Cargando…
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...
Autores principales: | Zhang, Pingde, Liu, Stephanie Si, Ngan, Hextan Yuen Sheung |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416758/ https://www.ncbi.nlm.nih.gov/pubmed/22900074 http://dx.doi.org/10.1371/journal.pone.0042985 |
Ejemplares similares
-
C‐Jun N‐terminal kinase signalling pathway in response to cisplatin
por: Yan, Dong, et al.
Publicado: (2016) -
Crosstalk between c-Jun and TAp73α/β contributes to the apoptosis–survival balance
por: Koeppel, Max, et al.
Publicado: (2011) -
TAp73 promotes anabolism
por: Amelio, Ivano, et al.
Publicado: (2014) -
Relative expression of TAp73 and ΔNp73 isoforms
por: Conforti, Franco, et al.
Publicado: (2012) -
Protein Synthesis Inhibition and Activation of the c-Jun N-Terminal Kinase Are Potential Contributors to Cisplatin Ototoxicity
por: Nicholas, Brian D., et al.
Publicado: (2017)