What is he best known for?
The fields of study he is best known for:
Acetylcholine receptor, Genetics, Mutation, Molecular biology and CHRNE are his primary areas of study.
His research in Acetylcholine receptor intersects with topics in Agonist and Endocrinology.
His Endocrinology study which covers Postsynaptic potential that intersects with Neurotransmission.
His study connects Computational biology and Genetics.
His research investigates the connection with Mutation and areas like Neuroscience which intersect with concerns in Protein kinase B, Ghrelin, IκBα and MAPK/ERK pathway.
The various areas that he examines in his Molecular biology study include Acetylcholinesterase, Missense mutation, Protein subunit, Mutant and COLQ.
His most cited work include:
- Increase of deleted mitochondrial DNA in the striatum in Parkinson's disease and senescence. (316 citations)
- Mutation of the acetylcholine receptor α subunit causes a slow-channel myasthenic syndrome by enhancing agonist binding affinity (235 citations)
- Myofibrillar myopathy: clinical, morphological and genetic studies in 63 patients (227 citations)
What are the main themes of his work throughout his whole career to date?
Kinji Ohno mainly investigates Genetics, Internal medicine, Acetylcholine receptor, Endocrinology and Cell biology.
His Acetylcholine receptor research is multidisciplinary, relying on both Mutation, Protein subunit and Neuromuscular junction.
His Mutation study typically links adjacent topics like Molecular biology.
His Molecular biology research includes elements of Mutant and Exon.
His study explores the link between Neuromuscular junction and topics such as Acetylcholinesterase that cross with problems in Acetylcholine and Choline acetyltransferase.
Endocrinology connects with themes related to Postsynaptic potential in his study.
He most often published in these fields:
- Genetics (24.51%)
- Internal medicine (24.18%)
- Acetylcholine receptor (24.51%)
What were the highlights of his more recent work (between 2017-2021)?
- Cell biology (20.92%)
- Computational biology (3.27%)
- Parkinson's disease (5.88%)
In recent papers he was focusing on the following fields of study:
Kinji Ohno focuses on Cell biology, Computational biology, Parkinson's disease, Neuromuscular junction and Acetylcholine receptor.
His biological study spans a wide range of topics, including COLQ, RNA polymerase II and Gene expression.
Kinji Ohno works mostly in the field of Neuromuscular junction, limiting it down to topics relating to Motor neuron and, in certain cases, Receptor, as a part of the same area of interest.
Kinji Ohno studies Agrin, a branch of Acetylcholine receptor.
He works mostly in the field of Agrin, limiting it down to concerns involving Mutation and, occasionally, Exon.
His study in Internal medicine is interdisciplinary in nature, drawing from both Endocrinology, Gut flora, Roseburia and Enterotype.
Between 2017 and 2021, his most popular works were:
- Rules and tools to predict the splicing effects of exonic and intronic mutations. (53 citations)
- Loss of Sfpq Causes Long-Gene Transcriptopathy in the Brain (41 citations)
- Ubiquitination of DNA Damage-Stalled RNAPII Promotes Transcription-Coupled Repair. (34 citations)
In his most recent research, the most cited papers focused on:
The scientist’s investigation covers issues in Cell biology, RNA polymerase II, Gene, Neuromuscular junction and Parkinson's disease.
The Sarcolemma research Kinji Ohno does as part of his general Cell biology study is frequently linked to other disciplines of science, such as Biglycan, therefore creating a link between diverse domains of science.
Kinji Ohno interconnects Ectodomain, Myogenesis, Axon and Acetylcholine receptor in the investigation of issues within Neuromuscular junction.
His work deals with themes such as Mutation and Motor Endplate, which intersect with Acetylcholine receptor.
The study incorporates disciplines such as Reactive oxygen species, Inhalation and Toxicity in addition to Parkinson's disease.
The concepts of his Congenital myasthenic syndrome study are interwoven with issues in Missense mutation and Exon.
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