...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Microtubule actin crosslinking factor 1 promotes osteoblast differentiation by promoting β‐catenin/TCF1/Runx2 signaling axis
【24h】

Microtubule actin crosslinking factor 1 promotes osteoblast differentiation by promoting β‐catenin/TCF1/Runx2 signaling axis

机译：1促进微管肌动蛋白交联因素成骨细胞分化,促进β连环蛋白/ TCF1应承担Runx2信号轴

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Osteoblast differentiation is a multistep process delicately regulated by many factors, including cytoskeletal dynamics and signaling pathways. Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes; however, its role in regulating osteoblast differentiation is still needed to be elucidated. To further uncover the functions and mechanisms of action of MACF1 in osteoblast differentiation, we examined effects of MACF1 knockdown (MACF1‐KD) in MC3T3‐E1 osteoblastic cells on their osteoblast differentiation and associated molecular mechanisms. The results showed that knockdown of MACF1 significantly suppressed mineralization of MC3T3‐E1 cells, down‐regulated the expression of key osteogenic genes alkaline phosphatase (ALP), runt‐related transcription factor 2 (Runx2) and type I collagen α1 (Col Iα1). Knockdown of MACF1 dramatically reduced the nuclear translocation of β‐catenin, decreased the transcriptional activation of T cell factor 1 (TCF1), and down‐regulated the expression of TCF1, lymphoid enhancer‐binding factor 1 (LEF1), and Runx2, a target gene of β‐catenin/TCF1. In addition, MACF1‐KD increased the active level of glycogen synthase kinase‐3β (GSK‐3β), which is a key regulator for β‐catenin signal transduction. Moreover, the reduction of nuclear β‐catenin amount and decreased expression of TCF1 and Runx2 were significantly reversed in MACF1‐KD cells when treated with lithium chloride, an agonist for β‐catenin by inhibiting GSK‐3β activity. Taken together, these findings suggest that knockdown of MACF1 in osteoblastic cells inhibits osteoblast differentiation through suppressing the β‐catenin/TCF1‐Runx2 axis. Thus, a novel role of MACF1 in and a new mechanistic insight of osteoblast differentiation are uncovered.
机译：成骨细胞分化是一个多步骤的过程精致受许多因素,包括细胞骨架动力学和信号通路。微管肌动蛋白交联因子1 (MACF1),一个关键的细胞骨架连接程序,已被证明关键角色在信号转导和多样化细胞过程;调节成骨细胞分化仍在需要阐明。MACF1行动的功能和机制成骨细胞分化,我们检查效果MACF1击倒(MACF1 KD)应承担的MC3T3 E1成骨细胞的成骨细胞的细胞分化和相关分子机制。MACF1显著抑制矿化地理MC3T3 E1细胞,调控的表达关键成骨基因碱性磷酸酶(ALP),矮子应承担的相关转录因子2 (Runx2)和I型胶原蛋白α1 (Col我α1)。大大降低了核易位地理β连环蛋白,降低了转录激活的T细胞因子1 (TCF1)量监管TCF1的表达,淋巴增强器检测结合因子1 (LEF1)和Runx2β连环蛋白/ TCF1应承担的目标基因。MACF1 KD增加糖原的活动程度合成酶激酶检测3β(GSK量3β),这是一个关键监管机构对β连环蛋白信号转导。此外,减少核β连环蛋白数量和降低TCF1和Runx2的表情显著逆转MACF1 KD应承担的细胞氯化锂处理时,受体激动剂为β连环蛋白通过抑制GSK 3β应承担的活动。总的来说,这些发现表明,击倒的MACF1抑制成骨细胞的细胞通过抑制成骨细胞分化β连环蛋白/ TCF1应承担Runx2应承担的轴。MACF1的和机械的见解成骨细胞分化是发现。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号