Biomedical Biotechnology Research Unit, Department of Biochemistry, Microbiology and Biotechnology, Rhodes University, Grahamstown, South Africa.
IUBMB Life. 2010 Jan;62(1):61-6. doi: 10.1002/iub.283.
Self-renewal of in vitro cultured mouse embryonic stem (mES) cells is dependent on the presence of leukemia inhibitory factor (LIF). LIF induces overexpression and tyrosine phosphorylation of STAT3 (signal transducer and activator of transcription 3) and its subsequent nuclear translocation. The molecular chaperone heat shock protein 90 (Hsp90) is involved in the activation and maturation of a wide variety of substrate proteins. We investigated the effect of LIF withdrawal on the protein expression levels of STAT3 and Hsp90 and on the interactions between STAT3 and Hsp90. Taken together the data presented here suggest that LIF promotes the interaction of Hsp90 with STAT3 during self-renewal, indicating a potentially pivotal role for Hsp90 in the LIF-based maintenance of self-renewal of mouse embryonic stem cells.
体外培养的小鼠胚胎干细胞（mES）的自我更新依赖于白血病抑制因子（LIF）的存在。LIF 诱导 STAT3（信号转导和转录激活因子 3）的过度表达和酪氨酸磷酸化及其随后的核转位。分子伴侣热休克蛋白 90（Hsp90）参与了各种底物蛋白的激活和成熟。我们研究了 LIF 撤出对 STAT3 和 Hsp90 的蛋白表达水平以及 STAT3 和 Hsp90 之间相互作用的影响。综合本文提供的数据表明，LIF 在自我更新过程中促进了 Hsp90 与 STAT3 的相互作用，表明 Hsp90 在基于 LIF 的维持小鼠胚胎干细胞的自我更新中可能起着关键作用。
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