What is he best known for?
The fields of study he is best known for:
His primary areas of study are Genetics, Polycystic kidney disease, Autosomal dominant polycystic kidney disease, Alport syndrome and Gene.
His work in Chromosome 16, Locus, Chromosome 17 and Chromosome 22 are all subfields of Genetics research.
His Polycystic kidney disease study combines topics in areas such as Hybridization probe and Genetic linkage.
His Alport syndrome research is multidisciplinary, incorporating perspectives in Alpha, Mutation, Gene Organization and Nephritis, Immunology.
His Mutation research is multidisciplinary, incorporating elements of Consanguinity and Glomerular basement membrane, Glomerulonephritis, Thin basement membrane disease.
In his study, Fusion protein is inextricably linked to PKD1, which falls within the broad field of Gene.
His most cited work include:
- A highly polymorphic DNA marker linked to adult polycystic kidney disease on chromosome 16 (605 citations)
- Type IV collagen: structure, gene organization, and role in human diseases. Molecular basis of Goodpasture and Alport syndromes and diffuse leiomyomatosis. (542 citations)
- Improved telomere detection using a telomere repeat probe (TTAGGG)n generated by PCR (465 citations)
What are the main themes of his work throughout his whole career to date?
His scientific interests lie mostly in Genetics, Molecular biology, Gene, Autosomal dominant polycystic kidney disease and Genetic marker.
His study involves Locus, PKD1, Chromosome 16, Gene mapping and Polycystic kidney disease, a branch of Genetics.
His Molecular biology research includes elements of Goodpasture syndrome, Alport syndrome, Gene mutation, Basement membrane and Candidate gene.
Stephen T. Reeders interconnects Alpha and Peptide sequence in the investigation of issues within Alport syndrome.
His study in Autosomal dominant polycystic kidney disease is interdisciplinary in nature, drawing from both Cystic kidney and Cell biology.
His studies deal with areas such as Genetic linkage, Allele and Restriction fragment length polymorphism as well as Genetic marker.
He most often published in these fields:
- Genetics (72.63%)
- Molecular biology (36.84%)
- Gene (31.58%)
What were the highlights of his more recent work (between 1993-1999)?
- Genetics (72.63%)
- Molecular biology (36.84%)
- Gene (31.58%)
In recent papers he was focusing on the following fields of study:
Genetics, Molecular biology, Gene, PKD1 and Autosomal dominant polycystic kidney disease are his primary areas of study.
His study in Gene mapping, Alport syndrome, Allele, Locus and Gene product are all subfields of Genetics.
As part of one scientific family, Stephen T. Reeders deals mainly with the area of Alport syndrome, narrowing it down to issues related to the Mutation, and often Glomerulonephritis, Consanguinity and Thin basement membrane disease.
His Molecular biology research integrates issues from Endocrinology, Gene mutation, Gene cluster, Internal medicine and Candidate gene.
Within one scientific family, Stephen T. Reeders focuses on topics pertaining to Polycystic kidney disease under Gene, and may sometimes address concerns connected to Structural motif.
Specifically, his work in Autosomal dominant polycystic kidney disease is concerned with the study of Polycystin-1.
Between 1993 and 1999, his most popular works were:
- Identification of Mutations in the Alpha-3(iv) and Alpha-4(iv) Collagen Genes in Autosomal Recessive Alport Syndrome (420 citations)
- Identification of Mutations in the Alpha-3(iv) and Alpha-4(iv) Collagen Genes in Autosomal Recessive Alport Syndrome (420 citations)
- Polycystic kidney disease: the complete structure of the PKD1 gene and its protein (380 citations)
In his most recent research, the most cited papers focused on:
Stephen T. Reeders mostly deals with Genetics, Alport syndrome, Gene, Autosomal dominant polycystic kidney disease and Polycystic kidney disease.
As part of his studies on Alport syndrome, Stephen T. Reeders often connects relevant areas like Mutation.
His research integrates issues of Alpha, Glomerular basement membrane, Glomerulonephritis, Thin basement membrane disease and Consanguinity in his study of Mutation.
His Gene study frequently draws connections to adjacent fields such as PKD1.
In the subject of general Autosomal dominant polycystic kidney disease, his work in Polycystin 2 and Polycystin-1 is often linked to TRPP, thereby combining diverse domains of study.
His Exon research is multidisciplinary, incorporating elements of Nonsense mutation, Missense mutation, Compound heterozygosity and Locus.
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