Zobrazeno 1 - 10
of 68
pro vyhledávání: '"Carmen, R Valdivia"'
Autor:
Jun Li, Fei Wang, Xinyan Liu, Zhixiao Yang, Xiaoyu Hua, Hongqiao Zhu, Carmen R. Valdivia, Li Xiao, Songyu Gao, Héctor H. Valdivia, Liang Xiao, Jinming Wang
Publikováno v:
Materials Today Bio, Vol 23, Iss , Pp 100859- (2023)
Background: Reducing Ca2+ content in the sarcoplasmic reticulum (SR) through ryanodine receptors (RyRs) by calcin is a potential intervention strategy for the SR Ca2+ overload triggered by β-adrenergic stress in acute heart diseases. Methods: OpiCal
Externí odkaz:
https://doaj.org/article/df2e2294dc5d439dab6fcf97292832cc
Autor:
Jingjing Zheng, Holly C. Dooge, Marta Pérez-Hernández, Yan-Ting Zhao, Xi Chen, Jonathan J. Hernandez, Carmen R. Valdivia, Julieta Palomeque, Eli Rothenberg, Mario Delmar, Héctor H. Valdivia, Francisco J. Alvarado
Publikováno v:
J Mol Cell Cardiol
Ryanodine receptor 2 (RyR2) is an ion channel in the heart responsible for releasing into the cytosol most of the Ca(2+) required for contraction. Proper regulation of RyR2 is critical, as highlighted by the association between channel dysfunction an
Autor:
Omid Haji-Ghassemi, Yu Seby Chen, Kellie Woll, Georgina B. Gurrola, Carmen R. Valdivia, Wenxuan Cai, Songhua Li, Hector H. Valdivia, Filip Van Petegem
Publikováno v:
Science Advances. 9
Calcins are peptides from scorpion venom with the unique ability to cross cell membranes, gaining access to intracellular targets. Ryanodine Receptors (RyR) are intracellular ion channels that control release of Ca 2+ from the endoplasmic and sarcopl
Autor:
Claudia, Tito, Ilaria, Genovese, Flavia, Giamogante, Anna, Benedetti, Selenia, Miglietta, Lucia, Barazzuol, Loredana, Cristiano, Alessia, Iaiza, Sabatino, Carolini, Luciana De Angelis, Silvia, Masciarelli, Stefania Annarita Nottola, Giuseppe, Familiari, Vincenzo, Petrozza, Mattia, Lauriola, Tamagnone, Luca, Andrea, Ilari, Tito, Calì, Hector, H Valdivia, Carmen, R Valdivia, Gianni, Colotti, Francesco, Fazi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=od______2601::1f5c95a5955c98b87171767cf9470bdd
https://hdl.handle.net/10807/244014
https://hdl.handle.net/10807/244014
Autor:
Maria Musgaard, Elisa Venturi, Rebecca Sitsapesan, Ming Lei, Charalampos Sigalas, Jianshu Hu, Carmen R. Valdivia, Abigail D. Wilson, Héctor H. Valdivia
Key points RyR2 mutations can cause type-1 catecholaminergic polymorphic ventricular tachycardia (CPVT1), a lethal, autosomal-dominant arrhythmic disease. However, the changes in RyR2 ion-channel function that result from the many different patient m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::856e051f82ca4a632db88c66eec0d104
https://ora.ox.ac.uk/objects/uuid:7421fc54-4b61-4e5e-b05c-68743bb73ce3
https://ora.ox.ac.uk/objects/uuid:7421fc54-4b61-4e5e-b05c-68743bb73ce3
Autor:
Abigail D, Wilson, Jianshu, Hu, Charalampos, Sigalas, Elisa, Venturi, Héctor H, Valdivia, Carmen R, Valdivia, Ming, Lei, Maria, Musgaard, Rebecca, Sitsapesan
Publikováno v:
J Physiol
Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is a lethal genetic disease causing arrhythmias and sudden cardiac death in children and young adults and is linked to mutations in the cardiac ryanodine receptor (RyR2). The effect
Autor:
Yuriana Aguilar-Sanchez, Olivier Villejoubert, Feliciano Protasi, Liheng Yin, Camille Rabesahala de Meritens, Julio L. Álvarez, Pascale Gerbaud, Ernst Niggli, Romain Perrier, Pierre Joanne, Héctor H. Valdivia, F. Anthony Lai, Spyros Zissimopoulos, Riccardo Rizzetto, Esther Zorio, Elena Marques-Sule, Linwei Li, Yue Yi Wang, Yadan Zhang, Alexandra Zahradnikova Jr, Carmen R. Valdivia, Simona Boncompagni, Jean-Pierre Benitah, Valérie Nicolas, Ana Maria Gomez, Josefina Ramos-Franco, Philippe Mateo, Miguel Fernandez-Tenorio
Publikováno v:
CIRCULATION RESEARCH
r-IIS La Fe. Repositorio Institucional de Producción Científica del Instituto de Investigación Sanitaria La Fe
instname
Circulation Research
Circulation Research, American Heart Association, 2021, 129 (3), pp.e35-e52. ⟨10.1161/CIRCRESAHA.121.319094⟩
Circ Res
r-IIS La Fe. Repositorio Institucional de Producción Científica del Instituto de Investigación Sanitaria La Fe
instname
Circulation Research
Circulation Research, American Heart Association, 2021, 129 (3), pp.e35-e52. ⟨10.1161/CIRCRESAHA.121.319094⟩
Circ Res
Rationale: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare disease, manifested by syncope or sudden death in children or young adults under stress conditions. Mutations in the Ca 2+ release channel/RyR2 (type 2 ryanodine recept
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::65e2200fcbc412196d1bcdf3e2b9efab
https://fundanet.iislafe.san.gva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=14580
https://fundanet.iislafe.san.gva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=14580
Autor:
Eva Delpón, Rafael J. Ramirez, Marcos Matamoros, Todd J. Herron, Daniela Ponce-Balbuena, Kuljeet Kaur, Héctor H. Valdivia, Manuel Zarzoso, Francisco J. Alvarado, B. Cicero Willis, Eric N. Jiménez-Vázquez, F. Javier Díez-Guerra, José Jalife, Ricardo Caballero, Carmen R. Valdivia, Andre Monteiro da Rocha, Guadalupe Guerrero-Serna, Marta Pérez-Hernández, Katherine Campbell
Publikováno v:
Circulation Research. 122:1501-1516
Rationale: In cardiomyocytes, Na V 1.5 and Kir2.1 channels interact dynamically as part of membrane bound macromolecular complexes. Objective: The objective of this study was to test whether Na V 1.5 and Kir2.1 preassemble during early forward traffi
Autor:
Michael J. Ackerman, David J. Tester, Carmen R. Valdivia, Bi-Hua Tan, Jonathan C. Makielski, Matteo Vatta, Argelia Medeiros-Domingo, Jianding Cheng, David W. Van Norstrand
Publikováno v:
Cardiogenetics, Vol 1, Iss 1, Pp e13-e13 (2011)
The SNTA1-encoded α1-syntrophin (SNTA1) missense mutation, p.A257G, causes long QT syndrome (LQTS) by pathogenic accentuation of Nav1.5’s sodium current (INa). Subsequently, we found p.A257G in combination with the SNTA1 polymorphism, p.P74L in 4
Externí odkaz:
https://doaj.org/article/36be61019c1e42da8b8003167d38a7b0
Publikováno v:
Circulation Research. 122:1327-1329
With the completion of the human genome in 2003, it became evident what had been suspected for a time through isolated bits of data: a surprisingly small proportion of the genome—only ≈2%!—was actually translated into proteins (DNA→RNA→prot