Author

Teresa Mortera Blanco

Karolinska InstitutetORCID 0000-0002-8399-1430Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Research Focus:protein structure prediction· 2 Assay:proteomics· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1

Frequent Co-Authors

Ann-Charlotte BjörklundiD· 3 shared Indira BarbosaiD· 3 shared Pedro Luís MouraiD· 3 shared Christina Maria Perraki· 2 shared Eva Hellström‐LindbergiD· 2 shared Janne LehtiöiD· 2 shared Mikaela Hillberg Widfeldt· 2 shared Rui Mamede BrancaiD· 2 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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Curved chords = mutual co-authorship

3 shared papersCancer Biology

Ann-Charlotte BjörklundORCID

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3 papers

Recent·Most cited

Proteomics of steady-state and culture-derived human erythropoiesis reveals the dynamics of erythroid stress

Christina Maria Perraki, Kovi Rishya Shrung, Sadaf Fazeli, Yaroslav Kaminskiy, Ann-Charlotte Björklund, Indira Barbosa, Mikaela Hillberg Widfeldt, Janne Lehtiö, Eva Hellström‐Lindberg, Teresa Mortera Blanco, Rui Mamede Branca, Pedro Luís Moura

This study compares proteomic profiles of steady-state and cultured human erythroid progenitors, revealing how culture-induced stress alters protein expression and erythroid maturation dynamics.

bioRxiv · Oct 14, 2026 · PreprintPhysiology

RNA splicing factor mutations drive myeloid neoplasm oncogenesis through protein complex poisoning

Pedro Luís Moura, Rui Mamede Branca, Yaroslav Kaminskiy, Ioannis Siavelis, Kovi R Shrung, Sophia Hofmann, Christina Maria Perraki, Alexandra Argyriou, Sadaf Fazeli, Masahiro M Nakagawa, Teresa Mortera Blanco, Steffen Boettcher, Caroline Kubaczka, Thorsten M. Schlaeger, Maria Creignou, , Eva Hellström-Lindberg

This study identifies how RNA splicing factor mutations drive myeloid neoplasm by disrupting proteomic networks through mis-splicing, validated via single-cell transcriptomics and proteomics.

bioRxiv · Sep 30, 2026 · PreprintCancer Biology

SF3B1-mutant mis-splicing of UBA1 confers a targetable therapeutic vulnerability through UBA1 inhibition

Jonas Thier, Sophia Hofmann, Katharina Miria Kirchhof, Gabriele Todisco, Teresa Mortera Blanco, Ingrid Lilienthal, Dimitris C. Kanellis, Indira Barbosa, Ann-Charlotte Björklund, André G. Deslauriers, Jiří Bártek, Nikolas Herold, Elli Papaemmanuil, Eirini P. Papapetrou, Eva Hellström‐Lindberg, , Vanessa Lundin

This study identifies UBA1 mis-splicing as a therapeutic target in SF3B1-mutant myelodysplastic syndromes, showing that UBA1 inhibition sensitizes these cells to treatment.

Leukemia · Aug 26, 2025Peer-reviewedCancer Biology