Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Ma. Luisa Ordonez-Sanchez"'
Autor:
Luz E. Guillen Pineda, Ernesto Roldan-Valadez, Jannette Furuzawa-Carballeda, Suzanne B.R. Jacobs, Patricia Clark, Ivette Cruz-Bautista, Ma. Luisa Ordonez-Sanchez, Alexandro J Martagón Rosado, Jose C. Florez, Elena Zambrano, Tannia Viveros Ruiz, Paloma Almeda-Valdes, Joaquin Azpiroz, Alicia Huerta-Chagoya, Donaji V Gómez Velasco, Magdalena del Rocío Sevilla-González, Claudia J Bautista, Carlos A. Aguilar-Salinas, Karen Guadalupe Rodríguez-Álvarez, Liliana Muñoz Hernandez, Hortensia Moreno-Macías, Miguel Herrera-Hernandez, Olimpia Arellano Campos, Geoffrey A. Walford, María Teresa Tusié Luna, Omar Yaxmehen Bello-Chavolla
Publikováno v:
European Journal of Endocrinology. 180:99-107
Objective A haplotype at chromosome 17p13 that reduces expression and function of the solute carrier transporter SLC16A11 is associated with increased risk for type 2 diabetes in Mexicans. We aim to investigate the detailed metabolic profile of SLC16
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0f39a4d124d675385938fbdb02ac292e
https://doi.org/10.1530/eje-18-0677
https://doi.org/10.1530/eje-18-0677
Autor:
Dalia Cuenca, Jose Luis Ventura-Gallegos, Paloma Almeda-Valdes, María Teresa Tusié-Luna, Alfredo Reza-Albarran, Laura Ventura-Ayala, Ma. Luisa Ordoñez-Sánchez, Yayoi Segura-Kato, Francisco Javier Gomez-Perez, Michelle De Puy Conte, Lizbet Ruilova Gonzalez, Alejandro Zentella-Dehesa
Publikováno v:
Molecular Genetics and Metabolism Reports, Vol 35, Iss , Pp 100965- (2023)
Severe insulin resistance can be caused by rare genetic defects in the insulin receptor known as insulin receptoropathies. These genetic defects cause a wide spectrum of clinical manifestations ranging from mild syndromes to lethal disorders. Among t
Externí odkaz:
https://doaj.org/article/54dc240e5dbb40a293e3a8ce3a47ce6c
Autor:
Carlos A. Aguilar-Salinas, Ma. Luisa Velasco-Pérez, Ma. Luisa Ordonez-Sanchez, Salvador Ramírez-Jiménez, Eduardo García-García, Marcelo Arellano Torres, Melchor Alpizar, Juan A. Rull, Juan Ramón Martínez-François, Eduardo Reyes-Rodríguez, Francisco J. Gómez-Pérez, Aarón Domínguez-López, Ma. Teresa Tusié-Luna
Publikováno v:
The Journal of Clinical Endocrinology & Metabolism. 86:220-226
The objective of this study was to investigate possible defects in the insulin sensitivity and/or the acute insulin response in a group of Mexican patients displaying early-onset type 2 diabetes and to evaluate the contribution of mutations in three
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::ce9cf9cc70e55f084a509f9c5aa923b9
https://doi.org/10.1210/jcem.86.1.7134
https://doi.org/10.1210/jcem.86.1.7134
Autor:
Ma. Luisa Ordonez-Sanchez, Xochitl Felix-Lopez, Ma. Teresa Tusié-Luna, Alejandro Zentella-Dehesa, Salvador Ramírez-Jiménez, José Luis Ventura-Gallegos, Laura Riba
Publikováno v:
Journal of pediatric endocrinologymetabolism : JPEM. 16(7)
Steroid 21-hydroxylase deficiency is the major cause of congenital adrenal hyperplasia, an autosomic recessive disorder that affects the synthesis of aldosterone and cortisol. The disease presents a wide spectrum of clinical phenotypes as a result of
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4d007492d0ff88e6fdd86bd958cccd28
https://pubmed.ncbi.nlm.nih.gov/14513879
https://pubmed.ncbi.nlm.nih.gov/14513879
Autor:
F. Mendoza-Morfin, Ma. Luisa Ordonez-Sanchez, Salvador Ramírez-Jiménez, Juan Pablo Méndez, Nelly Altamirano-Bustamante, Carlos Robles-Valdés, Javier Cabello-Villegas, Raúl Calzada-León, Ma. Teresa Tusié-Luna, Margarita Teran-Garcia
Publikováno v:
Human genetics. 98(3)
Steroid 21-hydroxylase deficiency is caused by mutations in the CYP21 gene. Approximately 95% of mutant alleles are generated by recombination events between the acitve gene CYP21 and its highly homologous pseudogene, CYP21P. Deletion alleles are gen
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::efaf846d8ebaf57892e5e4a7bc2e0572
https://pubmed.ncbi.nlm.nih.gov/8707311
https://pubmed.ncbi.nlm.nih.gov/8707311