J
John-Paul Upton
Researcher at University of California, San Francisco
Publications - 11
Citations - 2747
John-Paul Upton is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Unfolded protein response & Endoplasmic reticulum. The author has an hindex of 11, co-authored 11 publications receiving 2334 citations. Previous affiliations of John-Paul Upton include Wellcome Trust Centre for Cell-Matrix Research & Genentech.
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Journal ArticleDOI
IRE1α Kinase Activation Modes Control Alternate Endoribonuclease Outputs to Determine Divergent Cell Fates
Dan Han,Dan Han,Alana G. Lerner,Alana G. Lerner,Lieselotte Vande Walle,Lieselotte Vande Walle,John-Paul Upton,Weihong Xu,Andrew Hagen,Andrew Hagen,Bradley J. Backes,Bradley J. Backes,Scott A. Oakes,Feroz R. Papa,Feroz R. Papa +14 more
TL;DR: Using chemical genetics, it is shown that kinase inhibitors bypass autophosphorylation to activate the RNase by an alternate mode that enforces XBP1 splicing and averts mRNA decay and apoptosis.
Journal ArticleDOI
IRE1α Induces Thioredoxin-Interacting Protein to Activate the NLRP3 Inflammasome and Promote Programmed Cell Death under Irremediable ER Stress
Alana G. Lerner,John-Paul Upton,P. V.K. Praveen,Rajarshi Ghosh,Yoshimi Nakagawa,Aeid Igbaria,Sarah Shen,Vinh Son Nguyen,Bradley J. Backes,Myriam Heiman,Myriam Heiman,Myriam Heiman,Nathaniel Heintz,Paul Greengard,Simon T. Hui,Qizhi Tang,Ala Trusina,Scott A. Oakes,Feroz R. Papa +18 more
TL;DR: The IRE1α-TXNIP pathway is used in the terminal UPR to promote sterile inflammation and programmed cell death and may be targeted to develop effective treatments for cell degenerative diseases.
Journal ArticleDOI
IRE1α Cleaves Select microRNAs During ER Stress to Derepress Translation of Proapoptotic Caspase-2
John-Paul Upton,Likun Wang,Dan Han,Eric S. Wang,Noelle E. Huskey,Lionel Lim,Morgan L. Truitt,Michael T. McManus,Davide Ruggero,Andrei Goga,Feroz R. Papa,Scott A. Oakes +11 more
TL;DR: It is reported that sustained IRE1α RNase activation caused rapid decay of select microRNAs that normally repress translation of Caspase-2 mRNA, and thus sharply elevates protein levels of this initiator protease of the mitochondrial apoptotic pathway.
Journal ArticleDOI
USP7 small-molecule inhibitors interfere with ubiquitin binding
Lorna Kategaya,Paola Di Lello,Lionel Rouge,Richard Pastor,Kevin R Clark,Jason Drummond,Tracy Kleinheinz,Eva Lin,John-Paul Upton,Sumit Prakash,Johanna Heideker,Mark McCleland,Maria Stella Ritorto,Dario R. Alessi,Matthias Trost,Travis W. Bainbridge,Michael C. M. Kwok,Taylur P. Ma,Zachary Stiffler,Bradley B. Brasher,Yinyan Tang,Priyadarshini Jaishankar,Brian R. Hearn,Adam R. Renslo,Michelle R. Arkin,Frederick Cohen,Kebing Yu,Frank Peale,Florian Gnad,Matthew T. Chang,Christiaan Klijn,Elizabeth Blackwood,Scott E. Martin,William F. Forrest,James A. Ernst,Chudi Ndubaku,Xiaojing Wang,Maureen Beresini,Vickie Tsui,Carsten Schwerdtfeger,Robert A. Blake,Jeremy Murray,Till Maurer,Ingrid E. Wertz +43 more
TL;DR: Engineering compounds that inhibit USP7 activity by attenuating ubiquitin binding suggests opportunities for developing other deubiquitinase inhibitors and may be a strategy more broadly applicable to inhibiting proteins that require ubiquit in binding for full functional activity.
Journal ArticleDOI
Caspase-2 cleavage of BID is a critical apoptotic signal downstream of endoplasmic reticulum stress.
John-Paul Upton,Kathryn Austgen,Mari Nishino,Kristen M. Coakley,Andrew Hagen,Dan Han,Feroz R. Papa,Scott A. Oakes +7 more
TL;DR: A novel signaling pathway that couples the ER and mitochondria and establishes a principal apoptotic effector downstream of ER stress is defined and caspase-2 is identified as the premitochondrial protease that cleaves BID in response to ER stress.