Thomas Wieland spends much of his time researching Genetics, Cell biology, Exome sequencing, Endocrinology and Internal medicine. The various areas that Thomas Wieland examines in his Genetics study include Lactic acidosis and Neuroscience. His Exome sequencing research is mostly focused on the topic Exome.
The concepts of his Endocrinology study are interwoven with issues in Ryanodine receptor 2, Ryanodine receptor, Angiogenesis, Ca2+/calmodulin-dependent protein kinase and Somatic cell. His Aldosterone and Secondary hypertension study in the realm of Internal medicine interacts with subjects such as Familial hyperaldosteronism and Calcium ion homeostasis. His G protein research is multidisciplinary, incorporating perspectives in G protein-coupled receptor and GTP'.
His primary areas of study are Cell biology, G protein, Biochemistry, Internal medicine and Genetics. His study focuses on the intersection of G protein and fields such as Molecular biology with connections in the field of Protein kinase C. As part of one scientific family, Thomas Wieland deals mainly with the area of Internal medicine, narrowing it down to issues related to the Endocrinology, and often Angiogenesis.
His research investigates the link between Genetics and topics such as Bioinformatics that cross with problems in Candidate gene. As a part of the same scientific study, Thomas Wieland usually deals with the Heterotrimeric G protein, concentrating on Nucleoside Diphosphate Kinase B and frequently concerns with Gene knockdown. He studies Exome sequencing, namely Exome.
Thomas Wieland mainly investigates Cell biology, Gene knockdown, Downregulation and upregulation, Nucleoside Diphosphate Kinase B and Internal medicine. The study incorporates disciplines such as Receptor, Leukemia and Caspase 1 in addition to Cell biology. Thomas Wieland has researched Receptor in several fields, including Secretion and Cell fractionation.
His work is dedicated to discovering how Downregulation and upregulation, Nucleoside-diphosphate kinase are connected with Glutamine, Phosphorylation, Molecular biology, Nucleoside triphosphate and Biosynthesis and other disciplines. The Internal medicine study combines topics in areas such as Induced pluripotent stem cell and Cardiology. His biological study spans a wide range of topics, including Heterotrimeric G protein, G protein, Molecular Pharmacology and Neuroscience.
Thomas Wieland mostly deals with Transcriptome, Computational biology, Induced pluripotent stem cell, Ajmaline and Internal medicine. His Transcriptome study incorporates themes from Proteomics, Protein abundance, Codon usage bias, Messenger RNA and Sequence. His study in Computational biology is interdisciplinary in nature, drawing from both Proteome, RNA-Seq, Human proteins, Genome and Human proteome project.
His studies in Induced pluripotent stem cell integrate themes in fields like Brugada syndrome, Enhancer, Stem cell, Pharmacology and Cellular model. His research in Ajmaline intersects with topics in Sodium channel, Phenotype, Amiodarone, Flecainide and Mexiletine. As a part of the same scientific family, he mostly works in the field of Internal medicine, focusing on Cardiology and, on occasion, Channel blocker.
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Transcriptome and genome sequencing uncovers functional variation in humans
Tuuli Lappalainen;Michael Sammeth;Marc R. Friedländer;Peter A. C. ‘t Hoen.
The genetic architecture of type 2 diabetes
Christian Fuchsberger;Christian Fuchsberger;Jason A. Flannick;Jason A. Flannick;Tanya M. Teslovich;Anubha Mahajan.
Range of genetic mutations associated with severe non-syndromic sporadic intellectual disability: an exome sequencing study.
Anita Rauch;Dagmar Wieczorek;Elisabeth Graf;Thomas Wieland.
The Lancet (2012)
Enhanced Sarcoplasmic Reticulum Ca2+ Leak and Increased Na+-Ca2+ Exchanger Function Underlie Delayed Afterdepolarizations in Patients With Chronic Atrial Fibrillation
Niels Voigt;Na Li;Qiongling Wang;Wei Wang.
Haploinsufficiency of TBK1 causes familial ALS and fronto-temporal dementia
Axel Freischmidt;Thomas Wieland;Benjamin Richter;Wolfgang Ruf.
Nature Neuroscience (2015)
Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension.
Felix Beuschlein;Sheerazed Boulkroun;Sheerazed Boulkroun;Andrea Osswald;Thomas Wieland.
Nature Genetics (2013)
Angiopoietin-2 differentially regulates angiogenesis through TIE2 and integrin signaling
Moritz Felcht;Robert Luck;Alexander Schering;Philipp Seidel.
Journal of Clinical Investigation (2012)
Mutations in the deubiquitinase gene USP8 cause Cushing's disease
Martin Reincke;Silviu Sbiera;Akira Hayakawa;Marily Theodoropoulou.
Nature Genetics (2015)
Calmodulin mutations associated with recurrent cardiac arrest in infants
Lia Crotti;Christopher N. Johnson;Elisabeth Graf;Gaetano M. De Ferrari.
Constitutive Activation of PKA Catalytic Subunit in Adrenal Cushing's Syndrome
Felix Beuschlein;Martin Fassnacht;Guillaume Assié;Davide Calebiro.
The New England Journal of Medicine (2014)
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