The scientist’s investigation covers issues in Genetics, Exome, Human genetics, Disease and Exome sequencing. All of his Genetics and Phenotype, Gene duplication, Genomics, Chromosome and Gene investigations are sub-components of the entire Genetics study. His Exome research focuses on subjects like Genetic heterogeneity, which are linked to Robinow syndrome, Frameshift mutation, Dwarfism, Exon and Sanger sequencing.
In his study, which falls under the umbrella issue of Human genetics, Bohring–Opitz syndrome, Failure to thrive, Proband and Locus heterogeneity is strongly linked to Bioinformatics. His Disease research includes themes of Human Phenotype Ontology and Pediatrics. In his work, Mutation is strongly intertwined with PTEN, which is a subfield of Exome sequencing.
His primary areas of investigation include Genetics, Exome sequencing, Disease, Pediatrics and Osteogenesis imperfecta. His Genetics study focuses mostly on Missense mutation, Gene, Phenotype, Allele and Exome. His Exome sequencing research also works with subjects such as
His Disease study frequently draws parallels with other fields, such as Family history. V. Reid Sutton has researched Pediatrics in several fields, including Young adult, Body mass index and Cohort. His Osteogenesis imperfecta study integrates concerns from other disciplines, such as Ambulatory, Clinical research, Rehabilitation and Mobility Limitation.
His main research concerns Genetics, Robinow syndrome, Missense mutation, Osteogenesis imperfecta and Phenotype. His study connects Skeletal abnormalities and Genetics. His Robinow syndrome research is multidisciplinary, relying on both Osteosclerosis, Physical examination and Locus heterogeneity.
The various areas that V. Reid Sutton examines in his Missense mutation study include Metabolic disorder, CAD and Allele. His biological study spans a wide range of topics, including Pregnancy, Low birth weight, Clinical research, Diabetes mellitus and Neonatal intensive care unit. His study in Phenotype is interdisciplinary in nature, drawing from both Mutant, Genome, Nonsense and CRISPR.
V. Reid Sutton mainly investigates Genetics, Pediatrics, Exome sequencing, Robinow syndrome and Locus heterogeneity. His research on Genetics frequently connects to adjacent areas such as Metabolic disorder. His research in Pediatrics intersects with topics in Hearing loss, Intellectual disability and Obstructive sleep apnea.
His Exome sequencing research is multidisciplinary, incorporating perspectives in Sanger sequencing, Genetic heterogeneity, Wnt signaling pathway and Locus. His Robinow syndrome study combines topics in areas such as Genetic disorder, Brachydactyly, Physical examination, Mesomelia and Clinodactyly. His Missense mutation research incorporates elements of Proband, Osteochondrodysplasia, Genomics, Allele and Short stature.
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.
The Genetic Basis of Mendelian Phenotypes: Discoveries, Challenges, and Opportunities
Jessica X. Chong;Kati J. Buckingham;Shalini N. Jhangiani;Corinne Boehm.
American Journal of Human Genetics (2015)
Resolution of Disease Phenotypes Resulting from Multilocus Genomic Variation
Jennifer E. Posey;Tamar Harel;Pengfei Liu;Jill A. Rosenfeld.
The New England Journal of Medicine (2017)
Chromosome 1p36 deletions: the clinical phenotype and molecular characterization of a common newly delineated syndrome.
Stuart K. Shapira;Christopher McCaskill;Hope Northrup;Aimee S. Spikes.
American Journal of Human Genetics (1997)
Mutations in X-linked PORCN, a putative regulator of Wnt signaling, cause focal dermal hypoplasia
Xiaoling Wang;V Reid Sutton;J Omar Peraza-Llanes;Zhiyin Yu.
Nature Genetics (2007)
Clinical delineation and natural history of the PIK3CA-related overgrowth spectrum.
Kim M Keppler-Noreuil;Julie C Sapp;Marjorie J Lindhurst;Victoria Er Parker.
American Journal of Medical Genetics Part A (2014)
Mosaic overgrowth with fibroadipose hyperplasia is caused by somatic activating mutations in PIK3CA
Marjorie J Lindhurst;Victoria E R Parker;Felicity Payne;Julie C Sapp.
Nature Genetics (2012)
22q11.2 Distal Deletion: A Recurrent Genomic Disorder Distinct from DiGeorge Syndrome and Velocardiofacial Syndrome
Shay Ben-Shachar;Zhishuo Ou;Chad A. Shaw;John W. Belmont.
American Journal of Human Genetics (2008)
Microarray‐based CGH detects chromosomal mosaicism not revealed by conventional cytogenetics
Sau W. Cheung;Chad A. Shaw;Daryl A. Scott;Ankita Patel.
American Journal of Medical Genetics Part A (2007)
Asprosin is a centrally acting orexigenic hormone.
Clemens Duerrschmid;Yanlin He;Chunmei Wang;Chia Li.
Nature Medicine (2017)
Molecular diagnostic experience of whole-exome sequencing in adult patients
Jennifer E. Posey;Jill A. Rosenfeld;Regis A. James;Matthew Bainbridge.
Genetics in Medicine (2016)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: