2020 - Fellow of the American Academy of Arts and Sciences
2009 - Fellow of the Royal Society, United Kingdom
Karen P. Steel mainly investigates Genetics, Mutant, Cell biology, Gene and Inner ear. Her Genetics research includes themes of Molecular biology and Hearing loss. In most of her Mutant studies, her work intersects topics such as Mutation.
Her Cell biology research incorporates themes from Hair cell and Organ of Corti. The concepts of her Gene study are interwoven with issues in Evolutionary biology and Sexual dimorphism. Inner ear is a primary field of her research addressed under Anatomy.
Karen P. Steel mainly focuses on Genetics, Mutant, Gene, Cell biology and Inner ear. As part of her studies on Genetics, Karen P. Steel often connects relevant subjects like Hearing loss. The study incorporates disciplines such as Molecular biology, Allele and Missense mutation in addition to Mutant.
Her work investigates the relationship between Cell biology and topics such as Hair cell that intersect with problems in Heterozygote advantage. Her Inner ear study integrates concerns from other disciplines, such as Cochlea and Pathology. Karen P. Steel combines subjects such as Inner ear morphogenesis and Exon with her study of Mutation.
Her primary areas of investigation include Genetics, Gene, Hearing loss, Phenotype and Hair cell. She interconnects Exome sequencing, Genetic heterogeneity and Internal medicine in the investigation of issues within Hearing loss. Her Phenotype research is multidisciplinary, incorporating elements of Quantitative trait locus, Genotype and Sexual dimorphism.
Karen P. Steel has researched Hair cell in several fields, including Organ of Corti and Cell biology. Her Mutant study also includes fields such as
Gene, Genetics, Phenotype, Hearing loss and Mutant are her primary areas of study. Many of her research projects under Genetics are closely connected to Retinopathy with Retinopathy, tying the diverse disciplines of science together. Her Phenotype study incorporates themes from Genome-wide association study, Allele and Sexual dimorphism.
The Hearing loss study combines topics in areas such as Endocochlear potential, Inner ear, Organ of Corti and Genetic heterogeneity. Her Inner ear study combines topics in areas such as SOX2, Penetrance and Ectopic expression. Her Mutant research is multidisciplinary, relying on both Evolutionary biology, Sex characteristics, Phenotypic trait, Quantitative trait locus and Genotype.
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A type VII myosin encoded by the mouse deafness gene shaker-1.
F. Gibson;J. Walsh;P. Mburu;A. Varela.
Nature (1995)
A systematic, genome-wide, phenotype-driven mutagenesis programme for gene function studies in the mouse.
P M Nolan;J Peters;M Strivens;D Rogers.
Nature Genetics (2000)
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)
Mutations in the seed region of human miR-96 are responsible for nonsyndromic progressive hearing loss.
Ángeles Mencía;Silvia Modamio-Høybjør;Nick Redshaw;Matías Morín.
Nature Genetics (2009)
The mouse Snell's waltzer deafness gene encodes an unconventional myosin required for structural integrity of inner ear hair cells
Karen B. Avraham;Tama Hasson;Karen P. Steel;David M. Kingsley.
Nature Genetics (1995)
TRP-2/DT, a new early melanoblast marker, shows that steel growth factor (c-kit ligand) is a survival factor.
Karen P Steel;Duncan R. Davidson;Ian Jackson.
Development (1992)
Sox2 is required for sensory organ development in the mammalian inner ear
Amy E. Kiernan;Anna L. Pelling;Keith K. H. Leung;Anna S. P. Tang.
Nature (2005)
Wnt5a functions in planar cell polarity regulation in mice
Dong Qian;Chonnettia Jones;Agnieszka Rzadzinska;Sharayne Mark.
Developmental Biology (2007)
Another role for melanocytes: their importance for normal stria vascularis development in the mammalian inner ear.
K.P. Steel;C. Barkway.
Development (1989)
Mutations in Cdh23, encoding a new type of cadherin, cause stereocilia disorganization in waltzer, the mouse model for Usher syndrome type 1D.
Federica Di Palma;Ralph H. Holme;Elizabeth C. Bryda;Inna A. Belyantseva.
Nature Genetics (2001)
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