World's Best Scientists 2026 revealed!

D-Index & Metrics

Biology and Biochemistry

D-Index
85
Citations
26278
World Ranking
3147
National Ranking
242

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Mutation

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 most cited work include:

  • Transcriptome and genome sequencing uncovers functional variation in humans (1417 citations)
  • Range of genetic mutations associated with severe non-syndromic sporadic intellectual disability: an exome sequencing study. (766 citations)
  • The genetic architecture of type 2 diabetes (674 citations)

What are the main themes of his work throughout his whole career to date?

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.

He most often published in these fields:

  • Cell biology (32.23%)
  • G protein (23.08%)
  • Biochemistry (21.25%)

What were the highlights of his more recent work (between 2018-2021)?

  • Cell biology (32.23%)
  • Gene knockdown (2.93%)
  • Downregulation and upregulation (4.40%)

In recent papers he was focusing on the following fields of study:

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.

Between 2018 and 2021, his most popular works were:

  • A deep proteome and transcriptome abundance atlas of 29 healthy human tissues (164 citations)
  • Quantification and discovery of sequence determinants of protein-per-mRNA amount in 29 human tissues (28 citations)
  • A cellular model of Brugada syndrome with SCN10A variants using human-induced pluripotent stem cell-derived cardiomyocytes. (10 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Enzyme
  • Mutation

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.

Best Publications

  • 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

  • Haploinsufficiency of TBK1 causes familial ALS and fronto-temporal dementia

    Axel Freischmidt;Thomas Wieland;Benjamin Richter;Wolfgang Ruf

  • A deep proteome and transcriptome abundance atlas of 29 healthy human tissues

    Dongxue Wang;Basak Eraslan;Basak Eraslan;Thomas Wieland;Björn M. Hallström

  • 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

  • Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension.

    Felix Beuschlein;Sheerazed Boulkroun;Sheerazed Boulkroun;Andrea Osswald;Thomas Wieland

  • Mutations in the deubiquitinase gene USP8 cause Cushing's disease

    Martin Reincke;Silviu Sbiera;Akira Hayakawa;Marily Theodoropoulou

  • Angiopoietin-2 differentially regulates angiogenesis through TIE2 and integrin signaling

    Moritz Felcht;Robert Luck;Alexander Schering;Philipp Seidel

  • 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

  • Exome Sequencing Reveals De Novo WDR45 Mutations Causing a Phenotypically Distinct, X-Linked Dominant Form of NBIA

    Tobias B. Haack;Penelope Hogarth;Michael C. Kruer;Allison Gregory

  • How reliable are G-protein-coupled receptor antibodies?

    Martin C. Michel;Thomas Wieland;Gozoh Tsujimoto

  • A major transmembrane protein of Golgi-derived COPI-coated vesicles involved in coatomer binding.

    K Sohn;L Orci;M Ravazzola;M Amherdt

  • Mutations in DNMT1 cause autosomal dominant cerebellar ataxia, deafness and narcolepsy

    Juliane Winkelmann;Ling Lin;Barbara Schormair;Birgitte R. Kornum

  • Structure of Gαq-p63RhoGEF-RhoA Complex Reveals a Pathway for the Activation of RhoA by GPCRs

    Susanne Lutz;Aruna Shankaranarayanan;Aruna Shankaranarayanan;Cassandra Coco;Marc Ridilla;Marc Ridilla

  • Loss-of-function mutations in MGME1 impair mtDNA replication and cause multisystemic mitochondrial disease

    Cornelia Kornblum;Thomas J Nicholls;Tobias B Haack;Susanne Schöler

  • The Guanine Nucleotide Exchange Factor p63RhoGEF, a Specific Link between Gq/11-coupled Receptor Signaling and RhoA

    Susanne Lutz;Andrea Freichel-Blomquist;Yang Yang;Ulrich Rümenapp

  • ENHANCED G PROTEIN ACTIVATION IN IMMORTALIZED LYMPHOBLASTS FROM PATIENTS WITH ESSENTIAL HYPERTENSION

    W Siffert;D Rosskopf;A Moritz;T Wieland

  • The genetic architecture of type 2 diabetes

    Christian Fuchsberger;Jason Flannick;Tanya M. Teslovich;Anubha Mahajan

Frequent Co-Authors

Tim M. Strom
Tim M. Strom Technical University of Munich
Thomas Meitinger
Thomas Meitinger Technical University of Munich
Karl H. Jakobs
Karl H. Jakobs University of Duisburg-Essen
Holger Prokisch
Holger Prokisch Technical University of Munich
Martina Schmidt
Martina Schmidt Johannes Gutenberg University of Mainz
Tobias B. Haack
Tobias B. Haack University of Tübingen
Dagmar Wieczorek
Dagmar Wieczorek Heinrich Heine University Düsseldorf
Marie Loh
Marie Loh Nanyang Technological University
Shaun Purcell
Shaun Purcell Harvard Medical School
Jochen Utikal
Jochen Utikal German Cancer Research Center

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