Author

Natalia Jiménez-Moreno

Edinburgh Cancer ResearchORCID 0000-0002-3934-7015Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Katie Winnington-Ingram· 3 shared Simon WilkinsoniD· 3 shared Alain J. Kemp· 2 shared Alex von KriegsheimiD· 2 shared Ann P. WheeleriD· 2 shared Arianna KarageorgiouiD· 2 shared Carla Salomo-ColliD· 2 shared Ashish DhiriD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersCell Biology

Katie Winnington-Ingram

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3 papers

Recent·Most cited

ER-liquid condensate contacts sequester FAM134B/C and RhoA to govern cell morphology

Natalia Jiménez-Moreno, Arianna Karageorgiou, Katie Winnington-Ingram, Jimi C. Wills, Chinmayi Pednekar, Melina Overhoff, Katherine Paine, Matthew Pearson, Lukas Gerasimavicius, Ann P. Wheeler, Natalia L. Kononenko, Joseph A. Marsh, Paul Verkade, Alex von Kriegsheim, Jon D. Lane, Simon Wilkinson

The paper identifies ER-liquid condensates that sequester FAM134B/C and RhoA, affecting cell morphology and cancer invasion.

Molecular Cell · Aug 17, 2026Peer-reviewedCell Biology

Dysproteostasis primes pancreatic epithelial state changes in KRAS-mediated oncogenesis

Carla Salomo-Coll, Marisa Di Monaco, Jocelyn Holkham, Matthew Denman Smith, Morwenna Muir, Philippe Emmanuel Gautier, Hywel Dunn-Davies, Xiaozhong Zheng, Roopesh Krishnankutty, Alain J. Kemp, Katie Winnington-Ingram, Alex von Kriegsheim, Jennifer P. Morton, Natalia Jiménez-Moreno, Damian J. Mole, Simon Wilkinson

This study shows that proteostatic failure in ER-phagy, driven by Kras, leads to protein aggregates that prime acinar-ductal metaplasia and pancreatic cancer.

Developmental Cell · Aug 15, 2025Peer-reviewedCancer Biology

Chronic lysosome damage boosts interferon responses to Palbociclib dependent upon the mitochondrion

Mihaela Božić, Tian En Lim, Carla Salomo-Coll, Arianna Karageorgiou, Alain J. Kemp, Katie Winnington-Ingram, Laura C. Murphy, Ashish Dhir, Ann P. Wheeler, Natalia Jiménez-Moreno, Simon Wilkinson

The paper shows chronic lysosome damage from Palbociclib treatment in cancer cells triggers interferon responses via mitochondrial nucleic acid release, dependent on lysosome-mitochondrion contacts.

bioRxiv · Mar 13, 2025 · PreprintCell Biology