Janus 激酶-2 的耗竭促进了小鼠胚胎干细胞的神经元分化。
Depletion of Janus kinase-2 promotes neuronal differentiation of mouse embryonic stem cells.
机构信息
Biodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Biodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
出版信息
BMB Rep. 2021 Dec;54(12):626-631. doi: 10.5483/BMBRep.2021.54.12.154.
Janus kinase 2 (JAK2), a non-receptor tyrosine kinase, is a critical component of cytokine and growth factor signaling pathways regulating hematopoietic cell proliferation. JAK2 mutations are associated with multiple myeloproliferative neoplasms. Although physiological and pathological functions of JAK2 in hematopoietic tissues are well-known, such functions of JAK2 in the nervous system are not well studied yet. The present study demonstrated that JAK2 could negatively regulate neuronal differentiation of mouse embryonic stem cells (ESCs). Depletion of JAK2 stimulated neuronal differentiation of mouse ESCs and activated glycogen synthase kinase 3ꞵ, Fyn, and cyclin-dependent kinase 5. Knockdown of JAK2 resulted in accumulation of GTPbound Rac1, a Rho GTPase implicated in the regulation of cytoskeletal dynamics. These findings suggest that JAK2 might negatively regulate neuronal differentiation by suppressing the GSK-3β/Fyn/CDK5 signaling pathway responsible for morphological maturation. [BMB Reports 2021; 54(12): 626-631].
Janus 激酶 2（JAK2）是一种非受体酪氨酸激酶，是调节造血细胞增殖的细胞因子和生长因子信号通路的关键组成部分。JAK2 突变与多种骨髓增殖性肿瘤有关。尽管 JAK2 在造血组织中的生理和病理功能众所周知，但 JAK2 在神经系统中的功能尚未得到充分研究。本研究表明，JAK2 可负调控小鼠胚胎干细胞（ESCs）的神经元分化。JAK2 的耗竭刺激了小鼠 ESCs 的神经元分化，并激活了糖原合酶激酶 3β、Fyn 和周期蛋白依赖性激酶 5。JAK2 的敲低导致 GTP 结合 Rac1 的积累，Rac1 是一种参与细胞骨架动力学调节的 Rho GTPase。这些发现表明，JAK2 可能通过抑制负责形态成熟的 GSK-3β/Fyn/CDK5 信号通路来负调控神经元分化。[BMB 报告 2021；54(12):626-631]。
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