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α3β1 integrin promotes cell survival via multiple interactions between 14-3-3 isoforms and proapoptotic proteins

Cited 21 time in Web of Science Cited 24 time in Scopus
Authors
Oh, Ju-Eun; Jang, Da Hyun; Kim, Hyunsoo; Kang, Hyun Ki; Chung, Chong-Pyoung; Park, Won Ho; Min, Byung-Moo
Issue Date
2009-11
Publisher
Elsevier
Citation
EXPERIMENTAL CELL RESEARCH 315 (2009) 3187-3200
Keywords
Laminin-5PPFLMLLKGSTR motifKeratinocyte survivalAnti-apoptosis14-3-3ζ/p-Bad complex14-3-3σ/p-YAP complex
Abstract
Laminin-5 and α3β1 integrin promote keratinocyte survival; however, the downstream signaling pathways for laminin-5/α3β1 integrin-mediated cell survival had not been fully established. We report the unexpected finding of multiple interactions between 14-3-3 isoforms and proapoptotic proteins in the survival signaling pathway. Ln5-P4 motif within human laminin-5 α3 chain promotes cell survival and anti-apoptosis by inactivating Bad and YAP. This effect is achieved through the formation of 14-3-3ζ/p-Bad and 14-3-3σ/p-YAP complexes, which is initiated by α3β1 integrin and FAK/PI3K/Akt signaling. These complexes result in cytoplasmic sequestration of Bad and YAP and their subsequent inactivation. An increase in Akt1 activity in cells induces 14-3-3ζ and σ, p-Bad, and p-YAP, promoting cell survival, whereas decreasing Akt activity suppresses the same proteins and inhibits cell survival. Suppression of 14-3-3ζ with RNA-interference inhibits cell viability and promotes apoptosis. These results reveal a new mechanism of cell survival whereby the formation of 14-3-3ζ/p-Bad and 14-3-3σ/p-YAP complexes is initiated by laminin-5 stimulation via the α3β1 integrin and FAK/PI3K/Akt signaling pathways, thereby resulting in cell survival and anti-apoptosis.
ISSN
0014-4827
Language
English
URI
http://hdl.handle.net/10371/69706
DOI
https://doi.org/10.1016/j.yexcr.2009.08.002
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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