Laurent Schild

Publications | Mémoires et thèses

La recherche avancée est accessible via Serval

Les publications peuvent être gérées en accédant à Serval via MyUnil


94 publications

2023 | 2019 | 2018 | 2017 | 2015 | 2014 | 2012 | 2011 | 2010 | 2009 | 2008 | 2007 | 2006 | 2005 | 2004 | 2003 | 2002 | 2001 | 2000 | 1999 | 1998 | 1997 | 1996 | 1995 | 1994 | 1991 | 1990 | 1988 | 1987 | 1986 | 1984 | 1983 |
 
A mild and transient form of autosomal recessive pseudohypoaldosteronism type 1 caused by a novel mutation in the SCNN1A gene.
Efthymiadou A., Gautschi I., van Bemmelen M.X., Sertedaki A., Giannakopoulos A., Chrousos G., Schild L., Chrysis D., 2023/07/01. American journal of physiology. Endocrinology and metabolism, 325 (1) pp. E1-E9. Peer-reviewed.
 
Imatinib Uptake into Cells is Not Mediated by Organic Cation Transporters OCT1, OCT2, or OCT3, But is Influenced by Extracellular pH.
Blanc Mettral J., Faller N., Cruchon S., Sottas L., Buclin T., Schild L., Choong E., Nahimana A., Decosterd L.A., 2019. Drug metabolism letters, 13 (2) pp. 102-110. Peer-reviewed.
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.
 
International union of basic and clinical pharmacology. XCI. structure, function, and pharmacology of acid-sensing ion channels and the epithelial Na+ channel.
Kellenberger S., Schild L., 2015. Pharmacological Reviews, 67 (1) pp. 1-35. 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.
Use-dependent block of the voltage-gated Na+ channel by tetrodotoxin and saxitoxin: Effect of pore mutations that change ionic selectivity.
Huang C.J., Schild L., Moczydlowski E.G., 2012. Journal of General Physiology, 140 (4) pp. 435-454. Peer-reviewed.
 
A homozygous missense mutation in SCNN1A is responsible for a transient neonatal form of pseudohypoaldosteronism type 1.
Dirlewanger M., Huser D., Zennaro M.C., Girardin E., Schild L., Schwitzgebel V.M., 2011. American Journal of Physiology. Endocrinology and Metabolism, 301 (3) pp. E467-E473.
 
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.
 
The epithelial sodium channel and the control of sodium balance.
Schild L., 2010. Biochimica et Biophysica Acta-Molecular Basis of Disease, 1802 (12) pp. 1159-1165. 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.
 
Direct visualization of the trimeric structure of the ASIC1a channel, using AFM imaging.
Carnally S.M., Dev H.S., Stewart A.P., Barrera N.P., Van Bemmelen M.X., Schild L., Henderson R.M., Edwardson J.M., 2008. Biochemical and Biophysical Research Communications, 372 (4) pp. 752-755.
 
ENaC and its regulatory proteins as drug targets for blood pressure control.
Rotin D., Schild L., 2008. Current Drug Targets, 9 (8) pp. 709-716.
 
Epithelial sodium channel: mendelian versus essential hypertension
Rossier B. C., Schild L., 2008. Hypertension, 52 (4) pp. 595-600. Peer-reviewed.
 
Cadmium trapping in an epithelial sodium channel pore mutant.
Takeda A.N., Gautschi I., van Bemmelen M.X., Schild L., 2007/11. Journal of Biological Chemistry, 282 (44) pp. 31928-31936. Peer-reviewed.
 
CYP3A5 and ABCB1 genes influence blood pressure and response to treatment, and their effect is modified by salt.
Eap C.B., Bochud M., Elston R.C., Bovet P., Maillard M.P., Nussberger J., Schild L., Shamlaye C., Burnier M., 2007. Hypertension, 49 (5) pp. 1007-14. Peer-reviewed.
 
Mineralocorticoid action in the aldosterone-sensitive distal nephron
Verrey F., Hummler E., Schild L., Rossier B.C., 2007. pp. 889-924 dans Alpern R.J., Herbert S.C. (eds.) The Kidney, Alpern R.J. Herbert S.C..
 
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.
 
Association of CYP3A5 genotypes with blood pressure and renal function in African families.
Bochud M., Eap C.B., Elston R.C., Bovet P., Maillard M., Schild L., Shamlaye C., Burnier M., 2006. Journal of hypertension, 24 (5) pp. 923-9. Peer-reviewed.
 
Functional domains of the epithelial sodium channel
Loffing J., Schild L., 2005/11. Journal of the American Society of Nephrology, 16 (11) pp. 3175-81.
Common variants of the beta and gamma subunits of the epithelial sodium channel and their relation to plasma renin and aldosterone levels in essential hypertension.
Hannila-Handelberg T., Kontula K., Tikkanen I., Tikkanen T., Fyhrquist F., Helin K., Fodstad H., Piippo K., Miettinen H.E., Virtamo J. et al., 2005/01. BMC Medical Genetics, 6 p. 4. Peer-reviewed.
 
Heritability of renal function in hypertensive families of African descent in the Seychelles (Indian Ocean).
Bochud M., Elston R.C., Maillard M., Bovet P., Schild L., Shamlaye C., Burnier M., 2005. Kidney international, 67 (1) pp. 61-9. Peer-reviewed.
 
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.
 
Renal Transport of Organic Ions and Uric Acid.
Schild L., Roch-Ramel F., Diezi J., 2005. dans Diseases of the Kidney and Urinary Trac, Lippincott Williams & Wilkins.
 
The CYP3A5 polymorphism is associated with ambulatory blood pressure increase with age in families of African descent
Bochud Murielle, Eap Chin-Bin, Elston Robert C., Bovet Pascal, Schild Laurent, Maillard Marc P., Burnier Michel, 2005. p. 367 dans , Journal of Hypertension. Peer-reviewed.
 
The CYP3A5 polymorphism is associated with urinary sodium excretion in families of African descent
Bochud Murielle, Elston Robert C., Bovet Pascal, Schild Laurent, Maillard Marc P., Burnier Michel, Eap Chin-Bin, 2005. p. 364 dans , Journal of Hypertension. Peer-reviewed.
 
Vasopressin-stimulated CFTR Cl- currents are increased in the renal collecting duct cells of a mouse model of Liddle's syndrome.
Chang C.T., Bens M., Hummler E., Boulkroun S., Schild L., Teulon J., Rossier B.C., Vandewalle A., 2005. Journal of Physiology, 562 (1) pp. 271-284. Peer-reviewed.
 
Loss-of-function mutations of the K(+) channel gene KCNJ2 constitute a rare cause of long QT syndrome
Fodstad H., Swan H., Auberson M., Gautschi I., Loffing J., Schild L., Kontula K., 2004/08. Journal of Molecular and Cellular Cardiology, 37 (2) pp. 593-602.
 
ERK1/2 controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell of the cortical collecting duct of the mouse kidney.
Michlig S., Mercier A., Doucet A., Schild L., Horisberger J.D., Rossier B.C., Firsov D., 2004. Journal of Biological Chemistry, 279 (49) pp. 51002-51012. Peer-reviewed.
 
The epithelial sodium channel: from molecule to disease
Schild L., 2004. Reviews of Physiology, Biochemistry and Pharmacology, 151 pp. 93-107.
 
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. 2219-2228. Peer-reviewed.
 
Affinity and specificity of interactions between Nedd4 isoforms and the epithelial Na+ channel.
Henry P.C., Kanelis V., O'Brien M.C., Kim B., Gautschi I., Forman-Kay J., Schild L., Rotin D., 2003/05. Journal of Biological Chemistry, 278 (22) pp. 20019-20028. Peer-reviewed.
 
Characterization of the ligand-binding site of the serotonin 5-HT3 receptor: the role of glutamate residues 97, 224, AND 235.
Schreiter C., Hovius R., Costioli M., Pick H., Kellenberger S., Schild L., Vogel H., 2003. Journal of Biological Chemistry, 278 (25) pp. 22709-22716.
 
Epithelial Na+ channel mutants causing Liddle's syndrome retain ability to respond to aldosterone and vasopressin.
Auberson M., Hoffmann-Pochon N., Vandewalle A., Kellenberger S., Schild L., 2003. American Journal of Physiology. Renal Physiology, 285 (3) pp. F459-F471.
 
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.
 
Liddle's syndrome associated with a point mutation in the extracellular domain of the epithelial sodium channel gamma subunit.
Hiltunen T.P., Hannila-Handelberg T., Petäjäniemi N., Kantola I., Tikkanen I., Virtamo J., Gautschi I., Schild L., Kontula K., 2002/12. Journal of hypertension, 20 (12) pp. 2383-2390. Peer-reviewed.
 
An external site controls closing of the epithelial Na+ channel ENaC.
Kellenberger S., Gautschi I., Schild L., 2002/09/01. The Journal of physiology, 543 (Pt 2) pp. 413-424. Peer-reviewed.
 
Epithelial sodium channel and the control of sodium balance: interaction between genetic and environmental factors.
Rossier B.C., Pradervand S., Schild L., Hummler E., 2002. Annual Review of Physiology, 64 pp. 877-897. Peer-reviewed.
 
Epithelial sodium channel/degenerin family of ion channels: a variety of functions for a shared structure.
Kellenberger S., Schild L., 2002. Physiological Reviews, 82 (3) pp. 735-767.
 
Use of constant denaturant capillary electrophoresis of pooled blood samples to identify single-nucleotide polymorphisms in the genes (Scnn1a and Scnn1b) encoding the alpha and beta subunits of the epithelial sodium channel.
Xue M.Z., Bonny O., Morgenthaler S., Bochud M., Mooser V., Thilly W.G., Schild L., Leong-Morgenthaler P.M., 2002. Clinical Chemistry, 48 (5) pp. 718-728. Peer-reviewed.
 
Mitochondrial polarization in rat hippocampal astrocytes is resistant to cytosolic Ca(2+) loads
Kahlert S., Schild L., Reiser G., 2001/12. Journal of Neuroscience Research, 66 (5) pp. 1019-27.
 
Micromachined impedance spectroscopy flow cytometer for cell analysis and particle sizing
Gawad S., Schild L., Renaud P. H., 2001/09. Lab on a Chip, 1 (1) pp. 76-82.
 
Trafficking and cell surface stability of ENaC
Rotin D., Kanelis V., Schild L., 2001/09. American Journal of Physiology. Renal Physiology, 281 (3) pp. F391-9.
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.
 
Renal Transport of Organic Ions and Uric Acid.
Roch-Ramel F., Schild L., 2001. pp. 243-264 dans Diseases of the Kidney and Urinary Tract, Oxford University Press.
 
Structure function relationships of ENaC and its role in sodium handling.
Schild L., Kellenberger S., 2001. Advances in Experimental Medicine and Biology, 502 pp. 305-314.
 
Control of Na+ Transport by Aldosterone.
Verrey F., Hummler E., Schild L., Rossier B.C., 2000. pp. 1441-1472 dans Seldin D.W., Giebisch G.H. (eds.) The Kidney, Lippincott Williams & Wilkins.
 
Regulation of the epithelial Na+ channel by Nedd4 and ubiquitination.
Staub O., Abriel H., Plant P., Ishikawa T., Kanelis V., Saleki R., Horisberger J.D., Schild L., Rotin D., 2000. Kidney International, 57 (3) pp. 809-815. Peer-reviewed.
 
Identification of a highly conserved sequence at the N-terminus of the epithelial Na+ channel alpha subunit involved in gating
Grunder S., Jaeger N. F., Gautschi I., Schild L., Rossier B. C., 1999/10. Pflügers Archiv : European Journal of Physiology, 438 (5) pp. 709-715. Peer-reviewed.
 
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.
 
Defective regulation of the epithelial Na+ channel by Nedd4 in Liddle's syndrome.
Abriel H., Loffing J., Rebhun J.F., Pratt J.H., Schild L., Horisberger J.D., Rotin D., Staub O., 1999. Journal of Clinical Investigation, 103 (5) pp. 667-673. Peer-reviewed.
 
Mutational analysis of cysteine-rich domains of the epithelium sodium channel (ENaC). Identification of cysteines essential for channel expression at the cell surface.
Firsov D., Robert-Nicoud M., Gruender S., Schild L., Rossier B.C., 1999. Journal of Biological Chemistry, 274 (5) pp. 2743-2749.
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.
 
Regulation of ENaC by interacting proteins and by ubiquitination.
Staub O, Plant P, Ishikawa T, Schild L, Rotin D, 1999. pp. 65-87 dans Amiloride-sensitive sodium channels, Physiology and functional diversity, Current Topics in Membranes, Academic Press.
 
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.
 
The heterotetrameric architecture of the epithelial sodium channel (ENaC).
Firsov D., Gautschi I., Merillat A.M., Rossier B.C., Schild L., 1998. EMBO Journal, 17 (2) pp. 344-352.
On the structural basis for size-selective permeation of organic cations through the voltage-gated sodium channel. Effect of alanine mutations at the DEKA locus on selectivity, inhibition by Ca2+ and H+, and molecular sieving
Sun Y. M., Favre I., Schild L., Moczydlowski E., 1997/12. Journal of General Physiology, 110 (6) pp. 693-715.
 
Regulation of stability and function of the epithelial Na+ channel (ENaC) by ubiquitination
Staub O., Gautschi I., Ishikawa T., Breitschopf K., Ciechanover A., Schild L., Rotin D., 1997/11. EMBO Journal, 16 (21) pp. 6325-36.
 
A mutation causing pseudohypoaldosteronism type 1 identifies a conserved glycine that is involved in the gating of the epithelial sodium channel.
Gründer S., Firsov D., Chang S.S., Jaeger N.F., Gautschi I., Schild L., Lifton R.P., Rossier B.C., 1997. EMBO Journal, 16 (5) pp. 899-907.
Identification of amino acid residues in the alpha, beta, and gamma subunits of the epithelial sodium channel (ENaC) involved in amiloride block and ion permeation.
Schild L., Schneeberger E., Gautschi I., Firsov D., 1997. Journal of General Physiology, 109 (1) pp. 15-26.
 
Physiologie et physiopathologie de la balance du sodium : apports récents de la génétique et de la biologie moléculaire
Horisberger J. D., Schild L., 1997. Médecine et Hygiène, 55 (2155) pp. 532-539.
 
On the structural basis for ionic selectivity among Na+, K+, and Ca2+ in the voltage-gated sodium channel
Favre I., Moczydlowski E., Schild L., 1996/12. Biophysical Journal, 71 (6) pp. 3110-25.
 
Identification of a PY motif in the epithelial Na channel subunits as a target sequence for mutations causing channel activation found in Liddle syndrome
Schild L., Lu Y., Gautschi I., Schneeberger E., Lifton R. P., Rossier B. C., 1996/05. EMBO Journal, 15 (10) pp. 2381-7. Peer-reviewed.
 
Liddle disease caused by a missense mutation of beta subunit of the epithelial sodium channel gene
Tamura H., Schild L., Enomoto N., Matsui N., Marumo F., Rossier B. C., 1996/04. Journal of Clinical Investigation, 97 (7) pp. 1780-4. Peer-reviewed.
 
Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1
Chang S. S., Grunder S., Hanukoglu A., Rosler A., Mathew P. M., Hanukoglu I., Schild L., Lu Y., Shimkets R. A., Nelson-Williams C. et al., 1996/03. Nature Genetics, 12 (3) pp. 248-53. Peer-reviewed.
 
Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: a quantitative approach.
Firsov D., Schild L., Gautschi I., Mérillat A.M., Schneeberger E., Rossier B.C., 1996. Proceedings of the National Academy of Sciences of the United States of America, 93 (26) pp. 15370-15375.
 
Génétique du canal sodium épithélial: nouveaux développements dans la compréhension du contrôle de la pression sanguine et de la réabsorption de liquide dans les voies aériennes et le poumon
Rossier B.C., Hummler E., Horisberger J.-D., Schild L., 1996. Médecine / Sciences, 12 pp. 795-97.
 
Indirect coupling of urate and p-aminohippurate transport to sodium in human brush-border membrane vesicles
Roch-Ramel F., Guisan B., Schild L., 1996/01. American Journal of Physiology, 270 (1 Pt 2) pp. F61-8.
 
The ENaC channel as the primary determinant of two human diseases: Liddle syndrome and pseudohypoaldosteronism
Schild L., 1996. Nephrologie, 17 (7) pp. 395-400.
 
A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity
Hansson J. H., Schild L., Lu Y., Wilson T. A., Gautschi I., Shimkets R., Nelson-Williams C., Rossier B. C., Lifton R. P., 1995/12. Proceedings of the National Academy of Sciences of the United States of America, 92 (25) pp. 11495-9. Peer-reviewed.
 
Expression cloning of the epithelial sodium channel
Canessa C. M., Horisberger J. D., Schild L., Rossier B. C., 1995/10. Kidney International, 48 (4) pp. 950-5.
 
Hypertension caused by a truncated epithelial sodium channel gamma subunit: genetic heterogeneity of Liddle syndrome
Hansson J. H., Nelson-Williams C., Suzuki H., Schild L., Shimkets R., Lu Y., Canessa C., Iwasaki T., Rossier B., Lifton R. P., 1995/09. Nature Genetics, 11 (1) pp. 76-82. Peer-reviewed.
 
Specificity for block by saxitoxin and divalent cations at a residue which determines sensitivity of sodium channel subtypes to guanidinium toxins.
Favre I., Moczydlowski E., Schild L., 1995/08. The Journal of general physiology, 106 (2) pp. 203-229. Peer-reviewed.
 
The highly selective low-conductance epithelial Na channel of Xenopus laevis A6 kidney cells
Puoti A., May A., Canessa C. M., Horisberger J. D., Schild L., Rossier B. C., 1995/07. American Journal of Physiology, 269 (1 Pt 1) pp. C188-97.
 
A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system
Schild L., Canessa C. M., Shimkets R. A., Gautschi I., Lifton R. P., Rossier B. C., 1995/06. Proceedings of the National Academy of Sciences of the United States of America, 92 (12) pp. 5699-703. Peer-reviewed.
 
Epithelial sodium channels
Rossier B. C., Canessa C. M., Schild L., Horisberger J. D., 1994/09. Current Opinion in Nephrology and Hypertension, 3 (5) pp. 487-96.
 
Permeation of Na+ through open and Zn(2+)-occupied conductance states of cardiac sodium channels modified by batrachotoxin: exploring ion-ion interactions in a multi-ion channel
Schild L., Moczydlowski E., 1994/03. Biophysical Journal, 66 (3 Pt 1) pp. 654-66.
 
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.
 
Competitive binding interaction between Zn2+ and saxitoxin in cardiac Na+ channels. Evidence for a sulfhydryl group in the Zn2+/saxitoxin binding site
Schild L., Moczydlowski E., 1991/03. Biophysical Journal, 59 (3) pp. 523-37.
 
Basolateral transport pathways for K+ and Cl- in rabbit proximal tubule: effects on cell volume
Schild L., Aronson P. S., Giebisch G., 1991/01. American Journal of Physiology, 260 (1 Pt 2) pp. F101-9.
 
Divalent cation selectivity for external block of voltage-dependent Na+ channels prolonged by batrachotoxin. Zn2+ induces discrete substates in cardiac Na+ channels.
Ravindran A., Schild L., Moczydlowski E., 1991/01. The Journal of general physiology, 97 (1) pp. 89-115. Peer-reviewed.
 
Zn2(+)-induced subconductance events in cardiac Na+ channels prolonged by batrachotoxin. Current-voltage behavior and single-channel kinetics.
Schild L., Ravindran A., Moczydlowski E., 1991/01. The Journal of general physiology, 97 (1) pp. 117-142. Peer-reviewed.
 
Effects of apical membrane Cl(-)-formate exchange on cell volume in rabbit proximal tubule
Schild L., Aronson P. S., Giebisch G., 1990/03. American Journal of Physiology, 258 (3 Pt 2) pp. F530-6.
 
Transport of salicylate in proximal tubule (S2 segment) isolated from rabbit kidney
Schild L., Roch-Ramel F., 1988/04. American Journal of Physiology, 254 (4 Pt 2) pp. F554-61.
 
Chloride transport in the proximal renal tubule
Schild L., Giebisch G., Green R., 1988. Annual Review of Physiology, 50 pp. 97-110.
 
Effect of formate on volume reabsorption in the rabbit proximal tubule
Schild L., Giebisch G., Karniski L. P., Aronson P. S., 1987/01. Journal of Clinical Investigation, 79 (1) pp. 32-8.
 
Chloride transport in the mammalian proximal tubule
Schild L., Giebisch G., Karniski L., Aronson P. S., 1986. Pflügers Archiv : European Journal of Physiology, 407 (Suppl 2) pp. S156-S159.
 
Mechanisms involved in the reabsorption of salicylate in the proximal tubule of rabbits
Schild L., Roch-Ramel F., 1984. Progress in Clinical and Biological Research, 164 pp. 417-22.
 
Secretion of tetraethylammonium by proximal tubules of rabbit kidneys
Schali C., Schild L., Overney J., Roch-Ramel F., 1983/08. American Journal of Physiology, 245 (2) pp. F238-46.
Partagez:
Unicentre - CH-1015 Lausanne
Suisse
Tél. +41 21 692 11 11
Swiss University