miR-1224-5p inhibits the proliferation in glioma cells.钱进徐英纳栾文康史岩尤永平Journal of Clinical Neurosurgery / Linchuang Shenjingwaike Zazhi钱进;徐英纳;栾文康;史岩;尤永平.miR-1224-5p在胶质瘤中的表达及其对胶质瘤细胞增殖的影响.临床神经外科杂志.2016.325-327...
MiR-1224-5p modulates osteogenesis by coordinating osteoblast/osteoclast differentiation via the Rap1 signaling target ADCY2 Experimental & Molecular Medicine (2022) -1Comment pubmed: 35831436 doi: 10.1038/s12276-022-00799-9 issn: 2092-6413
MCE 国际站:mmu-miR-1224-5p mimic 产品活性:mmu-miR-1224-5p mimic 是一种化学合成的miRNA模拟物,能模拟内源性miRNA,上调miRNA活性,用于功能获得性(gain-of-function)研究。 研究领域:Epigenetics 作用靶点:MicroRNA 相关产品:hsa-miR-4728-3p agomir | hsa-miR-126-3p agomir | rno-miR-6323 antagomir |...
Target prediction algorithms identified a consensus miR-1224-5p recognition site in the 3鈥睻TR of the cAMP response element-binding protein (CREB1) gene, and this sequence was shown to directly confer miR-1224-5p repression in luciferase reporter assays. Furthermore, exogenous miR-1224-5p ...
MicroRNAs (miRNAs) broadly regulate normal biological functions of bone and the progression of fracture healing and osteoporosis. Recently, it has been reported that miR-1224-5p in fracture plasma is a potential therapy for osteogenesis. To investigate t
Hu等人发现,miR-1224-5p通过rap1信号通路靶向ADCY2,促进成骨细胞分化。Huang等证实,来自间充质干细胞的外泌体miR-19b可通过WWP1/Smurf2介导的KLF5/b-catenin信号通路增强BMSCs的成骨作用。在该研究中,miR-365-2-5p在M2-exos...
目的研究血浆外泌体源性miR-1224-5p在重症肌无力(MG)患者中的表达差异,并探讨其对 MG的诊断价值.方法收集2017年3月至2018年7月广西医科大学第一附属医院就诊的 MG患者44例,同时收集性别,年龄匹配的44名健康人作为对照组.通过深度测序及实时荧光定量聚合酶链反应(qRT-PCR)检测患者和健康人血浆外泌体源性miRNA的...
Circ_HECW2 reduces mature miR-1224-5p by binding to pre-miR-1224, upregulating PDK2, and facilitating LPS-induced osteoblast apoptosis.BioMed CentralJournal of Orthopaedic Surgery and ResearchZhang, ChaoDepartment of Orthopedics, The First Hospital of Lanzhou University, Lanzhou, ChinaLi, Qiangqiang...
值得注意的是,失调的miRNAs抑制AMPK在肝脏中的表达和活性,促进NAFLD。例如,肝脏miR-33、miR34a、miR-1224-5p和miR-291b-3p在NAFLD中上调,通过抑制AMPK活性导致肝脏脂质代谢紊乱和肝脏脂肪变性。相反,抑制它们的过表达可提高AMPK活性,从而减少肝脏中的脂质积累。因此,miRNA/AMPK轴可能代表NAFLD治疗的潜在治疗靶点。
值得注意的是,失调的miRNAs抑制AMPK在肝脏中的表达和活性,促进NAFLD。例如,肝脏miR-33、miR34a、miR-1224-5p和miR-291b-3p在NAFLD中上调,通过抑制AMPK活性导致肝脏脂质代谢紊乱和肝脏脂肪变性。相反,抑制它们的过表达可提高AMPK活性,从而减少肝脏中的脂质积累。因此,miRNA/AMPK轴可能代表NAFLD治疗的潜在治疗靶点。