To be, or notch to be: mediating cell fate from embryogenesis to lymphopoiesis
Autor: | Elizabeth Quail, Mark N. Cruickshank, Daniela Ulgiati, Han Leng Ng |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Cell type Notch signaling pathway Embryonic Development Review Cell fate determination Biology 0601 Biochemistry and Cell Biology Biochemistry Microbiology 03 medical and health sciences 0302 clinical medicine Animals Humans Cell Lineage Lymphopoiesis Lymphocytes Progenitor cell Molecular Biology development Notch signaling B cell Receptors Notch leukemia Juxtacrine signalling Embryonic stem cell QR1-502 Cell biology 030104 developmental biology 030220 oncology & carcinogenesis Cellular model Signal Transduction |
Zdroj: | Biomolecules, Vol 11, Iss 849, p 849 (2021) Biomolecules |
Popis: | Notch signaling forms an evolutionarily conserved juxtacrine pathway crucial for cellular development. Initially identified in Drosophila wing morphogenesis, Notch signaling has since been demonstrated to play pivotal roles in governing mammalian cellular development in a large variety of cell types. Indeed, abolishing Notch constituents in mouse models result in embryonic lethality, demonstrating that Notch signaling is critical for development and differentiation. In this review, we focus on the crucial role of Notch signaling in governing embryogenesis and differentiation of multiple progenitor cell types. Using hematopoiesis as a diverse cellular model, we highlight the role of Notch in regulating the cell fate of common lymphoid progenitors. Additionally, the influence of Notch through microenvironment interplay with lymphoid cells and how dysregulation influences disease processes is explored. Furthermore, bi-directional and lateral Notch signaling between ligand expressing source cells and target cells are investigated, indicating potentially novel therapeutic options for treatment of Notch-mediated diseases. Finally, we discuss the role of cis-inhibition in regulating Notch signaling in mammalian development. |
Databáze: | OpenAIRE |
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