Author

P. D. Mace

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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Biochemistry· 6 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 7 Organism:human· 6 Research Focus:protein folding & dynamics· 3 Research Focus:cell type annotation· 2 Research Focus:drug response / drug discovery· 2 Assay:protein structure· 2 Assay:proteomics· 2 Approach:biophysical modeling· 1

Frequent Co-Authors

A. E. Burgess· 3 shared J. L. Brewster· 3 shared S. A. Jamieson· 3 shared A. L. Cadell· 2 shared D. R. Croucher· 2 shared H. D. McMillan· 2 shared J. M. Murphy· 2 shared A. D. Axtman· 1 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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3 shared papersBiochemistry

A. E. Burgess

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

TRIB1 modulates transcriptional programming in breast cancer cells to regulate cell proliferation

H. D. McMillan, E. K. Papachristou, J. Hazlett, S. Omarjee, J. Carroll, M. Black, P. D. Mace, A. Dunbier

This study shows TRIB1 promotes breast cancer cell proliferation by regulating MYC expression and cell cycle progression through interactions with β-catenin and ER-driven transcription.

bioRxiv · Jul 6, 2023 · PreprintCancer Biology

Nanobodies identify an activated state of the TRIB2 pseudokinase

S. A. Jamieson, M. Pudjihartono, C. Horne, R. C. Day, J. M. Murphy, P. D. Mace

This study identifies nanobodies that recognize an activated conformation of TRIB2 pseudokinase, revealing structural insights and potential for inhibitor development.

bioRxiv · Apr 29, 2022Biochemistry

Oncogenic truncations of ASXL1 enhance a motif for BRD4 ET-domain binding

A. E. Burgess, T. Kleffmann, P. D. Mace

This study identifies a molecular mechanism by which ASXL1 truncations enhance BRD4 binding through an ET-domain motif, potentially altering transcriptional regulation and offering therapeutic insights.

bioRxiv · Jul 15, 2021Biochemistry

Structural basis for active-site probes targeting Staphylococcus aureus serine hydrolase virulence factors

M. Fellner, C. S. Lentz, S. A. Jamieson, J. L. Brewster, L. Chen, M. Bogyo, P. D. Mace

The paper reports structures of Staphylococcus aureus serine hydrolases and their interactions with inhibitors, revealing functional insights and potential targets for therapeutic development.

bioRxiv · Apr 21, 2020 · PreprintBiochemistry

A cryptic tubulin-binding domain links MEKK1 to microtubule remodelling

P. Filipcik, S. L. Latham, A. L. Cadell, C. L. Day, D. R. Croucher, P. D. Mace

This paper identifies a previously unknown TOG domain in MEKK1 that binds curved tubulin heterodimers, and shows mutations disrupting this interaction are enriched in tumors.

bioRxiv · Apr 7, 2020 · PreprintBiochemistry

Mechanism of preferential complex formation by Apoptosis Signal-regulating Kinases

S. J. Trevelyan, J. L. Brewster, A. E. Burgess, J. M. Crowther, A. L. Cadell, B. L. Parker, D. R. Croucher, R. C. Dobson, J. M. Murphy, P. D. Mace

This study identifies the mechanism by which ASK1-3 kinases form preferential heterocomplexes through their SAM domains, revealing structural insights into their role in inflammatory signaling.

bioRxiv · Jul 5, 2019Biochemistry

Substrate binding allosterically relieves autoinhibition of the TRIB1 pseudokinase

S. A. Jamieson, Z. Ruan, A. E. Burgess, J. R. Curry, H. D. McMillan, J. L. Brewster, A. K. Dunbier, A. D. Axtman, K. Natarajan, P. D. Mace

The paper shows that substrate binding to TRIB1 pseudokinase induces allosteric changes enabling complex formation with COP1 ubiquitin ligase.

bioRxiv · May 3, 2018Biochemistry