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https://doi.org/10.14670/HH-18-744


Título: | The diverse functions of DYRK2 in response to cellular stress |
Fecha de publicación: | 2024 |
Editorial: | Universidad de Murcia, Departamento de Biologia Celular e Histiologia |
Cita bibliográfica: | Histology and Histopathology Vol. 39, nº11 (2024) |
ISSN: | 0213-3911 1699-5848 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Cellular stress Homeostasis DYRK2 Kinase DNA damage Primary cilia |
Resumen: | To maintain microenvironmental and cellular homeostasis, cells respond to multiple stresses by activating characteristic cellular mechanisms consisting of receptors, signal transducers, and effectors. Dysfunction of these mechanisms can trigger multiple human diseases as well as cancers. Dual-specificity tyrosine-regulated kinases (DYRKs) are members of the CMGC group and are evolutionarily conserved from yeast to mammals. Previous studies revealed that DYRK2 has important roles in the regulation of the cell cycle and survival in cancer cells. On the other hand, recent studies show that DYRK2 also exhibits significant functions in multiple cellular stress responses and in maintaining cellular homeostasis. Hence, the further elucidation of mechanisms underlying DYRK2’s diverse responses to various stresses helps to promote the advancement of innovative clinical therapies and pharmacological drugs. This review summarizes the molecular mechanisms of DYRK2, particularly focusing on cellular stress responses. |
Autor/es principal/es: | Kawamura, Akira Yoshida, Saishu Yoshida, Kiyotsugu |
URI: | http://hdl.handle.net/10201/144869 |
DOI: | https://doi.org/10.14670/HH-18-744 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 8 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
Aparece en las colecciones: | Vol.39,nº11 (2024) |
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Kawamura-39-1427-1434-2024.pdf | 667,43 kB | Adobe PDF | ![]() Visualizar/Abrir |
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