Zobrazeno 1 - 10
of 48
pro vyhledávání: '"Jordi Magrané"'
Autor:
Hong Lin, Jordi Magrane, Amy Rattelle, Anna Stepanova, Alexander Galkin, Elisia M. Clark, Yi Na Dong, Sarah M. Halawani, David R. Lynch
Publikováno v:
Disease Models & Mechanisms, Vol 11, Iss 1 (2018)
Externí odkaz:
https://doaj.org/article/97cbd0599aa94169adb7d5b8df7ca5e5
Autor:
Jordi Magrané, Manuel Reina, Roser Pagan, Ana Luna, Ricardo P. Casaroli-Marano, Bo Angelin, Mats Gåfvels, Senén Vilaró
Publikováno v:
Journal of Lipid Research, Vol 39, Iss 11, Pp 2172-2181 (1998)
The very low density lipoprotein (VLDL) receptor is a member of the low density lipoprotein supergene family of receptors in which differential splicing of mRNA has been reported. We present several lines of evidence showing that bovine aortic endoth
Externí odkaz:
https://doaj.org/article/3a79e5a6c18141f19e4b7076233703ba
Autor:
Wencheng Liu, Cristofol Vives-Bauza, Rebeca Acín-Peréz, Ai Yamamoto, Yingcai Tan, Yanping Li, Jordi Magrané, Mihaela A Stavarache, Sebastian Shaffer, Simon Chang, Michael G Kaplitt, Xin-Yun Huang, M Flint Beal, Giovanni Manfredi, Chenjian Li
Publikováno v:
PLoS ONE, Vol 4, Iss 2, p e4597 (2009)
Mutations in PTEN induced kinase 1 (PINK1), a mitochondrial Ser/Thr kinase, cause an autosomal recessive form of Parkinson's disease (PD), PARK6. Here, we report that PINK1 exists as a dimer in mitochondrial protein complexes that co-migrate with res
Externí odkaz:
https://doaj.org/article/852a8703ec6941798c2d544d3cb17f23
Autor:
Belem Yoval-Sánchez, Ivan Guerrero, Fariha Ansari, Zoya Niatsetskaya, Max Siragusa, Jordi Magrane, Vadim Ten, Csaba Konrad, Marten Szibor, Alexander Galkin
Publikováno v:
Redox Biology, Vol 77, Iss , Pp 103378- (2024)
Alternative oxidase (AOX) is an enzyme that transfers electrons from reduced quinone directly to oxygen without proton translocation. When AOX from Ciona intestinalis is xenotopically expressed in mice, it can substitute the combined electron-transfe
Externí odkaz:
https://doaj.org/article/fe85487d601545029e197c41e815ccf3
Autor:
Anna Stepanova, David A. Lynch, Amy Rattelle, Yi Na Dong, Hong Lin, Jordi Magrané, Alexander Galkin, Elisia M. Clark, Sarah M. Halawani
Publikováno v:
Disease Models & Mechanisms, Vol 10, Iss 11, Pp 1343-1352 (2017)
Disease Models & Mechanisms
Disease Models & Mechanisms
Friedreich ataxia (FRDA), the most common recessive inherited ataxia, results from deficiency of frataxin, a small mitochondrial protein crucial for iron-sulphur cluster formation and ATP production. Frataxin deficiency is associated with mitochondri
Autor:
Anna Stepanova, Jordi Magrané
Publikováno v:
Molecular and cellular neurosciences. 102
Friedreich's ataxia is a multisystemic genetic disorder within the family of mitochondrial diseases that is characterized by reduced levels of the essential mitochondrial protein frataxin. Based on clinical evidence, the peripheral nervous system is
Autor:
Jordi Magrané, Linlin Sun, Wen-Biao Gan, Guang Yang, Chao Chen, Elina Shtridler, Joseph Cichon
Publikováno v:
J Neurosci Methods
Background The genetically encoded calcium (Ca2+) sensor GCaMP6 has been widely used for imaging Ca2+ transients in neuronal somata, dendrites, and synapses. New method Here we describe five new transgenic mouse lines expressing GCaMP6F (fast) or GCa
Autor:
Alexander Galkin, David A. Lynch, Yi Na Dong, Anna Stepanova, Amy Rattelle, Hong Lin, Jordi Magrané, Elisia M. Clark, Sarah M. Halawani
Publikováno v:
Disease Models & Mechanisms
Disease Models & Mechanisms, Vol 11, Iss 1 (2018)
Disease Models & Mechanisms, Vol 11, Iss 1 (2018)
Friedreich ataxia (FRDA), the most common recessive inherited ataxia, results from deficiency of frataxin, a small mitochondrial protein crucial for iron-sulphur cluster formation and ATP production. Frataxin deficiency is associated with mitochondri
Autor:
Alberto Lleó, Martí Colom-Cadena, Laia Muñoz, Jordi Clarimón, Cristina Guardia-Laguarta, Nahuai Badiola, Marc Suárez-Calvet, Marta Pera, Jordi Magrané, Olivia Belbin
Publikováno v:
Journal of Neurochemistry. 128:330-339
Autosomal-dominant Alzheimer's disease (ADAD) is a genetic disorder caused by mutations in Amyloid Precursor Protein (APP) or Presenilin (PSEN) genes. Studying the mechanisms underlying these mutations can provide insight into the pathways that lead
Publikováno v:
Human Molecular Genetics. 23:1413-1424
Neuronal mitochondrial morphology abnormalities occur in models of familial amyotrophic lateral sclerosis (ALS) associated with SOD1 and TDP43 mutations. These abnormalities have been linked to mitochondrial axonal transport defects, but the temporal