D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 47 Citations 7,486 87 World Ranking 11936 National Ranking 5136

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Mutation

Richard T. Swank mainly investigates Molecular biology, Gene, Genetics, Mutation and Mutant. His studies deal with areas such as Positional cloning and Rab as well as Molecular biology. His research in the fields of Phenotype, Transgene, Locus and Chromosome 19 overlaps with other disciplines such as Hermanski-Pudlak Syndrome.

He combines subjects such as Secretion and Biogenesis with his study of Phenotype. His work focuses on many connections between Mutation and other disciplines, such as Griscelli syndrome, that overlap with his field of interest in Homologous chromosome, Drosophila Protein, Vacuole, Vesicular transport protein and Melanosome transport. To a larger extent, Richard T. Swank studies Biochemistry with the aim of understanding Mutant.

His most cited work include:

  • Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1). (355 citations)
  • A Mutation in Rab27a causes the vesicle transport defects observed in ashen mice (354 citations)
  • The beta3A subunit gene (Ap3b1) of the AP-3 adaptor complex is altered in the mouse hypopigmentation mutant pearl, a model for Hermansky-Pudlak syndrome and night blindness (227 citations)

What are the main themes of his work throughout his whole career to date?

His primary areas of study are Molecular biology, Mutant, Gene, Genetics and Cell biology. The concepts of his Molecular biology study are interwoven with issues in Mutation, Biochemistry, Transfection, Ratón and Beta-glucuronidase. His work carried out in the field of Mutation brings together such families of science as Griscelli syndrome, Oculocutaneous albinism, Albinism and Coding region.

As a part of the same scientific family, Richard T. Swank mostly works in the field of Mutant, focusing on Platelet and, on occasion, Pathology and Adenine nucleotide. Richard T. Swank works mostly in the field of Gene, limiting it down to concerns involving Von Willebrand disease and, occasionally, Ristocetin. The various areas that he examines in his Cell biology study include Melanosome, Biogenesis and Lysosome.

He most often published in these fields:

  • Molecular biology (39.00%)
  • Mutant (36.00%)
  • Gene (34.00%)

What were the highlights of his more recent work (between 2000-2017)?

  • Cell biology (28.00%)
  • Organelle (19.00%)
  • Mutant (36.00%)

In recent papers he was focusing on the following fields of study:

His primary areas of study are Cell biology, Organelle, Mutant, Gene and Platelet. The Cell biology study combines topics in areas such as Biogenesis, Lysosome, Melanosome, Griscelli syndrome and Thrombocytopathy. His studies in Mutant integrate themes in fields like Molecular biology, Lamellar granule, Glutathione and Melanin.

Many of his studies involve connections with topics such as Mutation and Molecular biology. His research on Gene concerns the broader Genetics. His Platelet study combines topics in areas such as Rab, Adenosine triphosphate and Prenylation, Enzyme.

Between 2000 and 2017, his most popular works were:

  • Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1). (355 citations)
  • Murine Hermansky-Pudlak syndrome genes: regulators of lysosome-related organelles. (173 citations)
  • Mutation of a new gene causes a unique form of Hermansky–Pudlak syndrome in a genetic isolate of central Puerto Rico (171 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Enzyme
  • Mutation

His primary areas of investigation include Mutation, Gene, Genetics, Biogenesis and Phenotype. He has researched Mutation in several fields, including Molecular biology and Oculocutaneous albinism. Richard T. Swank performs integrative study on Gene and Hermanski-Pudlak Syndrome in his works.

His biological study spans a wide range of topics, including Lysosome and Organelle, Cell biology. His Phenotype research is multidisciplinary, incorporating elements of Melanosome, Mutant and Organelle biogenesis. His Mutant study introduces a deeper knowledge of Biochemistry.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1).

Wei Li;Qing Zhang;Naoki Oiso;Edward K Novak.
Nature Genetics (2003)

441 Citations

A Mutation in Rab27a causes the vesicle transport defects observed in ashen mice

Scott M. Wilson;Richard Yip;Deborah A. Swing;T. Norene O'Sullivan.
Proceedings of the National Academy of Sciences of the United States of America (2000)

435 Citations

Mutations in Orthologous Genes in Human Spondyloepimetaphyseal Dysplasia and the Brachymorphic Mouse

Faiyaz ul Haque M;King Lm;Krakow D;Krakow D;Cantor Rm.
Nature Genetics (1998)

269 Citations

Mouse Models of Hermansky Pudlak Syndrome: A Review

Richard T. Swank;Edward K. Novak;Michael P. McGARRY;Michael E. Rusiniak.
Pigment Cell Research (1998)

267 Citations

Murine Hermansky-Pudlak syndrome genes: regulators of lysosome-related organelles.

Wei Li;Michael E. Rusiniak;Sreenivasulu Chintala;Rashi Gautam.
BioEssays (2004)

265 Citations

Mutation of a new gene causes a unique form of Hermansky–Pudlak syndrome in a genetic isolate of central Puerto Rico

Yair Anikster;Marjan Huizing;James White;Yuriy O. Shevchenko.
Nature Genetics (2001)

261 Citations

The beta3A subunit gene (Ap3b1) of the AP-3 adaptor complex is altered in the mouse hypopigmentation mutant pearl, a model for Hermansky-Pudlak syndrome and night blindness

Lijun Feng;Albert B. Seymour;Shelley Jiang;Agnes To.
Human Molecular Genetics (1999)

260 Citations

Genetic control of glucuronidase induction in mice.

Richard T. Swank;Kenneth Paigen;Roger E. Ganschow.
Journal of Molecular Biology (1973)

206 Citations

Hermansky-Pudlak syndrome is caused by mutations in HPS4 , the human homolog of the mouse light-ear gene

Tamio Suzuki;Wei Li;Qing Zhang;Amna Karim.
Nature Genetics (2002)

205 Citations

Kidney and Retinal Defects (Krd), a Transgene-Induced Mutation with a Deletion of Mouse Chromosome 19 That Includes the Pax2 Locus

Scot A. Keller;Julie M. Jones;Ann Boyle;Lon L. Barrow.
Genomics (1994)

203 Citations

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