What is he best known for?
The fields of study he is best known for:
His main research concerns Genetics, MMP20, Amelogenesis imperfecta, FAM83H and Allele.
His work on Gene mutation, Locus, Candidate gene and Papillon–Lefèvre syndrome as part of general Genetics research is frequently linked to Cathepsin C, thereby connecting diverse disciplines of science.
The concepts of his Papillon–Lefèvre syndrome study are interwoven with issues in Stop codon and Frameshift mutation, Exon.
His biological study spans a wide range of topics, including Amelogenin and ENAM.
His study looks at the intersection of ENAM and topics like AMELX with Amelogenesis.
His research in Allele intersects with topics in Periodontitis, Genome, Periodontal disease and Etiology.
His most cited work include:
- Phenotype and Course of Hutchinson–Gilford Progeria Syndrome (469 citations)
- Mutations of the UMOD gene are responsible for medullary cystic kidney disease 2 and familial juvenile hyperuricaemic nephropathy (355 citations)
- Genes and Gene Polymorphisms Associated with Periodontal Disease (265 citations)
What are the main themes of his work throughout his whole career to date?
His primary areas of investigation include Genetics, Amelogenesis imperfecta, Gene mutation, Dentistry and Molecular biology.
Many of his research projects under Genetics are closely connected to Cathepsin C with Cathepsin C, tying the diverse disciplines of science together.
He combines subjects such as Amelogenin and Phenotype with his study of Amelogenesis imperfecta.
The Gene mutation study combines topics in areas such as Endocrinology, Tamm–Horsfall protein, Internal medicine and Haplotype.
Thomas C. Hart has included themes like Craniosynostosis, Orthodontics, Heritability, Etiology and Craniofacial in his Dentistry study.
His Molecular biology research includes themes of Insertion, Mutant, Heterozygote advantage, Frameshift mutation and SOS1.
He most often published in these fields:
- Genetics (43.86%)
- Amelogenesis imperfecta (17.54%)
- Gene mutation (17.54%)
What were the highlights of his more recent work (between 2007-2013)?
- Genetics (43.86%)
- Gene mutation (17.54%)
- Internal medicine (12.28%)
In recent papers he was focusing on the following fields of study:
His primary scientific interests are in Genetics, Gene mutation, Internal medicine, Endocrinology and Amelogenesis imperfecta.
Within one scientific family, he focuses on topics pertaining to MMP20 under Genetics, and may sometimes address concerns connected to AMELX and ENAM.
His Gene mutation study incorporates themes from Hyperkeratosis and Severe periodontitis.
His study in Internal medicine is interdisciplinary in nature, drawing from both Microbiome and Immunology.
In general Endocrinology, his work in Kidney disease, Kidney and Klotho is often linked to Methylmalonic acid linking many areas of study.
His Amelogenesis imperfecta study combines topics from a wide range of disciplines, such as Patient satisfaction, Oral and maxillofacial pathology and Masticatory force.
Between 2007 and 2013, his most popular works were:
- Phenotype and Course of Hutchinson–Gilford Progeria Syndrome (469 citations)
- Dominant Renin Gene Mutations Associated with Early-Onset Hyperuricemia, Anemia, and Chronic Kidney Failure (107 citations)
- Amelogenesis Imperfecta: Genotype-Phenotype Studies in 71 Families (95 citations)
In his most recent research, the most cited papers focused on:
Genetics, Amelogenesis imperfecta, ENAM, MMP20 and Gene mutation are his primary areas of study.
His work in Allele, Phenotype, Genetic association, Locus and Frameshift mutation is related to Genetics.
His studies deal with areas such as SNP genotyping, Single-nucleotide polymorphism and Promoter as well as Allele.
His Phenotype research incorporates themes from Molecular biology, Dentin dysplasia, Dentinogenesis imperfecta, Exon and Haplotype.
Thomas C. Hart specializes in Amelogenesis imperfecta, namely FAM83H.
Thomas C. Hart interconnects Amelogenin, AMELX, Enamel hypoplasia and Candidate gene in the investigation of issues within ENAM.
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