Author

Lorna M. FitzPatrick

Manchester Metropolitan University

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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Molecular Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 2 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Assay:metabolomics· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

Ángeles AlmeidaiD· 1 shared Aseel M. SharairehiD· 1 shared Brenda Morant-FerrandoiD· 1 shared Carlos Vicente‐GutiérreziD· 1 shared Catherine B. LawrenceiD· 1 shared Christopher D. Thompton· 1 shared Christopher HoyleiD· 1 shared Costantina Buondelmonte· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperNeuroscience

Ángeles AlmeidaORCID

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Author profile →

2 papers

Recent·Most cited

Brazilin is a Natural Product Inhibitor of the NLRP3 Inflammasome

Emily McMahon, Sherihan El‐Sayed, Jack Green, Christopher Hoyle, Lorna M. FitzPatrick, Emma V. Jones, Eve Corrie, Rebecca L. Kelly, Mairi Challinor, Sally Freeman, Richard A. Bryce, Catherine B. Lawrence, David Brough, Paul R. Kasher

This study identifies brazilin as a natural product inhibitor of the NLRP3 inflammasome, effective in multiple models and suggesting its potential as a therapeutic scaffold.

iScience · Jan 21, 2024Peer-reviewedMolecular Biology

Mitochondrial collapse links PFKFB3-promoted glycolysis with CLN7/MFSD8 neuronal ceroid lipofuscinosis pathogenesis

Irene López-Fabuel, Marina García Macia, Costantina Buondelmonte, Olga Burmistrova, Nicoló Bonora, Brenda Morant-Ferrando, Paula Alonso-Batan, Carlos Vicente‐Gutiérrez, Daniel Jiménez-Blasco, Rubén Quintana–Cabrera, Emilio Fernández, Aseel M. Sharaireh, Marta Guevara‐Ferrer, Lorna M. FitzPatrick, Christopher D. Thompton, , Juan Pedro Bolaños

This study identifies a metabolic shift driven by PFKFB3 in CLN7 disease, showing that targeting glycolysis can alleviate disease hallmarks in a mouse model and patient-derived cells.

bioRxiv · Oct 20, 2020 · PreprintNeuroscience