Author

David Gordon

John Radcliffe Hospital

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

Same name, identified by ORCID

Biology Disciplines

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Neuroscience· 2 Genetics· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Organism:human· 1 Approach:statistical model· 1 Research Focus:variant effect prediction· 1

Frequent Co-Authors

Kevin TalbotiD· 2 shared Aïda Masmoudi· 1 shared Andrew Paul TosoliniiD· 1 shared Anny DevoyiD· 1 shared Eleni ChristoforidouiD· 1 shared Elizabeth FisheriD· 1 shared Fabio A. SimoesiD· 1 shared Giampietro SchiavoiD· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

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2 shared papersNeuroscience

Kevin TalbotORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The ALS-associated TDP-43M337V mutation dysregulates microglia-derived extracellular microRNAs in a sex-specific manner

Eleni Christoforidou, Libby Moody, Greig Joilin, Fabio A. Simoes, David Gordon, Kevin Talbot, Majid Hafezparast

This study shows that the TDP-43M337V mutation in microglia alters miRNA release in a sex-specific way, potentially affecting ALS progression.

bioRxiv · Nov 30, 2023 · PreprintNeuroscience

Novel frameshift variant in MYL2 reveals molecular differences between dominant and recessive forms of hypertrophic cardiomyopathy

Sathiyanarayanan Manivannan, Sihem Darouich, Aïda Masmoudi, David Gordon, Gloria A. Zender, Zhe Han, Sara M. Fitzgerald‐Butt, Peter White, Kim L. McBride, Maher Kharrat, Vidu Garg

The paper identifies a novel recessive frameshift variant in MYL2 causing severe infantile-onset HCM and shows molecular differences between recessive and dominant MYL2 variants.

PLoS Genetics · May 26, 2020Peer-reviewedGenetics

ALS mice carrying pathological mutant TDP-43, but not mutant FUS, display axonal transport defects in vivo

James N. Sleigh, Andrew Paul Tosolini, David Gordon, Anny Devoy, Pietro Fratta, Elizabeth Fisher, Kevin Talbot, Giampietro Schiavo

The paper examines axonal transport defects in two ALS mouse models, finding that TDP-43 mutations cause transport issues while FUS mutations do not.

Cell Reports · Mar 1, 2020Peer-reviewedNeuroscience