What is he best known for?
The fields of study he is best known for:
His main research concerns Genetics, ATRX, Gene, Chromatin and Phenotype.
His multidisciplinary approach integrates Genetics and Transcriptional Regulator ATRX in his work.
His studies deal with areas such as Death-associated protein 6, Cellular differentiation, Telomere and Heterochromatin, Heterochromatin protein 1 as well as ATRX.
His work in Chromatin addresses issues such as DNA methylation, which are connected to fields such as Mutation, Subtelomere, SWI/SNF and Embryonic stem cell.
His research investigates the connection between Phenotype and topics such as X chromosome that intersect with issues in Point mutation and DNA repair.
Richard J. Gibbons works mostly in the field of Epigenetics, limiting it down to topics relating to Transcription factor and, in certain cases, DNA binding site, as a part of the same area of interest.
His most cited work include:
- Distinct Factors Control Histone Variant H3.3 Localization at Specific Genomic Regions (864 citations)
- Large-scale discovery of novel genetic causes of developmental disorders (661 citations)
- Mutations in a Putative Global Transcriptional Regulator Cause X-linked Mental Retardation With Alpha-Thalassemia (ATR-X Syndrome) (497 citations)
What are the main themes of his work throughout his whole career to date?
Richard J. Gibbons focuses on Genetics, ATRX, Gene, Thalassemia and Cancer research.
All of his Genetics and X chromosome, Phenotype, Chromatin, Mutation and Epigenetics investigations are sub-components of the entire Genetics study.
His work carried out in the field of X chromosome brings together such families of science as Alpha and Genetic linkage.
Richard J. Gibbons combines subjects such as Death-associated protein 6, Alpha-thalassemia, Point mutation, Heterochromatin and Histone with his study of ATRX.
The various areas that Richard J. Gibbons examines in his Alpha-thalassemia study include Genetic counseling, Disease and Immunology.
His Thalassemia research also works with subjects such as
- Pediatrics most often made with reference to Hemoglobinopathy,
- Molecular biology most often made with reference to Globin.
He most often published in these fields:
- Genetics (62.84%)
- ATRX (50.68%)
- Gene (29.05%)
What were the highlights of his more recent work (between 2014-2021)?
- Genetics (62.84%)
- ATRX (50.68%)
- Gene (29.05%)
In recent papers he was focusing on the following fields of study:
Richard J. Gibbons mainly focuses on Genetics, ATRX, Gene, Thalassemia and Histone.
Regulation of gene expression, Replication factor C and Eukaryotic DNA replication are the subjects of his Genetics studies.
The ATRX study combines topics in areas such as Death-associated protein 6, Cancer research, Chromatin, Telomere and Epigenetics.
His Death-associated protein 6 research integrates issues from Heterochromatin and Genomic imprinting.
His Cancer research research includes themes of Mutation and Mutant.
Richard J. Gibbons has included themes like Low birth weight, Molecular biology, Anemia and Globin in his Thalassemia study.
Between 2014 and 2021, his most popular works were:
- Large-scale discovery of novel genetic causes of developmental disorders (661 citations)
- The Fanconi Anemia Pathway Maintains Genome Stability by Coordinating Replication and Transcription (197 citations)
- Genetic dissection of the α-globin super-enhancer in vivo (183 citations)
In his most recent research, the most cited papers focused on:
Genetics, ATRX, DNA replication, Cancer research and Bioinformatics are his primary areas of study.
His ATRX research is multidisciplinary, incorporating perspectives in Death-associated protein 6, CDKN2A and Genomic imprinting.
His DNA replication research includes elements of Telomere Homeostasis and Telomere.
His studies in Bioinformatics integrate themes in fields like Exome sequencing, Thalassemia, Beta thalassemia, Sickle cell anemia and Anemia.
His Exome sequencing study contributes to a more complete understanding of Gene.
The Chromatin study which covers Regulation of gene expression that intersects with Enhancer.
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