Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Alvaro Blanch"'
Publikováno v:
PLoS ONE, Vol 8, Iss 6, p e66436 (2013)
The p53 family of transcription factors is a key regulator of cell proliferation and death. In this report we identify the eukaryotic translation elongation factor 1-alpha 1 (eEF1A1) to be a novel p53 and p73 interacting protein. Previous studies hav
Externí odkaz:
https://doaj.org/article/b25259b0db3446f3a48d144d9e13069b
Autor:
Monika Podkowa, Daniel A. Morgenstern, Nikolaus E. Wolter, David L. Kaplan, Teresa Partridge, Jennifer K Wolter, Alvaro Blanch, Meredith S. Irwin, Lynn S. Cheng
Publikováno v:
Oncotarget
Neuroblastoma (NB) is a pediatric tumor of the sympathetic nervous system, which is often associated with elevated catecholamines. More than half of patients with metastatic NB relapse and survival is extremely poor with current therapies. In a high-
Publikováno v:
Journal of Biological Chemistry. 281:34096-34103
Mutations in p73 are rare in cancer. Emerging evidence suggests that the relative expression of various p73 isoforms may contribute to tumorigenesis. Alternative promoters and N-terminal splicing result in the transcription and processing of either f
Autor:
Alvaro Blanch, Teresa Caballero, Daniel Callejo, Margarita López-Trascasa, Olga Roche, Noelia Sastre
Publikováno v:
ResearcherID
Scopus-Elsevier
Scopus-Elsevier
Background Hereditary angioedema (HAE) is a rare disease caused by C1 inhibitor mutations. Although more than 100 mutations have been described, epidemiologic data are lacking; therefore, we developed a Spanish HAE patient registry. Objective To stud
Autor:
Peter J. Späth, E. Rusicke, Christoph Bucher, Alvaro Blanch, Olga Roche, Emanuela Pappalardo, István Karádi, Marco Cicardi, Mathias Juers, Inmaculada Martinez-Saguer, Roberto Giacomelli, Pál Novák Kaposi, Anthony J. Castaldo, Erik Waage Nielsen, Roberto Perricone, Arianna Kitzinger, Kalman Fay, Emel Aygören-Pürsün, Carlo Perricone, Christian Drouet, George Füst, Beáta Visy, C. Erik Hack, Vincenzo Penna, Hilary Longhurst, Tímea Kollár, George Harmat, István Nagy, Nicole Monnier, Éva Németh, Jan H. Nuijens, Bettina Fischer, Ursula Rauch, Peter L. Lakatos, Caterina De Carolis, Caroline O'Grady, Edit Takács, Margarita López-Trascasa, Henriette Farkas, Albrecht Gröner, George Szendei, Lilian Varga, Alvin E. Davis, Lennart Truedsson, Béla Fekete, John Jakenfelds, Andrea Zanichelli, Wolfhart Kreuz, Kayla Williams, Lajos Kalmar, Lorenza C. Zingale, Karen Binkley, Christiane Duponchel, Laurence Bouillet, Attila Tordai, Luigi Fontana, Angelo Agostoni, Konrad Bork
Publikováno v:
The Journal of Allergy and Clinical Immunology
Hereditary angioedema (HAE), a rare but life-threatening condition, manifests as acute attacks of facial, laryngeal, genital, or peripheral swelling or abdominal pain secondary to intra-abdominal edema. Resulting from mutations affecting C1 esterase
Publikováno v:
PLoS ONE, Vol 8, Iss 6, p e66436 (2013)
PLoS ONE
PLoS ONE
The p53 family of transcription factors is a key regulator of cell proliferation and death. In this report we identify the eukaryotic translation elongation factor 1-alpha 1 (eEF1A1) to be a novel p53 and p73 interacting protein. Previous studies hav
Autor:
I. Urrutia, Pedro M. Gamboa, Gumersindo Fontán, Margarita López-Trascasa, Olga Roche, Alvaro Blanch
Publikováno v:
The Journal of allergy and clinical immunology. 118(6)
Background C1 Inhibitor (C1-Inh) deficiency causes angioedema and can be hereditary (HAE), caused by mutations in the C1-Inh gene (C1NH), or acquired (AAE). Patients with HAE show a complement profile different from that of patients with AAE with nor
Autor:
Alvaro, Blanch, Olga, Roche, Eduardo, López-Granados, Gumersindo, Fontán, Margarita, López-Trascasa
Publikováno v:
Human mutation. 20(5)
Hereditary angioedema (HAE) is caused by mutations in the C1 inhibitor gene (SERPING1, C1NH) and the result is C1 inhibitor deficiency, either in levels or function. We have searched exon 8 for mutations by direct sequencing and analyzed the rest of
Publikováno v:
Cancer Research. 69:B1-B1
MDM2 is an E3 ligase that promotes ubiquitin-mediated destruction of p53. Cellular stresses such as DNA damage can lead to p53 activation due in part to MDM2 destabilization. Here, we show that the stability of MDM2 is regulated by an ubiquitin-like
Autor:
Alvaro Blanch, Olga Roche, Eduardo López-Granados, Gumersindo Fontán, Margarita López-Trascasa
Publikováno v:
Human Mutation. 21:102-102