David S. Williams spends much of his time researching Cell biology, Genetics, Retina, Cilium and Mutant. He has researched Cell biology in several fields, including Retinal degeneration, Photoreceptor outer segment, Macular degeneration, MYO7A and Opsin. His work on Retinitis pigmentosa, T cell and Candidate Gene Analysis as part of his general Genetics study is frequently connected to Disease gene identification, thereby bridging the divide between different branches of science.
His biological study spans a wide range of topics, including Retinal, Anatomy and Transducin. David S. Williams has included themes like Positional cloning, Microtubule, RPGRIP1L, Senior–Løken syndrome and Myosin in his Cilium study. In his study, Gene knockdown and Respiratory enzyme is strongly linked to Molecular biology, which falls under the umbrella field of Mutant.
David S. Williams mostly deals with Cell biology, Retina, Retinal, Internal medicine and Retinal pigment epithelium. His Cell biology research is multidisciplinary, incorporating perspectives in Retinal degeneration, Photoreceptor outer segment and Opsin. His Retinal degeneration study integrates concerns from other disciplines, such as Retinitis pigmentosa, MYO7A and Usher syndrome.
The study incorporates disciplines such as Mutant and Anatomy in addition to Retina. His Retinal study results in a more complete grasp of Biochemistry. The concepts of his Retinal pigment epithelium study are interwoven with issues in Phagosome and Melanosome.
David S. Williams mainly focuses on Cell biology, Internal medicine, Nanotechnology, Polymersome and Nanoparticle. David S. Williams works in the field of Cell biology, focusing on Myosin in particular. The various areas that David S. Williams examines in his Internal medicine study include Gastroenterology and Oncology.
His work in the fields of Drug delivery overlaps with other areas such as Biocompatible material. His Polymersome study incorporates themes from Vesicle, Membrane, Biophysics, Synthetic Organelles and Nanoreactor. His Nanoparticle research includes themes of Copolymer and Ethylene glycol.
His primary areas of investigation include Polymersome, Cell biology, Biophysics, Internal medicine and Nanotechnology. His research integrates issues of Photoreceptor outer segment, Real-time polymerase chain reaction, Nicotinamide, Cytoskeletal Organization and Metabolism in his study of Cell biology. In his study, which falls under the umbrella issue of Photoreceptor outer segment, Mutant protein, Retina, Phagosome, Retinal degeneration and Rhodopsin is strongly linked to Motility.
His Biophysics research incorporates elements of Coacervate, Protocell and Cell membrane. His work in the fields of Internal medicine, such as Prospective cohort study and Colorectal cancer, overlaps with other areas such as Minimal change disease, Nephropathy and Membranous nephropathy. As a part of the same scientific study, David S. Williams usually deals with the Nanotechnology, concentrating on Function and frequently concerns with Ethylene glycol.
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Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease.
Gorazd B. Stokin;Concepción Lillo;Tomás L. Falzone;Richard G. Brusch.
Science (2005)
The centrosomal protein nephrocystin-6 is mutated in Joubert syndrome and activates transcription factor ATF4
John A. Sayer;John A. Sayer;Edgar A. Otto;John F. O'Toole;Gudrun Nurnberg.
Nature Genetics (2006)
Toxicity of Familial ALS-Linked SOD1 Mutants from Selective Recruitment to Spinal Mitochondria
Jian Liu;Concepción Lillo;P.Andreas Jonsson;Christine Vande Velde.
Neuron (2004)
Cadherin 23 is a component of the tip link in hair-cell stereocilia.
Jan Siemens;Concepcion Lillo;Rachel A. Dumont;Anna Reynolds.
Nature (2004)
Path Decomposition and Continuity of Local Time for One‐Dimensional Diffusions, I
David Williams.
Proceedings of The London Mathematical Society (1974)
Genetic evidence for selective transport of opsin and arrestin by kinesin-II in mammalian photoreceptors.
Joseph R Marszalek;Xinran Liu;Elizabeth A Roberts;Daniel Chui.
Cell (2000)
Nephrocystin-5, a ciliary IQ domain protein, is mutated in Senior-Loken syndrome and interacts with RPGR and calmodulin
Edgar A. Otto;Bart Loeys;Hemant Khanna;Jan Hellemans.
Nature Genetics (2005)
In-frame deletion in a novel centrosomal/ciliary protein CEP290/NPHP6 perturbs its interaction with RPGR and results in early-onset retinal degeneration in the rd16 mouse
Bo Chang;Hemant Khanna;Norman Hawes;David Jimeno.
Human Molecular Genetics (2006)
Candidate exome capture identifies mutation of SDCCAG8 as the cause of a retinal-renal ciliopathy
Edgar A Otto;Toby W Hurd;Rannar Airik;Moumita Chaki.
Nature Genetics (2010)
Serotype-dependent packaging of large genes in adeno-associated viral vectors results in effective gene delivery in mice
Mariacarmela Allocca;Monica Doria;Marco Petrillo;Pasqualina Colella.
Journal of Clinical Investigation (2008)
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