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 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.
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.
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.
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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)
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)
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)
Mouse Models of Hermansky Pudlak Syndrome: A Review
Richard T. Swank;Edward K. Novak;Michael P. McGARRY;Michael E. Rusiniak.
Pigment Cell Research (1998)
Murine Hermansky-Pudlak syndrome genes: regulators of lysosome-related organelles.
Wei Li;Michael E. Rusiniak;Sreenivasulu Chintala;Rashi Gautam.
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)
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)
Genetic control of glucuronidase induction in mice.
Richard T. Swank;Kenneth Paigen;Roger E. Ganschow.
Journal of Molecular Biology (1973)
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)
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.
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