Zobrazeno 1 - 10
of 29
pro vyhledávání: '"Marta Loureiro"'
Autor:
Adela Guarás, Ester Perales-Clemente, Enrique Calvo, Rebeca Acín-Pérez, Marta Loureiro-Lopez, Claire Pujol, Isabel Martínez-Carrascoso, Estefanía Nuñez, Fernando García-Marqués, María Angeles Rodríguez-Hernández, Ana Cortés, Francisca Diaz, Acisclo Pérez-Martos, Carlos T. Moraes, Patricio Fernández-Silva, Aleksandra Trifunovic, Plácido Navas, Jesús Vazquez, Jose A. Enríquez
Publikováno v:
Cell Reports, Vol 15, Iss 1, Pp 197-209 (2016)
Electrons feed into the mitochondrial electron transport chain (mETC) from NAD- or FAD-dependent enzymes. A shift from glucose to fatty acids increases electron flux through FAD, which can saturate the oxidation capacity of the dedicated coenzyme Q (
Externí odkaz:
https://doaj.org/article/398fede521514fbaa72a53db1ef4ebdc
Publikováno v:
Saúde & Tecnologia, Vol 0, Iss 3, Pp 19-24 (2015)
Biotechnology allows plant and animal genetic modification, leading to genetic modified organisms (GMO). The GMO related benefits and risks are still surrounded in controversy, reason why the consumer has the right to decide about its consumption. Th
Externí odkaz:
https://doaj.org/article/1378f86cf2ee4f298a4644db5f789079
Autor:
Pedro M. Quirós, Yaiza Español, Rebeca Acín-Pérez, Francisco Rodríguez, Clea Bárcena, Kenta Watanabe, Enrique Calvo, Marta Loureiro, M. Soledad Fernández-García, Antonio Fueyo, Jesús Vázquez, José Antonio Enríquez, Carlos López-Otín
Publikováno v:
Cell Reports, Vol 8, Iss 2, Pp 542-556 (2014)
We generated mice deficient in Lon protease (LONP1), a major enzyme of the mitochondrial quality control machinery. Homozygous deletion of Lonp1 causes early embryonic lethality, whereas its haploinsufficiency protects against colorectal and skin tum
Externí odkaz:
https://doaj.org/article/c628e3a772344fb6bec50e4f632d1921
Publikováno v:
Acta Médica Portuguesa, Vol 28, Iss 6 (2015)
Palavras-chave: Criança; Escleroderma Sistémica.
Externí odkaz:
https://doaj.org/article/9e35ec7a34684c62a65578d4e9d34a40
Publikováno v:
Pediatric Reports, Vol 7, Iss 3 (2015)
Primary adrenal insufficiency is defined by the impaired synthesis of adrenocortical hormones due to an intrinsic disease of the adrenal cortex. Determining its etiology is crucial to allow adequate long-term management and genetic counseling. We rep
Externí odkaz:
https://doaj.org/article/052361c9580c4de4ab77b2b8c12ed0c0
Publikováno v:
Saúde & Tecnologia, Iss 03 (2009)
A biotecnologia permite modificar geneticamente plantas e animais, dando origem a organismos geneticamente modificados (OGM). Os benefícios e potenciais riscos relacionados com os transgénicos são controversos, pelo que o consumidor tem direito a
Externí odkaz:
https://doaj.org/article/a89dd827af884b0495f703992028dc60
Publikováno v:
Advances in Tourism, Technology and Systems ISBN: 9789811910395
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::723796f74f21eb5c68e6c2580d4120c6
https://doi.org/10.1007/978-981-19-1040-1_12
https://doi.org/10.1007/978-981-19-1040-1_12
Publikováno v:
Lecture Notes in Networks and Systems ISBN: 9783030936761
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::76515c33b44f94f8016139d7474cf52c
https://doi.org/10.1007/978-3-030-93677-8_37
https://doi.org/10.1007/978-3-030-93677-8_37
Autor:
Narcis A. Petriman, Marta Loureiro-López, Michael Taschner, Nevin K. Zacharia, Magdalena M. Georgieva, Niels Boegholm, André Mourão, Robert B. Russell, Jens S. Andersen, Esben Lorentzen
Publikováno v:
bioRxiv/The EMBO Journal
bioRxiv
bioRxiv
Cilia are ubiquitous eukaryotic organelles important to cellular motility, signalling and sensory reception. Cilium formation requires intraflagellar transport for trafficking of structural and signalling components. The large MDa IFT-B complex const
Publikováno v:
Comprehensible Science ISBN: 9783030857981
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::aacec9ecbeea83b7e6a89430150cdce9
https://doi.org/10.1007/978-3-030-85799-8_29
https://doi.org/10.1007/978-3-030-85799-8_29