Jonathan A. Deane
Genomics Institute of the Novartis Research Foundation
22 Papers
161 Citations
Jonathan A. Deane is an academic researcher from Genomics Institute of the Novartis Research Foundation. The author has contributed to research in topics: Phosphoinositide 3-kinase & Signal transduction. The author has an hindex of 13, co-authored 20 publications. Previous affiliations of Jonathan A. Deane include National Institutes of Health & University of California, Irvine.
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Papers
Autoreactive B Cell Responses to RNA-Related Antigens Due to TLR7 Gene Duplication
Prapaporn Pisitkun,Jonathan A. Deane,Michael J. Difilippantonio,Tatyana N. Tarasenko,Anne B. Satterthwaite,Silvia Bolland +5 more
TL;DR: It is reported that B cells containing the Y-linked autoimmune accelerator (Yaa) locus are intrinsically biased toward nucleolar antigens because of increased expression of TLR7, a single-stranded RNA-binding innate immune receptor.
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Control of Toll-like Receptor 7 Expression Is Essential to Restrict Autoimmunity and Dendritic Cell Proliferation
Jonathan A. Deane,Prapaporn Pisitkun,Rebecca S. Barrett,Lionel Feigenbaum,Terrence Town,Jerrold M. Ward,Richard A. Flavell,Silvia Bolland +7 more
TL;DR: It is demonstrated that duplication of the Tlr7 gene was the sole requirement for this accelerated autoimmunity, because reduction of TLR7 gene dosage abolished the Yaa phenotype.
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Phosphoinositide 3-kinase signaling is essential for ABL oncogene–mediated transformation of B-lineage cells
Michael G. Kharas,Jonathan A. Deane,Stephane Wong,Karen R O'Bosky,Naomi Rosenberg,Owen N. Witte,David A. Fruman +6 more
TL;DR: It is shown that activation of class I(A) PI3K and downstream inactivation of FOXO transcription factors are essential for survival of murine pro/pre-B cells transformed by v-ABL or BCR-ABl and a role is established in B-lineage transformation by ABL oncogenes.
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Enhanced T Cell Proliferation in Mice Lacking the p85β Subunit of Phosphoinositide 3-Kinase
Jonathan A. Deane,Matthew J. Trifilo,Claudine M. Yballe,Sangdun Choi,Thomas E. Lane,David A. Fruman +5 more
TL;DR: A unique role for p85β in limiting T cell expansion is suggested after a marked increase in proliferation and decreased death when stimulated with anti-CD3 plus IL-2 and in vivo following infection of p85 β-deficient mice with mouse hepatitis virus.
Sjögren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase
Jean S. Oak,Jonathan A. Deane,Jonathan A. Deane,Michael G. Kharas,Ji Luo,Thomas E. Lane,Lewis C. Cantley,David A. Fruman +7 more
TL;DR: It is shown that mice with T cell-specific loss of class IA phosphoinositide 3-kinase function develop organ-specific autoimmunity that resembles the human disease SS.
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