Author

D. P. Ball

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 6

Signature Assays, Organisms & Methods

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Approach:experimental assay· 6 Research Focus:host-pathogen & immune response· 4 Research Focus:cell signaling & trafficking· 3 Organism:human· 3 Research Focus:protein folding & dynamics· 3 Assay:proteomics· 2 Research Focus:cell type annotation· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

D. A. Bachovchin· 6 shared A. R. Griswold· 4 shared Q. Wang· 4 shared E. L. Orth-He· 3 shared H.-C. Huang· 3 shared S. D. Rao· 3 shared A. J. Chui· 2 shared C. M. O'Mara· 2 shared

Activity by Year

2019-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 42 mutual co-author links

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6 shared papersImmunology

D. A. Bachovchin

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6 papers

Recent·Most cited

The interaction between NLRP1 and oxidized TRX1 involves a transient disulfide bond

M. B. Geeson, J. C. Hsiao, L. P. Tsamouri, D. P. Ball, D. A. Bachovchin

This study identifies a transient disulfide bond between NLRP1 and oxidized TRX1, revealing how NLRP1 senses cellular redox state to regulate inflammasome formation.

bioRxiv · Sep 27, 2023Immunology

The NLRP1 and CARD8 inflammasomes detect reductive stress

Q. Wang, J. Hsiao, N. Yardeny, H.-C. Huang, C. M. O'Mara, E. L. Orth-He, D. P. Ball, D. A. Bachovchin

This study identifies chemical probes that induce reductive stress and shows that reductive stress and peptide accumulation together strongly activate NLRP1 and CARD8 inflammasomes.

bioRxiv · Mar 22, 2022Immunology

A ubiquitin-independent proteasome pathway controls the CARD8 inflammasome

J. C. Hsiao, A. R. Neugroschl, A. J. Chui, C. Y. Taabazuing, A. R. Griswold, Q. Wang, H.-C. Huang, E. L. Orth-He, D. P. Ball, G. Hiotis, D. A. Bachovchin

This study identifies a ubiquitin-independent proteasome pathway that degrades the CARD8 N-terminal fragment, releasing the inflammatory C-terminal fragment and activating the inflammasome.

bioRxiv · Mar 22, 2022 · PreprintImmunology

Cytosolic peptide accumulation activates the NLRP1 and CARD8 inflammasomes

E. L. Orth-He, H.-C. Huang, S. D. Rao, Q. Wang, Q. Chen, C. M. O'Mara, A. J. Chui, M. Saoi, A. R. Griswold, A. Bhattacharjee, D. P. Ball, J. R. Cross, D. A. Bachovchin

This study identifies cytosolic peptide accumulation as a danger signal that activates NLRP1 and CARD8 inflammasomes by promoting NT degradation and disrupting DPP9-mediated sequestration of CT fragments.

bioRxiv · Mar 22, 2022 · PreprintImmunology

Oxidized thioredoxin-1 restrains the NLRP1 inflammasome

D. P. Ball, A. E. Wang, C. D. Warren, Q. Wang, A. R. Griswold, S. D. Rao, D. A. Bachovchin

This study identifies oxidized thioredoxin-1 as a repressor of NLRP1 inflammasome activation, showing that mutations impair this interaction and cause autoinflammatory disease.

bioRxiv · Sep 20, 2021Immunology

Human caspase-1 autoproteolysis is required for ASC-dependent and -independent inflammasome activation

D. P. Ball, C. Y. Taabazuing, A. R. Griswold, E. L. Orth, S. D. Rao, I. B. Kotliar, D. C. Johnson, D. A. Bachovchin

This study shows that pro-caspase-1 autoproteolysis is required for both ASC-dependent and -independent inflammasome activation in human cells.

bioRxiv · Jun 24, 2019 · PreprintImmunology