Chloride channel, Biophysics, Biochemistry, Gating and Xenopus are his primary areas of study. Michael Pusch undertakes multidisciplinary studies into Chloride channel and Torpedo in his work. His research in Biophysics intersects with topics in Cytoplasm, Patch clamp and Ion transporter.
His Biochemistry study deals with Cell biology intersecting with Transmembrane domain. In his study, which falls under the umbrella issue of Gating, Valence, Molecular physics and Voltage is strongly linked to Electrophysiology. He has included themes like Amino acid, Sodium, Membrane potential and Tetrodotoxin in his Xenopus study.
The scientist’s investigation covers issues in Chloride channel, Biophysics, Gating, Biochemistry and Cell biology. His Chloride channel research is multidisciplinary, incorporating elements of Xenopus, Stereochemistry, Mutant and Binding site. His Biophysics study incorporates themes from Extracellular, Patch clamp, Intracellular and Ion channel.
Michael Pusch usually deals with Intracellular and limits it to topics linked to Skeletal muscle and HEK 293 cells. He focuses mostly in the field of Gating, narrowing it down to matters related to Analytical chemistry and, in some cases, Membrane. The Cell biology study combines topics in areas such as Osteopetrosis and Transmembrane domain.
Michael Pusch spends much of his time researching Cell biology, Chloride channel, Biophysics, Protein subunit and Gating. His studies in Cell biology integrate themes in fields like Osteopetrosis, Xenopus and Reabsorption. The Chloride channel study combines topics in areas such as HEK 293 cells, Kidney and Pharmacology.
His work deals with themes such as Biochemistry, Intracellular and Endosome, which intersect with Biophysics. His Protein subunit research includes themes of Mutation and Membrane protein. His work focuses on many connections between Gating and other disciplines, such as Binding site, that overlap with his field of interest in Allosteric regulation, Adamantane, Ligand, Mutagenesis and Potassium channel blocker.
Michael Pusch focuses on Biophysics, Chloride channel, Mutation, Genetics and Intracellular. His Biophysics research includes elements of Xenopus, Biochemistry, Calcium and Membrane protein. His research ties HEK 293 cells and Chloride channel together.
His Mutation research focuses on subjects like Protein subunit, which are linked to Mutant and Molecular biology. His Phenotype, CLCN1 and Dominance study, which is part of a larger body of work in Genetics, is frequently linked to Megalencephalic leukoencephalopathy with subcortical cysts, bridging the gap between disciplines. His Intracellular study incorporates themes from Homeostasis, Vacuole and TRPV6.
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Mutation in the neuronal voltage-gated sodium channel SCN1A in familial hemiplegic migraine.
Martin Dichgans;Tobias Freilinger;Gertrud Eckstein;Elena Babini.
The Lancet (2005)
Rates of diffusional exchange between small cells and a measuring patch pipette.
Michael Pusch;Erwin Neher.
Pflügers Archiv: European Journal of Physiology (1988)
A chloride channel widely expressed in epithelial and non-epithelial cells.
Astrid Thiemann;Stefan Gründer;Michael Pusch;Thomas J. Jentsch.
Mapping the site of block by tetrodotoxin and saxitoxin of sodium channel II.
Heinrich Terlau;Stefan H. Heinemann;Walter Stühmer;Michael Pusch.
FEBS Letters (1991)
Chloride/proton antiporter activity of mammalian CLC proteins ClC-4 and ClC-5
Alessandra Picollo;Michael Pusch.
Regions involved in the opening of CIC-2 chloride channel by voltage and cell volume.
Stefan Gründer;Astrid Thiemann;Michael Pusch;Thomas J. Jentsch.
Gating of the voltage-dependent chloride channel CIC-0 by the permeant anion
Michael Pusch;Uwe Ludewig;Annett Rehfeldt;Thomas J. Jentsch.
Two physically distinct pores in the dimeric ClC-0 chloride channel.
Uwe Ludewig;Michael Pusch;Thomas J. Jentsch.
Heteromultimeric CLC chloride channels with novel properties
Claudius Lorenz;Michael Pusch;Thomas J. Jentsch.
Proceedings of the National Academy of Sciences of the United States of America (1996)
Multimeric structure of ClC-1 chloride channel revealed by mutations in dominant myotonia congenita (Thomsen).
K Steinmeyer;C Lorenz;M Pusch;M C Koch.
The EMBO Journal (1994)
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