2014 - Fellow of the American Association for the Advancement of Science (AAAS)
His primary areas of investigation include Genetics, Mutation, Internal medicine, Endocrinology and Osteogenesis imperfecta. His research integrates issues of Procollagen peptidase and Type II collagen in his study of Genetics. The study incorporates disciplines such as Phenotype, Haploinsufficiency, Molecular biology and Candidate gene in addition to Mutation.
His Internal medicine research includes themes of Urea cycle disorder, Urea cycle, Cellular differentiation and Cell biology. His work in the fields of Myocyte overlaps with other areas such as Dobutamine. His Osteogenesis imperfecta study combines topics in areas such as Wnt signaling pathway, Type I collagen, Osteoid, Bruck syndrome and Osteoporosis.
Brendan Lee focuses on Internal medicine, Endocrinology, Genetics, Osteogenesis imperfecta and Molecular biology. His Internal medicine study which covers Urea cycle that intersects with Urea. The various areas that Brendan Lee examines in his Endocrinology study include Argininosuccinic acid and Arginine, Ornithine.
His study in Genetics concentrates on Gene, Mutation, Missense mutation, Exome sequencing and Phenotype. His Osteogenesis imperfecta research is multidisciplinary, incorporating perspectives in Type I collagen, Bruck syndrome, Osteoporosis, Cell biology and Pediatrics. His Molecular biology study incorporates themes from Viral vector, Transgene and Transduction.
His main research concerns Osteogenesis imperfecta, Genetics, Internal medicine, Exome sequencing and Pediatrics. His Osteogenesis imperfecta research incorporates themes from Clinical research, Bisphosphonate, Disease and Craniofacial. Genetics is a component of his Missense mutation, Gene, Intellectual disability, Phenotype and Hypotonia studies.
His study looks at the relationship between Internal medicine and topics such as Endocrinology, which overlap with Extracellular matrix. His biological study spans a wide range of topics, including Bioinformatics and Pathology. The Pediatrics study combines topics in areas such as Cohort and Natural history study.
His primary areas of study are Genetics, Missense mutation, Phenotype, Intellectual disability and Cell biology. His work carried out in the field of Missense mutation brings together such families of science as Germline, Genetic linkage, Genotype, Molecular genetics and Polymerase chain reaction. His studies deal with areas such as Fibronectin, Neurologic decline, Allele and Fibrillin as well as Phenotype.
His study in Cell biology is interdisciplinary in nature, drawing from both Peroxisome, Cellular differentiation, Intravital Imaging and Osteoblast. His Osteoblast study combines topics from a wide range of disciplines, such as Internal medicine, Endocrinology and Osteogenesis imperfecta. Many of his research projects under Endocrinology are closely connected to Induced pluripotent stem cell with Induced pluripotent stem cell, tying the diverse disciplines of science together.
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.
Linkage of Marfan syndrome and a phenotypically related disorder to two different fibrillin genes
Brendan Lee;Maurice Godfrey;Emilia Vitale;Hisae Hori.
Missense mutations abolishing DNA binding of the osteoblast-specific transcription factor OSF2/CBFA1 in cleidocranial dysplasia.
Brendan Lee;Kannan Thirunavukkarasu;Lei Zhou;Lucio Pastore.
Nature Genetics (1997)
Recurrent reciprocal 1q21.1 deletions and duplications associated with microcephaly or macrocephaly and developmental and behavioral abnormalities
Nicola Brunetti-Pierri;Jonathan S. Berg;Fernando Scaglia;John Belmont.
Nature Genetics (2008)
Limb and kidney defects in Lmx1b mutant mice suggest an involvement of LMX1B in human nail patella syndrome
Haixu Chen;Yi Lun;Dmitry Ovchinnikov;Hiroki Kokubo.
Nature Genetics (1998)
Mutations in LMX1B cause abnormal skeletal patterning and renal dysplasia in nail patella syndrome
Sandra D. Dreyer;Guang Zhou;Antonio Baldini;Andreas Winterpacht.
Nature Genetics (1998)
Cloning of the putative tumour suppressor gene for hereditary multiple exostoses (EXT1)
Jung Ahn;Hermann-Josef Lüdecke;Steffi Lindow;William A. Horton.
Nature Genetics (1995)
CRTAP is required for prolyl 3- hydroxylation and mutations cause recessive osteogenesis imperfecta.
Roy Morello;Terry K. Bertin;Yuqing Chen;Yuqing Chen;John Hicks.
Dimorphic effects of Notch signaling in bone homeostasis.
Feyza Engin;Zhenqiang Yao;Tao Yang;Guang Zhou.
Nature Medicine (2008)
Dominance of SOX9 function over RUNX2 during skeletogenesis
Guang Zhou;Qiping Zheng;Feyza Engin;Elda Munivez.
Proceedings of the National Academy of Sciences of the United States of America (2006)
Deficiency of Cartilage-Associated Protein in Recessive Lethal Osteogenesis Imperfecta
Aileen M. Barnes;Weizhong Chang;Roy Morello;Wayne A. Cabral.
The New England Journal of Medicine (2006)
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: