2015 - Fellow of the Royal Society, United Kingdom
Steve D.M. Brown mainly investigates Genetics, Gene, Genome, Mutant and Mutation. Phenotype, MYO7A, Allele, Genome-wide association study and Locus are the subjects of his Genetics studies. His Genome study incorporates themes from Embryonic stem cell, Mutagenesis, Signature-tagged mutagenesis, Computational biology and Human genetics.
His biological study spans a wide range of topics, including Hair cell, Neuroscience and Lissencephaly. The Mutation study combines topics in areas such as Key genes, Stereocilia bundle, Endocytosis, Cell biology and Apical membrane. His studies examine the connections between Cell biology and genetics, as well as such issues in Organ of Corti, with regards to Neural tube.
His main research concerns Genetics, Gene, Mutant, Phenotype and Genome. His study in Mutagenesis, Mutation, Human genetics, Locus and Gene mapping is carried out as part of his studies in Genetics. His studies in Gene integrate themes in fields like Computational biology and Function.
His Mutant study combines topics from a wide range of disciplines, such as Molecular biology, Embryonic stem cell, Anatomy and Cell biology. Steve D.M. Brown has researched Cell biology in several fields, including Hair cell and Inner ear. The study of Phenotype is intertwined with the study of Otitis in a number of ways.
His primary areas of investigation include Gene, Computational biology, Function, Phenotype and Genetics. Many of his research projects under Gene are closely connected to Identification with Identification, tying the diverse disciplines of science together. His Mutant research is multidisciplinary, incorporating perspectives in Nonsense mutation, Nephrocalcinosis, Molecular biology and Mitochondrial DNA.
His Computational biology research incorporates elements of Precision medicine, MEDLINE, Functional genomics, Gene knockout and Human genetics. The concepts of his Phenotype study are interwoven with issues in Enhancer and Mutation. His study in Genetics focuses on Allele, Genome editing, Mutation, CRISPR and In vivo.
The scientist’s investigation covers issues in Gene, Computational biology, Phenotype, Gene knockout and Function. Steve D.M. Brown works in the field of Gene, namely Novel gene. His Computational biology research is multidisciplinary, incorporating elements of Loss function, Phenomics and Knockout mouse.
His study explores the link between Phenotype and topics such as Candidate gene that cross with problems in Genotyping, Genome-wide association study, Genome, Promoter and Gene regulatory network. His research integrates issues of Human genetic variation, Mammalian gene, Functional genomics, Phenome and Genetic screen in his study of Gene knockout. Steve D.M. Brown interconnects Pleiotropy, Oxidative phosphorylation and Mutant in the investigation of issues within Function.
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α-Synuclein impairs macroautophagy: implications for Parkinson’s disease
Ashley R. Winslow;Chien-Wen Chen;Silvia Corrochano;Abraham Acevedo-Arozena.
Journal of Cell Biology (2010)
Mutation of Celsr1 disrupts planar polarity of inner ear hair cells and causes severe neural tube defects in the mouse.
John A. Curtin;Elizabeth Quint;Vicky Tsipouri;Ruth M. Arkell.
Current Biology (2003)
High-throughput discovery of novel developmental phenotypes
Mary E. Dickinson;Ann M. Flenniken;Xiao Ji;Lydia Teboul.
Mutations in the myosin VIIA gene cause non-syndromic recessive deafness.
X. Z. Liu;J. Walsh;P. Mburu;J. Kendrick-Jones.
Nature Genetics (1997)
Dynein mutations impair autophagic clearance of aggregate-prone proteins.
Brinda Ravikumar;Abraham Acevedo-Arozena;Sara Imarisio;Zdenek Berger.
Nature Genetics (2005)
The mouse ascending: perspectives for human-disease models.
Nadia Alicia Rosenthal;Steve Brown.
Nature Cell Biology (2007)
Autosomal dominant non-syndromic deafness caused by a mutation in the myosin VIIA gene
Xue Zhong Liu;James Walsh;Yuya Tamagawa;Ken Kitamura.
Nature Genetics (1997)
Mutations in α-Tubulin Cause Abnormal Neuronal Migration in Mice and Lissencephaly in Humans
David A. Keays;Guoling Tian;Karine Poirier;Guo Jen Huang.
A comparative phenotypic and genomic analysis of C57BL/6J and C57BL/6N mouse strains
Michelle M Simon;Simon Greenaway;Jacqueline K White;Helmut Fuchs.
Genome Biology (2013)
Defects in whirlin, a PDZ domain molecule involved in stereocilia elongation, cause deafness in the whirler mouse and families with DFNB31.
Philomena Mburu;Mirna Mustapha;Anabel Varela;Dominique Weil.
Nature Genetics (2003)
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