Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Antonio S. Gomes"'
Autor:
Prasanna K.R. Allu, Maria Dafne Cardamone, Antonio S. Gomes, Alessandra Dall'agnese, Carly Cederquist, Hui Pan, Jonathan M. Dreyfuss, Sven Enerbäck, C. Ronald Kahn
Publikováno v:
Molecular Metabolism, Vol 78, Iss , Pp 101825- (2023)
Objective: Insulin acts on the liver via changes in gene expression to maintain glucose and lipid homeostasis. This study aimed to the Forkhead box protein K1 (FOXK1) associated gene regulatory network as a transcriptional regulator of hepatic insuli
Externí odkaz:
https://doaj.org/article/d2e1cc8bad99432488ec8c7abd957cfd
Autor:
Jon M. Madison, Karen Duong, Ellen F. Vieux, Namrata D. Udeshi, Sumaiya Iqbal, Elise Requadt, Shaunt Fereshetian, Michael C. Lewis, Antonio S. Gomes, Kerry A. Pierce, Randall J. Platt, Feng Zhang, Arthur J. Campbell, Dennis Lal, Florence F. Wagner, Clary B. Clish, Steven A. Carr, Morgan Sheng, Edward M. Scolnick, Jeffrey R. Cottrell
Publikováno v:
iScience, Vol 24, Iss 1, Pp 101935- (2021)
Summary: Genetic variation of the 16p11.2 deletion locus containing the KCTD13 gene and of CUL3 is linked with autism. This genetic connection suggested that substrates of a CUL3-KCTD13 ubiquitin ligase may be involved in disease pathogenesis. Compar
Externí odkaz:
https://doaj.org/article/02815da01a7f40da86fd1e72b7901ade
Autor:
Raquel V Mendes, Nuno Figueiredo, Rita Fior, Antonio S. Gomes, Miguel Godinho Ferreira, Vanda Póvoa, Tânia Carvalho
Publikováno v:
Proceedings of the National Academy of Sciences of the United States of America
Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 2017, 114 (39), pp.E8234-E8243. ⟨10.1073/PNAS.1618389114⟩
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Agência para a Sociedade do Conhecimento (UMIC)-FCT-Sociedade da Informação
instacron:RCAAP
Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 2017, 114 (39), pp.E8234-E8243. ⟨10.1073/PNAS.1618389114⟩
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Agência para a Sociedade do Conhecimento (UMIC)-FCT-Sociedade da Informação
instacron:RCAAP
Cancer is as unique as the person fighting it. With the exception of a few biomarker-driven therapies, patients go through rounds of trial-and-error approaches to find the best treatment. Using patient-derived cell lines, we show that zebrafish larva
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6d6f8760c492502f929e142ecb87f287
https://hal.archives-ouvertes.fr/hal-02438810/file/394597_2_other__4rt928.pdf
https://hal.archives-ouvertes.fr/hal-02438810/file/394597_2_other__4rt928.pdf
Autor:
Jianghui Hou, Daniel A. Goodenough, Mingli Hou, Aparna Renigunta, Antonio S. Gomes, David L. Paul, Siegfried Waldegger
Publikováno v:
Proceedings of the National Academy of Sciences. 106:15350-15355
Claudins are tight junction integral membrane proteins that are key regulators of the paracellular pathway. Defects in claudin-16 (CLDN16) and CLDN19 function result in the inherited human renal disorder familial hypomagnesemia with hypercalciuria an
Autor:
Siegfried Waldegger, Antonio S. Gomes, Aparna Renigunta, Daniel A. Goodenough, Eveline E. Schneeberger, Martin Konrad, Jianghui Hou, David L. Paul
Publikováno v:
The Journal of clinical investigation. 118(2)
Tight junctions (TJs) play a key role in mediating paracellular ion reabsorption in the kidney. Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is an inherited disorder caused by mutations in the genes encoding the TJ protein
Autor:
Markus Bleich, Qingshang Yan, Jianghui Hou, Qixian Shan, Tong Wang, David L. Paul, Antonio S. Gomes, Daniel A. Goodenough
Publikováno v:
The Journal of biological chemistry. 282(23)
Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney. Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a human disorder caused by mutations in the tight junction protein claudin-16. Howev