H-Index & Metrics Best Publications

H-Index & Metrics

Discipline name H-index Citations Publications World Ranking National Ranking
Genetics and Molecular Biology D-index 60 Citations 18,352 142 World Ranking 2390 National Ranking 262

Research.com Recognitions

Awards & Achievements

2015 - Fellow of the Royal Society, United Kingdom

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Genetics
  • Mutation

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 most cited work include:

  • α-Synuclein impairs macroautophagy: implications for Parkinson’s disease (541 citations)
  • High-throughput discovery of novel developmental phenotypes (523 citations)
  • Mutation of Celsr1 disrupts planar polarity of inner ear hair cells and causes severe neural tube defects in the mouse. (493 citations)

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

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.

He most often published in these fields:

  • Genetics (49.51%)
  • Gene (27.94%)
  • Mutant (22.55%)

What were the highlights of his more recent work (between 2017-2021)?

  • Gene (27.94%)
  • Computational biology (13.24%)
  • Function (4.41%)

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

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.

Between 2017 and 2021, his most popular works were:

  • High-throughput mouse phenomics for characterizing mammalian gene function (38 citations)
  • Identification of genetic elements in metabolism by high-throughput mouse phenotyping. (36 citations)
  • Helios is a key transcriptional regulator of outer hair cell maturation (29 citations)

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

  • Gene
  • Mutation
  • Genetics

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.

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

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)

734 Citations

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)

626 Citations

High-throughput discovery of novel developmental phenotypes

Mary E. Dickinson;Ann M. Flenniken;Xiao Ji;Lydia Teboul.
Nature (2016)

561 Citations

Mutations in the myosin VIIA gene cause non-syndromic recessive deafness.

X. Z. Liu;J. Walsh;P. Mburu;J. Kendrick-Jones.
Nature Genetics (1997)

529 Citations

Dynein mutations impair autophagic clearance of aggregate-prone proteins.

Brinda Ravikumar;Abraham Acevedo-Arozena;Sara Imarisio;Zdenek Berger.
Nature Genetics (2005)

478 Citations

The mouse ascending: perspectives for human-disease models.

Nadia Alicia Rosenthal;Steve Brown.
Nature Cell Biology (2007)

408 Citations

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)

406 Citations

Mutations in α-Tubulin Cause Abnormal Neuronal Migration in Mice and Lissencephaly in Humans

David A. Keays;Guoling Tian;Karine Poirier;Guo Jen Huang.
Cell (2007)

385 Citations

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)

331 Citations

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)

328 Citations

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