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Visualitza Recerca: articles, congressos, llibres per autoria "Aligué, Rosa"

Ara mostrant els elements 1-4 de 4

A new negative feedback mechanism for MAPK pathway inactivation through Srk1 MAPKAP kinase

Marquina, Maribel; Lambea, Eva; Carmona, Mercè; Sánchez-Marinas, Marta; López-Aviles, Sandra; Ayté del Olmo, José; Hidalgo Hernando, Elena; Aligué, Rosa (Nature Research, 2022)

The fission yeast mitogen-activated kinase (MAPK) Sty1 is essential for cell survival in response to different environmental insults. In unstimulated cells, Sty1 forms an inactive ternary cytoplasmatic complex with the ...
p27Kip1, PCAF and PAX5 cooperate in the transcriptional regulation of specific target genes

Perearnau, Anna; Orlando, Serena; Islam, Abul, 1978-; Gallastegui Calvache, Edurne; Martínez, Jonatan; Jordan Vallès, Albert; Bigas Salvans, Anna; Aligué, Rosa; Pujol, Maria Jesús; Bachs Valldeneu, Oriol (Oxford University Press, 2017)

The cyclin-dependent kinase inhibitor p27Kip1 (p27) also behaves as a transcriptional repressor. Data showing that the p300/CBP-associated factor (PCAF) acetylates p27 inducing its degradation suggested that PCAF and p27 ...
Role of p27Kip1 as a transcriptional regulator

Bachs Valldeneu, Oriol; Gallastegui Calvache, Edurne; Orlando, Serena; Bigas Salvans, Anna; Morante-Redolat, José Manuel; Serratosa, Joan; Fariñas, Isabel; Aligué, Rosa; Pujol, Maria Jesús (Impact Journal, 2018)

The protein p27Kip1 is a member of the Cip/Kip family of cyclin-dependent kinase (Cdk) inhibitors. It interacts with both the catalytic and the regulatory subunit (cyclin) and introduces a region into the catalytic cleave ...
β-Catenin is required for T-cell leukemia initiation and MYC transcription downstream of Notch1.

Gekas, Christos; Teresa, D'Altri 1984-; Aligué, Rosa; González, Jessica; Espinosa Blay, Lluís; Bigas Salvans, Anna (Nature Publishing Group, 2016)

Notch activation is instrumental in the development of most T-cell acute lymphoblastic leukemia (T-ALL) cases, yet Notch mutations alone are not sufficient to recapitulate the full human disease in animal models. We here ...