Journal
BMB REPORTS
Volume 54, Issue 12, Pages 626-631Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2021.54.12.154
Keywords
Cyclin-dependent kinase 5 (CDK5); Embryonic stem cell; Glycogen synthase kinase 3 beta (GSK3 beta); Janus kinase-2 (JAK2); Neurogenesis; Neuronal differentiation
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Funding
- Defense Acquisi-tion Program Administration [ADD-911255201]
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JAK2 may negatively regulate neuronal differentiation by suppressing the GSK-3 beta/Fyn/CDK5 signaling pathway responsible for morphological maturation in the nervous system.
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 beta, Fyn, and cyclin-dependent kinase 5. Knockdown of JAK2 resulted in accumulation of GTP-bound 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-3 beta/Fyn/CDK5 signaling pathway responsible for morphological maturation.
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