Author

Rachel Seear

University of CambridgeORCID 0009-0008-6019-9679Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

James A. NathaniD· 2 shared Tekle PauzaiteiD· 2 shared Adrian Llewellyn HarrisiD· 1 shared Ahmed M. SalmaniD· 1 shared Alexander HandysideiD· 1 shared Anastasia C. HepburniD· 1 shared Anneliese O. SpeakiD· 1 shared Brian M. OrtmanniD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCancer Biology

James A. NathanORCID

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2 papers

Recent·Most cited

Cancer BiologyCancer ResearchPeer-reviewedApr 6, 2026

SET1B drives sustained HIF activity and disease progression in clear cell renal cell carcinoma.

Brian M. Ortmann, Tekle Pauzaite, James A.C. Bertlin…·James A. Nathan

This study shows SET1B maintains HIF activity in ccRCC, correlates with disease progression, and is a target for HIF-2 inhibitors.

1 citation

humanbulk RNA-seq

𝕏 PostBluesky

Cell BiologyThe EMBO JournalPeer-reviewedJul 15, 2024

Deubiquitinating enzyme mutagenesis screens identify a USP43 driven HIF-1 transcriptional response

Tekle Pauzaite, Niek Wit, Rachel Seear, James A. Nathan

The paper identifies USP43 as a deubiquitinating enzyme that enhances HIF-1 nuclear accumulation and target gene binding through interaction with 14-3-3 proteins under hypoxia.

11 citations

humangenetic perturbation / CRISPR

𝕏 PostBluesky