中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2013, 25(1): 47-53
BCR-ABL与Src家族激酶相互作用介导CML对抗癌药物伊马替尼耐受的研究进展
王冠明1,林 晨1*,陈小华1,李扬秋2
(1 暨南大学医学院微生物与免疫学系,广州 510632;2 暨南大学血液研究所,广州 510632)
摘 要:BCR/ABL融合蛋白是慢性粒细胞白血病(CML)的分子标志,具有高激酶活性,其在疾病发生、发展中扮演了极其重要的角色。伊马替尼(Imatinib)靶向抑制BCR-ABL,为CML慢性期的一线治疗药。BCR/ABL与Src家族激酶(Src-family kinases, SFK)之间也存在相互活化作用,通过激活众多信号通路,导致CML向急变期发展,并导致伊马替尼耐药。对有关BCR/ABL与SFK两者的相互作用机制及其生物学效应的研究进行总结。
关键词:慢性粒细胞白血病;BCR-ABL;Src家族激酶;伊马替尼耐药
 
Progress of the BCR-ABL and Src family kinases interactions leading CML to imatinib-resistance
WANG Guan-Ming1, LIN Chen1*, CHEN Xiao-Hua1, LI Yang-Qiu2
(1 Department of Microbiology and Immunology, Medical College, Jinan University, Guangzhou 510632, China; 2 Institute of Hematology, Medical College, Jinan University, Guangzhou 510632, China)
Abstract: BCR-ABL fusion protein is the molecular marker of chronic myeloid leukemia (CML), which has constitutive kinase activity, playing an essential role in the pathogenesis of CML. Imatinib specially inhibits BCR-ABL, which is considered as the frontline treatment in the chronic phase of CML(CP-CML).  Studies have shown that the interaction between BCR-ABL fusion protein and Src family kinases induces the activation of multiple signaling pathways  which are responsible for the transition from CP to BP of CML and induction of imatinib resistance. In this paper, we reviewed the progress of the BCR/ABL and Src family kinases interaction machanisms and their biological effects.
Key words: CML; BCR-ABL; Src family kinase; imatinib resistance
 
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