Emergence of the PI3-kinase pathway as a central modulator of normal and aberrant B cell differentiation.
Emergence of the PI3-kinase pathway as a central modulator of normal and aberrant B cell differentiation.
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DOI：
10.1016/j.coi.2011.01.001
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发表时间：
2011-04
影响因子：
7
通讯作者：
Rickert RC
中科院分区：
文献类型：
--
作者：
Baracho GV;Miletic AV;Omori SA;Cato MH;Rickert RC
磷酸肌醇 3-激酶 (PI3K) 定义了一个脂质激酶家族，可指导广泛的细胞过程和细胞命运决定。自从发现 PI3K 及其酶拮抗剂 PTEN 以来，人们对 PI3K 的关注主要集中在其致癌潜力上。近年来，对 B 淋巴细胞中 PI3K 信号传导的研究已经确定了该通路在影响 B 细胞分化和相关分子事件（例如 V(D)J 重组和类别转换重组）中的重要性。有趣的新发现还表明，B 细胞中的 PI3K 通路具有特异性，包括特定 PI3K 同工型的优先表达或使用以及 PTEN 和 SHIP 磷酸酶的反调节。 PI3K 衔接蛋白（CD19、BCAP、TC21）的作用也进行了修改，以反映共享和独特的特性。 Foxo1 作为 B 细胞分化的关键 PI3K 调节靶标的出现，将 PI3K/PTEN/SHIP 协调的膜近端调节事件与关键转录靶标结合起来。对 PI3K 信号传导调控和影响的深入了解已应用于 B 细胞恶性肿瘤的新治疗方法，也将成为 B 细胞依赖性自身免疫性疾病的一个重要考虑话题。
Phosphoinositide 3-kinase (PI3K) defines a family of lipid kinases that direct a wide range of cellular processes and cell fate decisions. Since its discovery, and that of its enzymatic antagonist PTEN, much of the focus on PI3K has been on its oncogenic potential. In recent years, studies of PI3K signaling in B lymphocytes have established the importance of this pathway in effecting B cell differentiation and associated molecular events such as V(D)J recombination and class switch recombination. Intriguing new findings also indicate that there is specificity in the PI3K pathway in B cells, including preferential expression or usage of particular PI3K isoforms and counter-regulation by the PTEN and SHIP phosphatases. The role of PI3K adaptor proteins (CD19, BCAP, TC21) has also undergone revision to reflect both shared and unique properties. The emergence of Foxo1 as a critical PI3K regulatory target for B cell differentiation has united membrane proximal regulatory events orchestrated by PI3K/PTEN/SHIP with key transcriptional targets. Insights into the regulation and impact of PI3K signaling has been brought to bear in new treatments for B cell malignancies, and will also be an important topic of consideration for B cell-dependent autoimmune diseases.
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影响因子：
30.5
作者：
通讯作者：
--
DOI：
10.1084/jem.20091962
发表时间：
2010-10-25
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Miletic AV;Anzelon-Mills AN;Mills DM;Omori SA;Pedersen IM;Shin DM;Ravetch JV;Bolland S;Morse HC 3rd;Rickert RC
通讯作者：
Rickert RC
影响因子：
4.1
作者：
Currie, RA;Walker, KS;Lucocq, J
通讯作者：
Lucocq, J
影响因子：
4.4
作者：
Doi, Tomomitsu;Obayashi, Kunie;Koyasu, Shigeo
通讯作者：
Koyasu, Shigeo
影响因子：
32.4
作者：
Hayashi, K;Yamamoto, M;Kitamura, D
通讯作者：
Kitamura, D