TAp73-mediated the activation of c-Jun N-terminal kinase enhances cellular chemosensitivity to cisplatin in ovarian cancer cells.
P73, one member of the tumor suppressor p53 family, shares highly structural and functional similarity to p53. Like p53, the transcriptionally active TAp73 can mediate cellular response to chemotherapeutic agents in human cancer cells by up-regulating the expressions of its pro-apoptotic target gene...
Guardado en:
Autores principales: | Pingde Zhang, Stephanie Si Liu, Hextan Yuen Sheung Ngan |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Public Library of Science (PLoS)
2012
|
Materias: | |
Acceso en línea: | https://doaj.org/article/8632a0fcc81c41eea1738630394de85f |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
Ejemplares similares
-
A machine learning approach to identify predictive molecular markers for cisplatin chemosensitivity following surgical resection in ovarian cancer
por: Nicholas Brian Shannon, et al.
Publicado: (2021) -
Short-term activation of the Jun N-terminal kinase pathway in apoptosis-deficient cells of Drosophila induces tumorigenesis
por: Noelia Pinal, et al.
Publicado: (2018) -
Low level of Lck kinase in Th2 cells limits expression of CD4 co-receptor and S73 phosphorylation of transcription factor c-Jun
por: Yury V. Shebzukhov, et al.
Publicado: (2017) -
c-Jun N-terminal kinase 1 (JNK1) modulates oligodendrocyte progenitor cell architecture, proliferation and myelination
por: Martina Lorenzati, et al.
Publicado: (2021) -
FK866 attenuates acute hepatic failure through c-jun-N-terminal kinase (JNK)-dependent autophagy
por: Enshuang Guo, et al.
Publicado: (2017)