2019 - Fellow of the Australian Academy of Health and Medical Science
Sally L. Dunwoodie mainly focuses on Genetics, Cell biology, Spondylocostal dysostosis, Notch signaling pathway and LFNG. Her is involved in several facets of Genetics study, as is seen by her studies on Mutation, Gene, Mutant, Transcription factor and Progenitor cell. Her Cell biology research is multidisciplinary, incorporating perspectives in Heart development, Heart morphogenesis, Paraxial mesoderm, Downregulation and upregulation and NODAL.
Sally L. Dunwoodie interconnects Embryonic stem cell, Cellular differentiation and Somitogenesis in the investigation of issues within Notch signaling pathway. Her LFNG research includes themes of Genetic linkage, Mendelian inheritance and Candidate gene. Her Signal transduction research is multidisciplinary, relying on both Molecular biology and Hypoxia.
The scientist’s investigation covers issues in Genetics, Cell biology, Gene, Notch signaling pathway and Spondylocostal dysostosis. Her Genetics and Mutation, Missense mutation, Mutant, Allele and Exome sequencing investigations all form part of her Genetics research activities. Her Cell biology study combines topics in areas such as Molecular biology, Gene expression, Transcription factor and Embryonic stem cell.
Her Gene research integrates issues from Embryo and Cohort. Her Notch signaling pathway research includes elements of Penetrance, Paraxial mesoderm and Somite, Somitogenesis. Her studies examine the connections between Spondylocostal dysostosis and genetics, as well as such issues in LFNG, with regards to Cancer research.
Her scientific interests lie mostly in Genetics, Gene, Missense mutation, Exome sequencing and Heart disease. Her research on Genetics frequently connects to adjacent areas such as Disease. Her work carried out in the field of Gene brings together such families of science as Inflammation and Cohort.
The various areas that Sally L. Dunwoodie examines in her Missense mutation study include Heterozygote advantage and Allele. Her biological study spans a wide range of topics, including Tetralogy of Fallot, Genetic variation, Locus and Rare disease. Her Exome research incorporates themes from Functional genomics, Notch signaling pathway and Loss of heterozygosity.
Her primary areas of investigation include Genetics, Exome sequencing, Disease, Heart disease and Penetrance. Sally L. Dunwoodie is studying Exome, which is a component of Genetics. Her Exome sequencing study incorporates themes from CLARITY, Tetralogy of Fallot, Genetic variation and Rare disease.
The concepts of her Disease study are interwoven with issues in Molecular pathology and Medical genetics. As part of one scientific family, Sally L. Dunwoodie deals mainly with the area of Molecular pathology, narrowing it down to issues related to the Cohort, and often Gene and Bioinformatics. Her Penetrance research incorporates elements of Genetic predisposition, In utero, Heart development, TBX1 and Physiology.
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The Role of Hypoxia in Development of the Mammalian Embryo
Sally L. Dunwoodie.
Developmental Cell (2009)
Mouse Dll3: a novel divergent Delta gene which may complement the function of other Delta homologues during early pattern formation in the mouse embryo
Sally L. Dunwoodie;Domingos Henrique;Stephen M. Harrison;Rosa S. P. Beddington.
SmcHD1, containing a structural-maintenance-of-chromosomes hinge domain, has a critical role in X inactivation.
Marnie E Blewitt;Anne-Valerie Gendrel;Zhenyi Pang;Duncan B Sparrow.
Nature Genetics (2008)
Murine T-box transcription factor Tbx20 acts as a repressor during heart development, and is essential for adult heart integrity, function and adaptation.
Fiona A Stennard;Mauro W Costa;Mauro W Costa;Donna Lai;Christine Biben.
Mutation of the LUNATIC FRINGE Gene in Humans Causes Spondylocostal Dysostosis with a Severe Vertebral Phenotype
D.B. Sparrow;G. Chapman;M.A. Wouters;N.V. Whittock.
American Journal of Human Genetics (2006)
Axial skeletal defects caused by mutation in the spondylocostal dysplasia/pudgy gene Dll3 are associated with disruption of the segmentation clock within the presomitic mesoderm.
Sally L. Dunwoodie;Sally L. Dunwoodie;Melanie Clements;Duncan B. Sparrow;Xin Sa.
TBX6 Null Variants and a Common Hypomorphic Allele in Congenital Scoliosis
Wu N;Ming X;Xiao J;Wu Z.
The New England Journal of Medicine (2015)
A Mechanism for Gene-Environment Interaction in the Etiology of Congenital Scoliosis
Duncan B. Sparrow;Duncan B. Sparrow;Gavin Chapman;Gavin Chapman;Allanceson J. Smith;Muhammad Z. Mattar.
Divergent functions and distinct localization of the Notch ligands DLL1 and DLL3 in vivo.
Insa Geffers;Katrin Serth;Gavin Chapman;Robert Jaekel.
Journal of Cell Biology (2007)
Notch inhibition by the ligand Delta-Like 3 defines the mechanism of abnormal vertebral segmentation in spondylocostal dysostosis
Gavin Chapman;Gavin Chapman;Duncan B. Sparrow;Duncan B. Sparrow;Elisabeth Kremmer;Sally L. Dunwoodie;Sally L. Dunwoodie.
Human Molecular Genetics (2011)
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