The scientist’s investigation covers issues in Fetal hemoglobin, Genetics, Immunology, Regulation of gene expression and Gene. Vijay G. Sankaran focuses mostly in the field of Fetal hemoglobin, narrowing it down to matters related to Disease and, in some cases, Bioinformatics and Anemia. His Genetics study integrates concerns from other disciplines, such as Hereditary persistence of fetal hemoglobin and Cancer research.
The Immunology study combines topics in areas such as Fetal haemoglobin, Carrier protein, Developmental physiology and Neuroscience. His study in Regulation of gene expression is interdisciplinary in nature, drawing from both Osteosarcoma, Gene expression profiling, Chromatin immunoprecipitation, Gene silencing and Genetically modified mouse. His biological study deals with issues like Molecular biology, which deal with fields such as Gene cluster, Repressor, RNA interference, Exome and Exome sequencing.
Genetics, Cell biology, Haematopoiesis, Erythropoiesis and Fetal hemoglobin are his primary areas of study. Genetics is a component of his Gene, Genome-wide association study, Blood cell, Locus and Transcription factor studies. His Cell biology research includes elements of Translation, microRNA, Cellular differentiation and Ribosomal protein.
CD34 is closely connected to Progenitor cell in his research, which is encompassed under the umbrella topic of Haematopoiesis. His Fetal hemoglobin study combines topics from a wide range of disciplines, such as Thalassemia, Hemoglobin, Immunology, Disease and Gene silencing. His work focuses on many connections between Immunology and other disciplines, such as Anemia, that overlap with his field of interest in Diamond–Blackfan anemia.
His primary areas of study are Computational biology, Haematopoiesis, Cell, Stem cell and Cell biology. The concepts of his Computational biology study are interwoven with issues in Genome-wide association study, Phenotype, Gene, Epigenomics and Cell type. Genome-wide association study is a subfield of Genetics that he explores.
His work carried out in the field of Haematopoiesis brings together such families of science as Published Erratum, GTPase, Progenitor cell, Erythropoiesis and Genome. Vijay G. Sankaran has included themes like Lineage, Transcriptome, Mitochondrial DNA, Chromatin and Clonal hematopoiesis in his Cell study. His studies in Cell biology integrate themes in fields like Protein biosynthesis, Translation, Messenger RNA, microRNA and Ribosome.
His primary scientific interests are in Genetics, Computational biology, Genome-wide association study, Blood cell and Genetic architecture. His study in Somatic cell, Stem cell and Haematopoiesis is carried out as part of his Genetics studies. His Somatic cell study incorporates themes from Locus, Human genetics, Germline and Genetic variation.
He has researched Genetic variation in several fields, including Disease and Immunology. His research integrates issues of Chromatin, Cell, Lineage commitment and Mitochondrial DNA in his study of Computational biology. His Blood cell research is multidisciplinary, incorporating perspectives in Allele and Mendelian inheritance.
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Human Fetal Hemoglobin Expression Is Regulated by the Developmental Stage-Specific Repressor BCL11A
Vijay G. Sankaran;Tobias F. Menne;Jian Xu;Thomas E. Akie.
Science (2008)
Genome-wide association study shows BCL11A associated with persistent fetal hemoglobin and amelioration of the phenotype of β-thalassemia
Manuela Uda;Renzo Galanello;Serena Sanna;Guillaume Lettre;Guillaume Lettre.
Proceedings of the National Academy of Sciences of the United States of America (2008)
DNA polymorphisms at the BCL11A, HBS1L-MYB, and β-globin loci associate with fetal hemoglobin levels and pain crises in sickle cell disease
Guillaume Lettre;Vijay G. Sankaran;Marcos André C. Bezerra;Aderson S. Araújo.
Proceedings of the National Academy of Sciences of the United States of America (2008)
Developmental and species-divergent globin switching are driven by BCL11A
Vijay G. Sankaran;Jian Xu;Tobias Ragoczy;Gregory C. Ippolito.
Nature (2009)
Transcriptional silencing of γ-globin by BCL11A involves long-range interactions and cooperation with SOX6
Jian Xu;Vijay G. Sankaran;Min Ni;Min Ni;Tobias F. Menne.
Genes & Development (2010)
Structural Basis for Discrimination of 3-Phosphoinositides by Pleckstrin Homology Domains
Kathryn M. Ferguson;Jennifer M. Kavran;Vijay G. Sankaran;Emmanuel Fournier.
Molecular Cell (2000)
Conditional mouse osteosarcoma, dependent on p53 loss and potentiated by loss of Rb, mimics the human disease
Carl R. Walkley;Rameez Qudsi;Vijay G. Sankaran;Jennifer A. Perry.
Genes & Development (2008)
Exome sequencing identifies GATA1 mutations resulting in Diamond-Blackfan anemia
Vijay G. Sankaran;Roxanne Ghazvinian;Ron Do;Prathapan Thiru.
Journal of Clinical Investigation (2012)
Correction of sickle cell disease in adult mice by interference with fetal hemoglobin silencing.
Jian Xu;Cong Peng;Vijay G. Sankaran;Vijay G. Sankaran;Zhen Shao.
Science (2011)
The Switch from Fetal to Adult Hemoglobin
Vijay G. Sankaran;Vijay G. Sankaran;Vijay G. Sankaran;Stuart H. Orkin;Stuart H. Orkin;Stuart H. Orkin.
Cold Spring Harbor Perspectives in Medicine (2013)
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