Torres Haydee M, Yeo Dongwook, Westendorf Jennifer J
Departments of Orthopedic Surgery and Biochemistry and Molecular Biology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Departments of Orthopedic Surgery and Biochemistry and Molecular Biology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Mol Cell. 2023 Oct 5;83(19):3397-3399. doi: 10.1016/j.molcel.2023.09.012.
In this issue, Abe et al report a novel mechanism by which RANKL stimulates osteoclast differentiation and bone resorption through non-coding RNAs that bind PGC-1β and convert the NCoR/HDAC3 co-repressor complex into a co-activator of AP-1- and NFκB-regulated genes.
在本期杂志中，阿部等人报道了一种新机制，通过该机制，核因子κB受体活化因子配体（RANKL）通过与过氧化物酶体增殖物激活受体γ共激活因子1β（PGC-1β）结合的非编码RNA刺激破骨细胞分化和骨吸收，并将核受体辅阻遏蛋白/组蛋白去乙酰化酶3（NCoR/HDAC3）共阻遏复合物转化为活化蛋白-1（AP-1）和核因子κB（NFκB）调节基因的共激活因子。
