Zobrazeno 1 - 10
of 42
pro vyhledávání: '"Leigh Pascoe"'
Autor:
Jean-Marc Victor, Gaëlle Debret, Annick Lesne, Leigh Pascoe, Pascal Carrivain, Gilles Wainrib, Jean-Pierre Hugot
Publikováno v:
PLoS ONE, Vol 11, Iss 6, p e0156138 (2016)
Numerous genetic and environmental risk factors play a role in human complex genetic disorders (CGD). However, their complex interplay remains to be modelled and explained in terms of disease mechanisms.Crohn's Disease (CD) was modeled as a modular n
Externí odkaz:
https://doaj.org/article/cfd64172d76e4103bdbd2ba784c1874b
Autor:
Raphaële Thiébaut, Sophie Esmiol, Patrick Lecine, Batoul Mahfouz, Aurelie Hermant, Cendrine Nicoletti, Stephane Parnis, Julie Perroy, Jean-Paul Borg, Leigh Pascoe, Jean-Pierre Hugot, Vincent Ollendorff
Publikováno v:
PLoS ONE, Vol 11, Iss 11, p e0165420 (2016)
NOD2 contributes to the innate immune response and to the homeostasis of the intestinal mucosa. In response to its bacterial ligand, NOD2 interacts with RICK and activates the NF-κB and MAPK pathways, inducing gene transcription and synthesis of pro
Externí odkaz:
https://doaj.org/article/d104d6b8fb8349ca8fc5fa70f2f07371
Autor:
Jean-Pierre Hugot, Stephane Parnis, Patrick Lécine, Jean-Paul Borg, Leigh Pascoe, Raphaële Thiébaut, Sophie Esmiol, Cendrine Nicoletti, Aurélie Hermant, Julie Perroy, Vincent Ollendorff, Batoul Mahfouz
Publikováno v:
PLoS ONE
PLoS ONE, Public Library of Science, 2016, 11, pp.165420-165420. ⟨10.1371/journal.pone.0165420⟩
Plos One 11 (11), 24 p.. (2016)
PLoS ONE, Vol 11, Iss 11, p e0165420 (2016)
PLoS ONE, 2016, 11 (11), 24 p. ⟨10.1371/journal.pone.0165420⟩
PLoS ONE, Public Library of Science, 2016, 11 (11), 24 p. ⟨10.1371/journ al.pone.0165 420⟩
PLoS ONE, Public Library of Science, 2016, 11 (11), 24 p. ⟨10.1371/journal.pone.0165420⟩
PLoS ONE, Public Library of Science, 2016, 11, pp.165420-165420. ⟨10.1371/journal.pone.0165420⟩
Plos One 11 (11), 24 p.. (2016)
PLoS ONE, Vol 11, Iss 11, p e0165420 (2016)
PLoS ONE, 2016, 11 (11), 24 p. ⟨10.1371/journal.pone.0165420⟩
PLoS ONE, Public Library of Science, 2016, 11 (11), 24 p. ⟨10.1371/journ al.pone.0165 420⟩
PLoS ONE, Public Library of Science, 2016, 11 (11), 24 p. ⟨10.1371/journal.pone.0165420⟩
International audience; NOD2 contributes to the innate immune response and to the homeostasis of the intestinal mucosa. In response to its bacterial ligand, NOD2 interacts with RICK and activates the NF-κB and MAPK pathways, inducing gene transcript
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::99e68a96198b45c742f939cf5f01f507
https://hal.archives-ouvertes.fr/hal-01475335/document
https://hal.archives-ouvertes.fr/hal-01475335/document
Autor:
Gilles Wainrib, Jean-Pierre Hugot, Gaëlle Debret, Annick Lesne, Pascal Carrivain, Jean-Marc Victor, Leigh Pascoe
Publikováno v:
PLoS ONE
PLoS ONE, 2016, 11 (6), pp.e0156138. ⟨10.1371/journal.pone.0156138⟩
PLoS ONE, Public Library of Science, 2016, 11 (6), pp.e0156138. ⟨10.1371/journal.pone.0156138⟩
PLoS ONE, Vol 11, Iss 6, p e0156138 (2016)
PLoS ONE, 2016, 11 (6), pp.e0156138. ⟨10.1371/journal.pone.0156138⟩
PLoS ONE, Public Library of Science, 2016, 11 (6), pp.e0156138. ⟨10.1371/journal.pone.0156138⟩
PLoS ONE, Vol 11, Iss 6, p e0156138 (2016)
International audience; BACKGROUND: Numerous genetic and environmental risk factors play a role in human complex genetic disorders (CGD). However, their complex interplay remains to be modelled and explained in terms of disease mechanisms.METHODS AND
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ad3e2d6541c1d3ab156a26e6f0bdbb68
https://hal.science/hal-02187347/document
https://hal.science/hal-02187347/document
Autor:
Jean-Frederic Colombel, J P Hugot, Miquel A. Gassull, Leigh Pascoe, Raphaële Thiébaut, Camille Jung, Yigael Finkel, Marc Lémann, M. O'Morain, Vibeke Binder, Françoise Merlin, S. Kotti, Curt Tysk, Sven Almer
Publikováno v:
The American Journal of Gastroenterology. 104:384-391
Inflammatory bowel disease (IBD), e.g., Crohn's disease (CD) and ulcerative colitis (UC), is a complex genetic disorder. Tumor necrosis factor (ligand) superfamily, member 15 (TNFSF15) has been previously identified as a susceptibility gene for CD in
Publikováno v:
European Journal of Human Genetics. 15:864-871
Estimation of genotype-specific risks at a disease susceptibility locus is an important question that is best carried out in a prospective study. Nevertheless it is usually desirable to make use of data from the families that have already been collec
Autor:
Paolo Mulatero, Leigh Pascoe, Yves Morel, Kathleen M. Curnow, Stephanie Portrat, Jean-Louis Chaussain
Publikováno v:
The Journal of Clinical Endocrinology & Metabolism. 86:3197-3201
Chromosomal rearrangements are natural experiments that can provide unique insights into in vivo regulation of genes and physiological systems. We have studied a patient with congenital adrenal hyperplasia and steroid 11beta-hydroxylase deficiency wh
Autor:
Brian S. Nunez, Perrin C. White, Kathleen M. Curnow, D. Randy McMillan, Heli Nikkila, Leigh Pascoe
Publikováno v:
Molecular Endocrinology. 14:1351-1364
cDNA clones encoding a novel putative G protein-coupled receptor have been characterized. The receptor is widely expressed in normal solid tissues. Consisting of 1967 amino acid residues, this receptor is one of the largest known and is therefore ref
Autor:
Jean Fiet, Hervé Galons, Ahmed Boudi, Micheline Gourmelen, Gilles Morineau, Leigh Pascoe, Jean-Michel Marc, Pierre Corvol
Publikováno v:
Hypertension. 34:435-441
Abstract —Apparent mineralocorticoid excess is a recessively inherited hypertensive syndrome caused by mutations in the 11β-hydroxysteroid dehydrogenase type 2 gene, which encodes the enzyme normally responsible for converting cortisol to inactive
Autor:
Kathleen M. Curnow, Yves Morel, J. Tourniaire, S. Portrat-Doyen, Leigh Pascoe, O. Richard, Paolo Mulatero, B. Aupetit-Faisant
Publikováno v:
The Journal of Clinical Endocrinology & Metabolism. 83:4156-4161
Isolated deficiencies in aldosterone biosynthesis are caused by mutations in the CYP11B2 (aldosterone synthase) gene. Patients with this deficiency have impaired aldosterone synthesis, exhibit increased plasma renin activity, secrete increased amount