423-3p 通过自噬促进 NHAs 向反应性星形胶质细胞(RAs)转化。
In an miRNA array between two types of exosomes from gliomas, miR-423-3p was highly expressed in H-GDEs and played an important role in autophagy, resulting in the activation of NHAs. The mechanism by which hypoxic glioma cells react with NHAs to create an immunosuppressive microenvironment ...
货号:cgr-miR-423-3p 原价:￥4030 现价:￥3098.38节省:￥931.62 规格:1 kits 说明:cgr-miR-423-3p 特异性茎环引物试剂盒 ￥615 产品参数 ---说明书下载--- microRNAs(miRNAs)是一类长度约19~24nt的非编码单链RNA,通过碱基互补配对的方式与靶基因的29’UTR区部分或完全互补,剪切靶基因的转录产物或者抑制转录...
Cell Mol Biol Lett (2021) 26:6 https://doi.org/10.1186/s11658-021-00247-y Cellular & Molecular Biology Letters RESEARCH Open Access ZNF674‑AS1 antagonizes miR‑423‑3p to induce G0/G1 cell cycle arrest in non‑small cell lung cancer cells Yu Liu1, Risheng Huang2*, De...
miR-101-3p和miR-423-5p的体外功能分析表明,用相应的模拟物处理MB细胞可显著抑制肿瘤细胞的增殖、集落形成能力、迁移能力和侵袭能力,促进细胞凋亡。此外,miR-101-3p和miR-423-5p被发现通过直接靶向一个共同的基因FOXP4。miR-101-3p还靶向组蛋白...
S2A, B). We also compared the expression of miR-101-3p and miR-423-5p in peripheral blood mononuclear cells (PBMCs) from MB patients and healthy controls and found that the expression of both miRNAs was higher in the PBMCs of MB patients (Fig. 1F). To determine whether plasma-derived...
在机制方面证明巨噬细胞的载脂蛋白载体主要递送靶向胰岛素样生长因子结合蛋白5(IGFBP5)的miR-143-3p,以破坏牙周骨稳态。综上所述,研究表明,Pg相关PD中的巨噬细胞发生凋亡,并产生富含miR-143-3p的ApoVs来沉默IGFBP5,导致成骨破骨细...
Liu X, Su X, Xu S, Wang H, Han D, Li J, Huang M and Cao X. MicroRNA in vivo precipitation iden- tifies miR-151-3p as a computational unpre- dictable miRNA to target Stat3 and inhibits in- nate IL-6 production. Cell Mol Immunol 2018; 15: 99-110....
miR-423-3p was significantly associated with smoker, age, and pathologic stage of LUAD patients.#Moreover, overexpressing miR-423-3p could facilitate LUAD cell proliferation, invasion, adhesion, and epithelial-mesenchymal transition (EMT) process, while depleted miR-423-3p caused repressive influence...