B
Ben G. Wen
Researcher at Genomics Institute of the Novartis Research Foundation
Publications - 5
Citations - 503
Ben G. Wen is an academic researcher from Genomics Institute of the Novartis Research Foundation. The author has contributed to research in topics: Antigen & Antibody. The author has an hindex of 5, co-authored 5 publications receiving 424 citations. Previous affiliations of Ben G. Wen include Novartis.
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Journal ArticleDOI
Proteasome inhibition for treatment of leishmaniasis, Chagas disease and sleeping sickness
Shilpi Khare,Advait Nagle,Agnes Biggart,Yin H. Lai,Fang Liang,Lauren C. Davis,S. Whitney Barnes,Casey J. N. Mathison,Elmarie Myburgh,Elmarie Myburgh,Mu-Yun Gao,J. Robert Gillespie,Xianzhong Liu,Jocelyn Tan,Monique Stinson,Ianne C. Rivera,Jaime Ballard,Vince Yeh,Todd Groessl,Glenn C. Federe,Hazel X. Y. Koh,John D. Venable,Badry Bursulaya,Michael Shapiro,Pranab Mishra,Glen Spraggon,Ansgar Brock,Jeremy C. Mottram,Jeremy C. Mottram,Frederick S. Buckner,Srinivasa P. S. Rao,Ben G. Wen,John R. Walker,Tove Tuntland,Valentina Molteni,Richard Glynne,Frantisek Supek +36 more
TL;DR: A selective inhibitor of the kinetoplastid proteasome (GNF6702) with unprecedented in vivo efficacy, which cleared parasites from mice in all three models of infection, underscores the possibility of developing a single class of drugs for these neglected diseases.
Journal ArticleDOI
Inositol (1,4,5) trisphosphate 3 kinase B controls positive selection of T cells and modulates Erk activity
Ben G. Wen,Mathew T. Pletcher,Masaki Warashina,Sun Hui Choe,Niusha Ziaee,Tim Wiltshire,Karsten Sauer,Michael P. Cooke +7 more
TL;DR: A nonsense mutation in the inositol (1,4,5) trisphosphate 3 kinase B (Itpkb) gene is revealed in Ms. T-less mice, suggesting a role for Itpkb in linking T cell receptor signaling to efficient and sustained Erk activation.
Journal ArticleDOI
Immunochemical termination of self-tolerance.
Jan Grünewald,Meng Lin Tsao,Roshan Perera,Liqun Dong,Frank Niessen,Ben G. Wen,Diane M. Kubitz,Vaughn V. Smider,Wolfram Ruf,Marc Nasoff,Richard A. Lerner,Peter G. Schultz +11 more
TL;DR: It is shown that site-specific incorporation of an immunogenic unnatural amino acid into a protein of interest produces high-titer antibodies that cross-react with WT protein, providing a general method for inducing an antibody response to specific epitopes of self- and foreign antigens that lead to a neutralizing immune response.
Journal ArticleDOI
Mechanistic studies of the immunochemical termination of self-tolerance with unnatural amino acids
Jan Grünewald,Grady S. Hunt,Liqun Dong,Frank Niessen,Ben G. Wen,Meng Lin Tsao,Meng Lin Tsao,Roshan Perera,Mingchao Kang,Bryan A. Laffitte,Sassan M. Azarian,Wolfram Ruf,Marc Nasoff,Richard A. Lerner,Peter G. Schultz,Peter G. Schultz,Vaughn V. Smider +16 more
TL;DR: The nature and durability of the polyclonal IgG antibody response is characterized and the generality of p-nitrophenylalanine (pNO2Phe)-induced loss of self-tolerance is established to generate effective immunotherapeutics against cancer-associated or other weakly immunogenic antigens.
Journal ArticleDOI
Inhibition of the Inositol Kinase Itpkb Augments Calcium Signaling in Lymphocytes and Reveals a Novel Strategy to Treat Autoimmune Disease
Andrew T. Miller,Carol Dahlberg,Mark L. Sandberg,Ben G. Wen,Daniel R. Beisner,John A. H. Hoerter,Albert E. Parker,Christian Schmedt,Monique Stinson,Jacqueline Avis,Cynthia Cienfuegos,Mark McPate,Pamela Tranter,Martin Gosling,Paul J. Groot-Kormelink,Janet Dawson,Shifeng Pan,Shin-Shay Tian,H. Martin Seidel,Michael P. Cooke +19 more
TL;DR: Evidence is provided for an alternative approach in which inhibition of the negative regulatory inositol kinase Itpkb in mature T lymphocytes results in enhanced intracellular calcium levels following antigen receptor activation leading to T cell death.