Nuclear Inositide Signaling in Myelodysplastic Syndromes
Nuclear Inositide Signaling in Myelodysplastic Syndromes
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DOI：
10.1002/jcb.22483
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发表时间：
2010-04-15
影响因子：
4
通讯作者：
Cocco, Lucio
中科院分区：
文献类型：
--
作者：
Follo, Matilde Y.;Mongiorgi, Sara;Cocco, Lucio
骨髓增生异常综合征（MDS）被定义为克隆性造血干细胞疾病，其特征是一种或多种骨髓谱系无效造血。尽管存在不同的形态学亚组，但 MDS 的自然病程是进展为急性髓系白血病 (AML)。然而，MDS 演变为 AML 的分子机制尚不完全清楚。肌醇是关键的细胞第二信使，在信号转导途径中具有明确的作用，并且由磷酸肌醇特异性磷脂酶 C (PI-PLC) beta 1 和 Akt 引发的核代谢在正常和病理条件下控制细胞周期进程和细胞凋亡之间的平衡中发挥着重要作用。最近的研究结果证明了核脂质信号通路所发挥的作用，它可能成为MDS有希望的治疗靶点。这篇评论将对这一主题的最新技术进行简明且最新的修订。 J.细胞。生物化学。 109：1065-1071，2010。(C) Wiley-Liss 公司。
Myelodysplastic syndromes (MDS) are defined as clonal hematopoietic stem-cell disorders characterized by ineffective hematopoiesis in one or more of the lineages of the bone marrow. Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML). However, the molecular mechanisms the underlying MDS evolution to AML are not completely understood. Inositides are key cellular second messengers with well-established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide-specific phospholipase C (PI-PLC) beta 1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions. Recent findings evidenced the role played by nuclear lipid signaling pathways, which could become promising therapeutic targets in MDS. This review will provide a concise and updated revision of the state of art on this topic. J. Cell. Biochem. 109: 1065-1071, 2010. (C) Wiley-Liss, Inc.