Author

T. Shutt

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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Cell Biology· 4 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Research Focus:cell type annotation· 3 Organism:human· 3 Research Focus:host-pathogen & immune response· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:drug response / drug discovery· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

A. Khan· 3 shared T. Zhao· 3 shared A. Ravandi· 2 shared F. Iqbal· 2 shared G. S. Shadel· 2 shared J. Deng· 2 shared P. Machiraju· 2 shared R. Sabouny· 2 shared

Activity by Year

2019-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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3 shared papersCell Biology

A. Khan

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Cooperative sensing of mitochondrial DNA by ZBP1 and cGAS promotes cardiotoxicity

Y. Lei, J. J. Vanportfliet, Y.-F. Chen, J. D. Bryant, Y. Li, D. Fails, S. Torres Odio, K. B. Ragan, J. Deng, A. Mohan, B. Wang, O. Brahms, S. Yates, M. Spencer, C. W. Tong, , A. P. West

This study shows that ZBP1 and cGAS cooperate to detect mitochondrial DNA, leading to cardiotoxicity, and that blocking this interaction protects against heart damage.

bioRxiv · May 30, 2022Immunology

Activation of the cGAS-STING innate immune response in cells with deficient mitochondrial topoisomerase TOP1MT

I. Al Khatib, J. Deng, Y. Lei, S. Torres-Odio, G. R. Rojas, L. E. Newman, B. K. Chung, S. A. Symes, H. Zhang, S.-y. N. Huang, Y. Pommier, A. Khan, G. S. Shadel, P. West, W. Gibson, T. Shutt

This study links TOP1MT deficiency and the P193L variant to mtDNA release and cGAS-STING activation, contributing to autoimmune disease susceptibility.

bioRxiv · Mar 8, 2022Cell Biology

Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

P. Sam, E. Calzada, M. G. Acoba, T. Zhao, Y. Watanabe, A. Nejatfard, J. Trinidad, T. Shutt, S. E. Neal, S. M. Claypool

The paper investigates the subcellular localization of Psd1 and shows that impaired phosphatidylethanolamine metabolism triggers an ER-assisted response to resolve nonfunctional mitochondrial precursors.

bioRxiv · Dec 10, 2020Cell Biology

Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes from Children with DCMA, a Mitochondrial Cardiomyopathy

L. Rohani, P. Machiraju, R. Sabouny, G. Meng, S. Liu, T. Zhao, F. Iqbal, A. Ravandi, J. C. Wu, A. Khan, T. Shutt, D. Rancourt, S. C. Greenway

This study uses iPSC-derived cardiomyocytes from DCMA patients to show reversible mitochondrial fragmentation and OPA1 isoform imbalance, suggesting SS-31 as a potential therapy.

Canadian Journal of Cardiology · Apr 1, 2020Peer-reviewedCell Biology

SS-31 Reverses Mitochondrial Fragmentation in Fibroblasts from Patients with DCMA, a Mitochondrial Cardiomyopathy

P. Machiraju, X. Wang, R. Sabouny, J. Huang, T. Zhao, F. Iqbal, M. King, D. Prasher, A. Lodha, A. Ravandi, B. Argiropoulos, D. Sinasac, A. Khan, T. Shutt, S. C. Greenway

This study shows that SS-31 reverses mitochondrial fragmentation and increases ROS in DCMA fibroblasts, suggesting it as a potential therapy for this mitochondrial cardiomyopathy.

bioRxiv · Jun 17, 2019Cell Biology