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Depletion of janus kinase-2 promotes neuronal differentiation of mouse embryonic stem cells
Baek-Soo Han1,2,3,*,# (Professor), Mihee Oh1,# (Research worker), Sun Young Kim1 (Research worker), Jeong-Su Byun1 (Research worker), Seonha Lee1 (Graduate student), Won-Kon Kim (Professor), Kyoung-Jin Oh (Professor), Eun-Woo Lee (Professor), Kwang-Hee Bae (Professor), Sang Chul Lee (Professor)
1Biodefense Research Center and 2Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology,
3Department of Functional Genomics, University of Science and Technology (UST) of Korea
Abstract
The non-receptor tyrosine kinase janus kinase 2 (JAK2) is a critical component of cytokine and growth factor signaling pathways regulating hematopoietic cell proliferation, and JAK2 mutations are associated with multiple myeloproliferative neoplasms. In contrast to hematopoietic tissue, the physiological and pathological functions of JAK2 in the nervous system are not well studied. Here we demonstrate that JAK2 negatively regulates neuronal differentiation of mouse embryonic stem cells (ESCs). Depletion of JAK2 stimulated neuronal differentiation of mouse ESCs and was associated with activation of glycogen synthase kinase 3ꞵ, Fyn, and cyclin-dependent kinase 5. Knockdown of JAK2 also resulted in accumulation of GTP-bound Rac1, a Rho GTPase implicated in the regulation of cytoskeletal dynamics. These findings suggest that JAK2 may negatively regulate neuronal differentiation by suppressing the GSK-3モ/Fyn/CDK5 signaling pathway responsible for morphological maturation.
Abstract, Accepted Manuscript(in press) [Submitted on October 30, 2021, Accepted on November 15, 2021]
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