What is he best known for?
The fields of study he is best known for:
His primary areas of investigation include Mitochondrial DNA, Genetics, Molecular biology, Cell biology and Mutation.
His research in Mitochondrial DNA intersects with topics in DNA and Mitochondrial fission.
His work on Mitochondrial DNA depletion syndrome, Respiratory chain and Mitochondrial DNA replication is typically connected to MPV17 and Premature aging as part of general Genetics study, connecting several disciplines of science.
His Molecular biology study frequently links to related topics such as Somatic cell.
Mitochondrion is the focus of his Cell biology research.
His studies in Mutation integrate themes in fields like Phenotype and Ageing.
His most cited work include:
- Premature ageing in mice expressing defective mitochondrial DNA polymerase (1994 citations)
- Human mitochondrial DNA deletions associated with mutations in the gene encoding Twinkle, a phage T7 gene 4-like protein localized in mitochondria. (715 citations)
- Somatic mtDNA mutations cause aging phenotypes without affecting reactive oxygen species production (458 citations)
What are the main themes of his work throughout his whole career to date?
Johannes N. Spelbrink spends much of his time researching Mitochondrial DNA, Genetics, Mitochondrion, Molecular biology and Cell biology.
The study incorporates disciplines such as Mutation, DNA, DNA replication and Helicase in addition to Mitochondrial DNA.
His work carried out in the field of Mitochondrion brings together such families of science as mitochondrial fusion, Oxidative phosphorylation, Internal medicine and Endocrinology.
His Molecular biology study incorporates themes from Gene expression, Recombination, Heteroplasmy, TFAM and Point mutation.
His biological study spans a wide range of topics, including Infantile onset spinocerebellar ataxia and Spinocerebellar ataxia.
His study in Cell biology is interdisciplinary in nature, drawing from both Nuclear DNA and Acetylation.
He most often published in these fields:
- Mitochondrial DNA (81.93%)
- Genetics (56.63%)
- Mitochondrion (55.42%)
What were the highlights of his more recent work (between 2013-2021)?
- Mitochondrial DNA (81.93%)
- Mitochondrion (55.42%)
- Genetics (56.63%)
In recent papers he was focusing on the following fields of study:
His primary scientific interests are in Mitochondrial DNA, Mitochondrion, Genetics, Helicase and Cell biology.
His study in Mitochondrial DNA focuses on Human mitochondrial genetics in particular.
His Mitochondrion research includes themes of Plasma protein binding and Cell growth.
His research integrates issues of DNA and Inner mitochondrial membrane in his study of Helicase.
His DNA research includes elements of Biophysics and RNA polymerase.
The concepts of his Cell biology study are interwoven with issues in Nuclear DNA, Cellular localization, Gene knockdown and Exonuclease.
Between 2013 and 2021, his most popular works were:
- TCA Cycle and Mitochondrial Membrane Potential Are Necessary for Diverse Biological Functions (236 citations)
- DNA Sequences Proximal to Human Mitochondrial DNA Deletion Breakpoints Prevalent in Human Disease Form G-quadruplexes, a Class of DNA Structures Inefficiently Unwound by the Mitochondrial Replicative Twinkle Helicase * (67 citations)
- CLPB Mutations Cause 3-Methylglutaconic Aciduria, Progressive Brain Atrophy, Intellectual Disability, Congenital Neutropenia, Cataracts, Movement Disorder (58 citations)
In his most recent research, the most cited papers focused on:
His main research concerns Mitochondrial DNA, Genetics, Mitochondrion, Human mitochondrial genetics and Exome sequencing.
His Mitochondrial DNA study typically links adjacent topics like DNA replication.
3-Methylglutaconic Aciduria and Congenital Neutropenia are the primary areas of interest in his Genetics study.
His Mitochondrion research integrates issues from Histone and Helicase.
The various areas that Johannes N. Spelbrink examines in his Human mitochondrial genetics study include mitochondrial fusion, Mitochondrial disease and Pontocerebellar hypoplasia.
His Exome sequencing study combines topics from a wide range of disciplines, such as Encephalopathy, Cerebral atrophy, Atrophy, CLPB and HAX1.
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