Ivan Gautschi

Publications | Mémoires et thèses

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19 publications

2018 | 2017 | 2015 | 2014 | 2010 | 2009 | 2006 | 2005 | 2003 | 2001 | 1999 | 1998 | 1994 |
Human Mutations in SLC2A9 (Glut9) Affect Transport Capacity for Urate.
Ruiz A., Gautschi I., Schild L., Bonny O., 2018. Frontiers in physiology, 9 p. 476. Peer-reviewed.
 
Deletion of Xenotropic and Polytropic Retrovirus Receptor 1 in mouse nephron causes renal Fanconi syndrome and hypophosphatemic rickets [857.9]
Ansermet C., Moor M., Centeno G., Auberson M., Hu D., Barron R., Nikolaeva S., Haenzi B., Katanaeva N., Gautschi I. et al., 2017/04/30., Annual Meeting of the American-Society-for-Pharmacology-and-Experimental-Therapeutics (ASPET) at Experimental Biology Meeting pp. n.p. dans Faseb Journal.
Renal Fanconi Syndrome and Hypophosphatemic Rickets in the Absence of Xenotropic and Polytropic Retroviral Receptor in the Nephron.
Ansermet C., Moor M.B., Centeno G., Auberson M., Hu D.Z., Baron R., Nikolaeva S., Haenzi B., Katanaeva N., Gautschi I. et al., 2017/04. Journal of the American Society of Nephrology : JASN, 28 (4) pp. 1073-1078. Peer-reviewed.
 
A Missense Mutation in the Extracellular Domain of αENaC Causes Liddle Syndrome.
Salih M., Gautschi I., van Bemmelen M.X., Di Benedetto M., Brooks A.S., Lugtenberg D., Schild L., Hoorn E.J., 2017. Journal of the American Society of Nephrology, 28 (11) pp. 3291-3299. Peer-reviewed.
Proton and non-proton activation of ASIC channels.
Gautschi I., van Bemmelen M.X., Schild L., 2017. PloS one, 12 (4) pp. e0175293. Peer-reviewed.
The Human Acid-Sensing Ion Channel ASIC1a: Evidence for a Homotetrameric Assembly State at the Cell Surface.
van Bemmelen M.X., Huser D., Gautschi I., Schild L., 2015. Plos One, 10 (8) pp. e0135191. Peer-reviewed.
 
Congenital ataxia and hemiplegic migraine with cerebral edema associated with a novel gain of function mutation in the calcium channel CACNA1A.
García Segarra N., Gautschi I., Mittaz-Crettol L., Kallay Zetchi C., Al-Qusairi L., Van Bemmelen M.X., Maeder P., Bonafé L., Schild L., Roulet-Perez E., 2014. Journal of the Neurological Sciences, 342 (1-2) pp. 69-78. Peer-reviewed.
Functional analysis of a missense mutation in the serine protease inhibitor SPINT2 associated with congenital sodium diarrhea.
Faller N., Gautschi I., Schild L., 2014. Plos One, 9 (4) pp. e94267. Peer-reviewed.
 
Licorice-induced hypertension and common variants of genes regulating renal sodium reabsorption.
Miettinen H.E., Piippo K., Hannila-Handelberg T., Paukku K., Hiltunen T.P., Gautschi I., Schild L., Kontula K., 2010. Annals of Medicine, 42 (6) pp. 465-474. Peer-reviewed.
 
Revealing a subclinical salt-losing phenotype in heterozygous carriers of the novel S562P mutation in the alpha subunit of the epithelial sodium channel.
Riepe F.G., van Bemmelen M.X., Cachat F., Plendl H., Gautschi I., Krone N., Holterhus P.M., Theintz G., Schild L., 2009. Clinical Endocrinology, 70 (2) pp. 252-258.
 
A gating mutation in the internal pore of ASIC1a.
Pfister Y., Gautschi I., Takeda A.N., van Bemmelen M., Kellenberger S., Schild L., 2006. Journal of Biological Chemistry, 281 (17) pp. 11787-11791.
 
Intracellular thiol-mediated modulation of epithelial sodium channel activity.
Kellenberger S., Gautschi I., Pfister Y., Schild L., 2005. Journal of Biological Chemistry, 280 (9) pp. 7739-7747.
 
Dysfunction of the epithelial sodium channel expressed in the kidney of a mouse model for Liddle syndrome
Pradervand S., Vandewalle A., Bens M., Gautschi I., Loffing J., Hummler E., Schild L., Rossier B. C., 2003/09. Journal of the American Society of Nephrology, 14 (9) pp. 2219-28. Peer-reviewed.
 
Mutations in the epithelial Na+ channel ENaC outer pore disrupt amiloride block by increasing its dissociation rate.
Kellenberger S., Gautschi I., Schild L., 2003. Molecular Pharmacology, 64 (4) pp. 848-856.
Permeability properties of ENaC selectivity filter mutants.
Kellenberger S., Auberson M., Gautschi I., Schneeberger E., Schild L., 2001. Journal of General Physiology, 118 (6) pp. 679-692.
 
A single point mutation in the pore region of the epithelial Na+ channel changes ion selectivity by modifying molecular sieving.
Kellenberger S., Gautschi I., Schild L., 1999. Proceedings of the National Academy of Sciences of the United States of America, 96 (7) pp. 4170-4175.
On the molecular basis of ion permeation in the epithelial Na+ channel.
Kellenberger S., Hoffmann-Pochon N., Gautschi I., Schneeberger E., Schild L., 1999. Journal of General Physiology, 114 (1) pp. 13-30.
 
Mutations causing Liddle syndrome reduce sodium-dependent downregulation of the epithelial sodium channel in the Xenopus oocyte expression system.
Kellenberger S., Gautschi I., Rossier B.C., Schild L., 1998. Journal of Clinical Investigation, 101 (12) pp. 2741-2750.
 
Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits.
Canessa C.M., Schild L., Buell G., Thorens B., Gautschi I., Horisberger J.D., Rossier B.C., 1994/02. Nature, 367 (6462) pp. 463-467. Peer-reviewed.
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