Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Heidi M. Sampson"'
Autor:
Suzana Maria Anjos, Renaud eRobert, Daniel Dirck Waller, Donglei eZhang, Haouaria eBalghi, Heidi M. Sampson, Fabiana eCiciriello, Pierre eLesimple, Graeme eCarlile, Julie eGoepp, Jie eLiao, Pasquale eFerraro, Romeo ePhillipe, Francoise eDantzer, John W Hanrahan, David Y. Thomas
Publikováno v:
Frontiers in Pharmacology, Vol 3 (2012)
Most cystic fibrosis is caused by mutations in CFTR that prevent its trafficking from the ER to the plasma membrane and is associated with exaggerated inflammation, altered metabolism and diminished responses to oxidative stress. PARP-1 is activated
Externí odkaz:
https://doaj.org/article/d7320003fcdd414a925c9ad65ad5025d
Autor:
Henry M. Krause, Jiho Yoo, Sunggeon Ko, Hyun Soo Cho, Cheryl H. Arrowsmith, Kwang Min Choe, Weontae Lee, Ji Hye Yun, Iksoo Chang, Hyeyon Kim, Heidi M. Sampson
Publikováno v:
Journal of Biological Chemistry. 286:31225-31231
The interaction between the orphan nuclear receptor FTZ-F1 (Fushi tarazu factor 1) and the segmentation gene protein FTZ is critical for specifying alternate parasegments in the Drosophila embryo. Here, we have determined the structure of the FTZ-F1
Autor:
Elizabeth Matthes, Graeme W. Carlile, John W. Hanrahan, David Y. Thomas, Renaud Robert, Jie Liao, Heidi M. Sampson
Publikováno v:
Chemistry & Biology. 18(2):231-242
SummaryMost cases of cystic fibrosis (CF) are attributable to the F508del allele of CFTR, which causes the protein to be retained in the endoplasmic reticulum (ER) and subsequently degraded. One strategy for CF therapy is to identify corrector compou
Autor:
Ping Yang, Keith Pardee, Heidi M. Sampson, Mandy M.S. Lam, Wendy White, Suya Liu, Shawn P. Williams, Jeff Reinking, Aled M. Edwards, Gilles A. Lajoie, Henry M. Krause
Publikováno v:
Cell. 122:195-207
SummaryNuclear receptors are a family of transcription factors with structurally conserved ligand binding domains that regulate their activity. Despite intensive efforts to identify ligands, most nuclear receptors are still “orphans.” Here, we de
Autor:
Andrew J. Simmonds, Daniela Hlousek, Anthony Percival-Smith, Carol Schwartz, Heidi M. Sampson, Henry M. Krause, John W. R. Copeland
Publikováno v:
The EMBO Journal. 20:510-519
To activate transcription, most nuclear receptor proteins require coactivators that bind to their ligand-binding domains (LBDs). The Drosophila FTZ-Factor1 (FTZ-F1) protein is a conserved member of the nuclear receptor superfamily, but was previously
Autor:
Show Ling Shyng, Yelena Kryukova, David Y. Thomas, Qing Zhou, Erik M. Olson, Heidi M. Sampson, Pei Chun Chen
Publikováno v:
The Journal of biological chemistry. 288(29)
ATP-sensitive potassium (KATP) channels consisting of sulfonylurea receptor 1 (SUR1) and the potassium channel Kir6.2 play a key role in insulin secretion by coupling metabolic signals to β-cell membrane potential. Mutations in SUR1 and Kir6.2 that
Publikováno v:
Trends in pharmacological sciences. 34(2)
Cystic fibrosis (CF) is a lethal disease caused by mutations in the CFTR gene. The most frequent mutation is deletion of a phenylalanine residue (ΔF508) that results in retention of the mutant, but otherwise functional, protein in the endoplasmic re
Autor:
David Y. Thomas, Heidi M. Sampson
Publikováno v:
Chemical Biology: Approaches to Drug Discovery and Development to Targeting Disease
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::57de4c80d19698eade8c7131b89bca66
https://doi.org/10.1002/9781118435762.ch20
https://doi.org/10.1002/9781118435762.ch20
Autor:
David Y. Thomas, Ryan M. Centko, Suzana M. Anjos, John W. Hanrahan, Donglei Zhang, Heidi M. Sampson, Jie Liao, Roger G. Linington, Robert A. Keyzers, Christopher A. Gray, Raymond J. Andersen, Renaud Robert, Graeme W. Carlile, Katrina A. Teske, David E. Williams, Yan Lu-Ping
Publikováno v:
Chemistrybiology. 19(10)
SummaryMutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause CF. The most common mutation, F508 deletion, causes CFTR misfolding and endoplasmic reticulum retention, preventing it from trafficking to the cell surface.
Autor:
Donglei Zhang, Jie Liao, Graeme W. Carlile, Pierre Lesimple, Heidi M. Sampson, Haouaria Balghi, Daniel D Waller, David Y. Thomas, Romeo Phillipe, Suzana M. Anjos, Françoise Dantzer, Julie Goepp, Pasquale Ferraro, Renaud Robert, Fabiana Ciciriello, John W. Hanrahan
Publikováno v:
Frontiers in Pharmacology, Vol 3 (2012)
Frontiers in Pharmacology
Frontiers in Pharmacology
Most cystic fibrosis is caused by mutations in CFTR that prevent its trafficking from the ER to the plasma membrane and is associated with exaggerated inflammation, altered metabolism, and diminished responses to oxidative stress. PARP-1 is activated
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b7ddc7e0be07ea010971b8615f5c6f40
http://journal.frontiersin.org/article/10.3389/fphar.2012.00165/abstract
http://journal.frontiersin.org/article/10.3389/fphar.2012.00165/abstract