Kisspeptin-10 binding to Gpr54 in osteoclasts prevents bone loss by activating Dusp18-mediated dephosphorylation of Src.
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ABSTRACT:
SUBMITTER: Li Z
PROVIDER: S-EPMC10861593 | biostudies-literature | 2024 Feb
REPOSITORIES: biostudies-literature
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Kisspeptin-10 binding to Gpr54 in osteoclasts prevents bone loss by activating Dusp18-mediated dephosphorylation of Src.
Li Zhenxi Z Yang Xinghai X Fu Ruifeng R Wu Zhipeng Z Xu Shengzhao S Jiao Jian J Qian Ming M Zhang Long L Wu Chunbiao C Xie Tianying T Yao Jiqiang J Wu Zhixiang Z Li Wenjun W Ma Guoli G You Yu Y Chen Yihua Y Zhang Han-Kun HK Cheng Yiyun Y Tang Xiaolong X Wu Pengfei P Lian Gewei G Wei Haifeng H Zhao Jian J Xu Jianrong J Ai Lianzhong L Siwko Stefan S Wang Yue Y Ding Jin J Song Gaojie G Luo Jian J Liu Mingyao M Xiao Jianru J
Nature communications 20240212 1
Osteoclasts are over-activated as we age, which results in bone loss. Src deficiency in mice leads to severe osteopetrosis due to a functional defect in osteoclasts, indicating that Src function is essential in osteoclasts. G-protein-coupled receptors (GPCRs) are the targets for ∼35% of approved drugs but it is still unclear how GPCRs regulate Src kinase activity. Here, we reveal that GPR54 activation by its natural ligand Kisspeptin-10 (Kp-10) causes Dusp18 to dephosphorylate Src at Tyr 416. Me ...[more]
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