Adaptor protein Abelson interactor 1 in homeostasis and disease.
Autor: | Petersen M; Division of Hematology/Oncology, Department of Medicine, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI, USA.; Center for the Biology of Aging, Brown University, Providence, RI, USA.; Legoretta Cancer Center, Brown University, Providence, RI, USA., Dubielecka P; Division of Hematology/Oncology, Department of Medicine, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI, USA. patrycja_dubielecka-szczerba@brown.edu.; Center for the Biology of Aging, Brown University, Providence, RI, USA. patrycja_dubielecka-szczerba@brown.edu.; Legoretta Cancer Center, Brown University, Providence, RI, USA. patrycja_dubielecka-szczerba@brown.edu. |
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Jazyk: | angličtina |
Zdroj: | Cell communication and signaling : CCS [Cell Commun Signal] 2024 Oct 01; Vol. 22 (1), pp. 468. Date of Electronic Publication: 2024 Oct 01. |
DOI: | 10.1186/s12964-024-01738-z |
Abstrakt: | Dysregulation of Abelson interactor 1 (ABI1) is associated with various states of disease including developmental defects, pathogen infections, and cancer. ABI1 is an adaptor protein predominantly known to regulate actin cytoskeleton organization processes such as those involved in cell adhesion, migration, and shape determination. Linked to cytoskeleton via vasodilator-stimulated phosphoprotein (VASP), Wiskott-Aldrich syndrome protein family (WAVE), and neural-Wiskott-Aldrich syndrome protein (N-WASP)-associated protein complexes, ABI1 coordinates regulation of various cytoplasmic protein signaling complexes dysregulated in disease states. The roles of ABI1 beyond actin cytoskeleton regulation are much less understood. This comprehensive, protein-centric review describes molecular roles of ABI1 as an adaptor molecule in the context of its dysregulation and associated disease outcomes to better understand disease state-specific protein signaling and affected interconnected biological processes. (© 2024. The Author(s).) |
Databáze: | MEDLINE |
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