Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation

Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. JNK1/2 are not only regulated by ROS—they in turn can also control ROS production. The prooxidant and cell death...

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Detalles Bibliográficos
Autores principales: Günther, Julia K., Nikolajevic, Aleksandar, Ebner, Susanne, Troppmair, Jakob, Khalid, Sana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284707/
https://www.ncbi.nlm.nih.gov/pubmed/32429320
http://dx.doi.org/10.3390/biology9050099

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284707/
https://www.ncbi.nlm.nih.gov/pubmed/32429320
http://dx.doi.org/10.3390/biology9050099

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