Depletion of Janus kinase-2 promotes neuronal differentiation of mouse embryonic stem cells

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Title
Depletion of Janus kinase-2 promotes neuronal differentiation of mouse embryonic stem cells
Author(s)
Mihee Oh; Sun Young Kim; Jeong Su Byun; Seonha Lee; Won Kon KimKyoung-Jin OhEun-Woo LeeKwang-Hee BaeSang Chul LeeBaek Soo Han
Bibliographic Citation
BMB Reports, vol. 54, no. 12, pp. 626-631
Publication Year
2021
Abstract
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 3?, 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.
Keyword
Cyclin-dependent kinase 5 (CDK5)Embryonic stem cellGlycogen synthase kinase 3β (GSK3 β)Janus kinase-2 (JAK2)NeurogenesisNeuronal differentiation
ISSN
1976-6696
Publisher
Korea Soc-Assoc-Inst
DOI
http://dx.doi.org/10.5483/BMBRep.2021.54.12.154
Type
Article
Appears in Collections:
Division of Research on National Challenges > Biodefense Research Center > 1. Journal Articles
Division of Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
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