Author

J. A. Marsh

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· 3 Cancer Biology· 2 Evolutionary Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Research Focus:chromatin & epigenetic regulation· 2 Assay:proteomics· 2 Approach:statistical model· 2

Frequent Co-Authors

L. Murphy· 2 shared M. Badonyi· 2 shared A. C. Purcell· 1 shared A. Coates· 1 shared A. Esin· 1 shared A. Ewing· 1 shared A. Fawkes· 1 shared A. Ferrer-Vacquer· 1 shared

Activity by Year

2017-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 12 mutual co-author links

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Curved chords = mutual co-authorship

2 shared papersCancer Biology

L. Murphy

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Mutational scanning reveals oncogenic CTNNB1 mutations have diverse effects on signalling and clinical traits

A. Krishna, A. Meynert, M. Kelder, A. Ewing, S. Sheraz, A. Ferrer-Vacquer, G. Grimes, H. Becher, R. Silk, C. A. Semple, T. Kendall, A.-K. Hadjantonakis, T. Bird, J. A. Marsh, P. Hohenstein, , D. D. Ozdemir

The paper quantifies signalling effects of CTNNB1 mutations across cancer types and finds weakly activating mutations correlate with worse prognosis in hepatocellular carcinoma.

bioRxiv · Nov 9, 2023 · PreprintCancer Biology

ALDH1A3-acetaldehyde metabolism potentiates transcriptionalheterogeneity in melanoma

Y. Lu, J. Travnickova, M. Badonyi, F. Rambow, A. Coates, Z. Khan, J. Marques, L. Murphy, P. Garcia-Martinez, R. Marais, P. Louphrasitthiphol, A. H. Y. Chan, C. J. Schofield, A. V. Kriegsheim, J. A. Marsh, , E. E. Patton

This study shows ALDH1A3 and ACSS2 coordinate acetaldehyde-acetyl-CoA metabolism with histone acetylation in melanoma, contributing to transcriptional heterogeneity and drug resistance.

bioRxiv · Oct 28, 2023Cancer Biology

Cell overgrowth during G1 arrest triggers an osmotic stress response and chronic p38 activation to promote cell cycle exit

L. Crozier, R. Foy, R. Adib, M. Badonyi, A. Kar, J. A. Holt, R. Wilson, C. Regnault, P. Whitfield, J. A. Marsh, A. T. Saurin, A. R. Barr, T. Ly

The paper shows that CDK4/6 inhibitor-induced G1 arrest causes cell overgrowth, triggering osmotic stress and p38-p53-p21 signaling to promote cell cycle exit.

bioRxiv · Sep 8, 2022Cell Biology

Longitudinal dynamics of clonal hematopoiesis identifies gene-specific fitness effects

N. A. Robertson, E. Latorre-Crespo, M. Terrada-Terradas, A. C. Purcell, B. J. Livesey, J. A. Marsh, L. Murphy, A. Fawkes, L. MacGillvray, M. Copland, R. E. Marioni, S. E. Harris, S. R. Cox, I. J. Deary, L. J. Schumacher, , T. Chandra

This study quantifies gene-specific fitness effects of CHIP drivers over 12 years using longitudinal sequencing data and a new DIF filtering method, showing gene-specific differences can inform personalized clinical management.

bioRxiv · May 27, 2021Cell Biology

A WDR35-dependent coatomer transports ciliary membrane proteins from the Golgi to the cilia

T. Quidwai, E. A. Hall, M. A. Keighren, W. Leng, P. Kiesel, J. N. Wells, L. C. Murphy, J. A. Marsh, G. Pigino, P. Mill

The paper shows WDR35 is part of a coatomer complex that transports ciliary membrane proteins from the Golgi to cilia, essential for cilia elongation.

bioRxiv · Dec 22, 2020 · PreprintCell Biology

The genetic basis and evolution of red blood cell sickling in deer

A. Esin, L. T. Bergendahl, V. Savolainen, J. A. Marsh, T. Warnecke

This study identifies the genetic basis of erythrocyte sickling in deer, revealing structural and evolutionary differences from human sickle cell disease.

bioRxiv · Jun 26, 2017Evolutionary Biology