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作 者:Fei Ao Fan Chen Minhong Lv Yuming Cao Jinfeng Xu Jingbo Xu Anskar Yu-Hung Leung Qiwen Yuan Li Wang Bailiang He
机构地区:[1]Guangdong Provincial Engineering Research Center of Molecular Imaging,The Fifth Affiliated Hospital,Sun Yatsen University,Zhuhai,Guangdong 519000,China [2]Department of Gynecology and Obstetrics,Perinatal Medical Center,The Fifth Affiliated Hospital,Sun Yat-sen University,Zhuhai,Guangdong 519000,China [3]Department of Hematology,The Fifth Affiliated Hospital,Sun Yat-sen University,Zhuhai,Guangdong 519000,China [4]Division of Haematology,Department of Medicine,School of Clinical Medicine,Li Ka Shing Faculty of Medicine,The University of Hong Kong,Hong Kong 999077,China
出 处:《Genes & Diseases》2024年第6期16-19,共4页基因与疾病(英文)
基 金:supported by grants from the National Natural Science Foundation of China (No.32000569);the Basic and Applied Basic Research Foundation of Guangdong Province,China (No.2019A1515110281).
摘 要:Gain-of-function somatic mutations of SET binding protein 1(SETBP1)result in the accumulation of SETBP protein and are detected in 17%of secondary acute myeloid leukemia(AML)patients.1 In fact,high expression of SETBP1 also drives adverse outcomes in human AML.However,the roles of SETBP1 during developmental hematopoiesis and AML progression are still not fully understood.Here we first sought to investigate the functions of SETBP1 in developmental hematopoiesis.
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