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Richard A. Wells
Researcher at Sunnybrook Health Sciences Centre
Publications - 119
Citations - 5348
Richard A. Wells is an academic researcher from Sunnybrook Health Sciences Centre. The author has contributed to research in topics: Eculizumab & Myelodysplastic syndromes. The author has an hindex of 31, co-authored 119 publications receiving 4674 citations. Previous affiliations of Richard A. Wells include John Radcliffe Hospital & University of Texas MD Anderson Cancer Center.
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Journal ArticleDOI
Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype
Daniel T. Starczynowski,Florian Kuchenbauer,Bob Argiropoulos,Sandy Sung,Ryan D. Morin,Andrew L Muranyi,Martin Hirst,Donna E. Hogge,Marco A. Marra,Richard A. Wells,Rena Buckstein,Wan L. Lam,R. Keith Humphries,Aly Karsan +13 more
TL;DR: Deletes chromosome 5q and identifies Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs.
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Targeted Deletion of a High-Affinity GATA-binding Site in the GATA-1 Promoter Leads to Selective Loss of the Eosinophil Lineage In Vivo
Channing Yu,Alan B. Cantor,Haidi Yang,Carol P. Browne,Richard A. Wells,Yuko Fujiwara,Stuart H. Orkin +6 more
TL;DR: Findings suggest that GATA-1 is required for specification of this lineage during hematopoietic development, and mice lacking the ability to produce eosinophils should prove useful in ascertaining the role of eosInophils in a variety of inflammatory or allergic disorders.
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Improved telomere detection using a telomere repeat probe (TTAGGG)n generated by PCR
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Origin of human chromosome 2: an ancestral telomere-telomere fusion.
TL;DR: The locus cloned in cosmids c8.1 and c29B is the relic of an ancient telomere-telomere fusion and marks the point at which two ancestral ape chromosomes fused to give rise to human chromosome 2.
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Fusion of retinoic acid receptor alpha to NuMA, the nuclear mitotic apparatus protein, by a variant translocation in acute promyelocytic leukaemia.
TL;DR: It is suggested that interference with retinoid signalling, and not disruption of PML organization, is essential to the APL phenotype and implicates for the first time an element of the mitotic apparatus in the molecular pathogenesis of human malignancy.