Akala Omobolaji O, Clarke Michael F
Stanford Institute for Stem Cell Biology and Regenerative Medicine, 1050 Arastradero Road, Palo Alto, CA 94304-1334, USA.
Curr Opin Genet Dev. 2006 Oct;16(5):496-501. doi: 10.1016/j.gde.2006.08.011. Epub 2006 Aug 17.
Recent studies have begun to elucidate the mechanisms controlling hematopoietic stem cell (HSC) self-renewal. Self-renewal requires the integration of survival signals and proliferation controls with the maintenance of an undifferentiated state. This demands a complex crosstalk between extrinsic signals from the microenvironment and the cell-intrinsic regulators of self-renewal. The Polycomb protein Bmi1 is absolutely required for the maintenance of both adult HSCs and neural stem cells. Evidence from studies in murine and human embryonic stem cells indicates that Polycomb group proteins play a dynamic role in concert with master transcriptional regulators in actively maintaining an undifferentiated state, suggesting that this mechanism applies to multiple types of stem cell. Recently, various new players that regulate HSC maintenance (e.g. Mcl1, Tel/Etv6, Gfi1, Pten and Stat5) have been identified. In order to better understand HSC self-renewal, we need to understand how these pathways are coordinated.
最近的研究已开始阐明控制造血干细胞（HSC）自我更新的机制。自我更新需要将存活信号、增殖控制与未分化状态的维持整合起来。这需要微环境的外在信号与自我更新的细胞内在调节因子之间进行复杂的相互作用。多梳蛋白Bmi1对于成体造血干细胞和神经干细胞的维持绝对必要。来自小鼠和人类胚胎干细胞研究的证据表明，多梳家族蛋白与主要转录调节因子协同发挥动态作用，积极维持未分化状态，这表明该机制适用于多种类型的干细胞。最近，已鉴定出各种调节造血干细胞维持的新因子（例如Mcl1、Tel/Etv6、Gfi1、Pten和Stat5）。为了更好地理解造血干细胞的自我更新，我们需要了解这些通路是如何协调的。
