Author

Kristbjorn O. Gudmundsson

Frederick National Laboratory for Cancer ResearchORCID 0000-0002-5995-2263Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 1 Developmental Biology· 1 Genetics· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Bjorg GudmundsdottiriD· 2 shared Jonathan R. KelleriD· 2 shared Baktiar O. KarimiD· 1 shared Ben TitleiD· 1 shared Brad L. JakubisoniD· 1 shared Dina M. SiganoiD· 1 shared Galya Monderer‐Rothkoff· 1 shared Gary T. PaulyiD· 1 shared

Activity by Year

2020-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersDevelopmental Biology

Bjorg GudmundsdottirORCID

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Author profile →

3 papers

Recent·Most cited

Id1 Promotes Clonal Hematopoiesis in Mice with Tet2 Loss of Function

Shweta Singh, Kristbjorn O. Gudmundsson, Tanmoy Sarkar, Brad L. Jakubison, Holly M. Morris, Sandra Sczerba Burkett, Baktiar O. Karim, Gary T. Pauly, Dina M. Sigano, Joel P. Schneider, Lino Tessarollo, Jonathan R. Keller

Genetic ablation of Id1 in Tet2-/- mice reduces clonal hematopoiesis by increasing CDKI expression, apoptosis, senescence, and differentiation while decreasing cell growth.

Science Advances · Aug 29, 2025Peer-reviewedCancer Biology

MLL1 complex is a critical regulator of fetal hemoglobin repression

Yufen Han, Bjorg Gudmundsdottir, Kristbjorn O. Gudmundsson, Kartik R. Roy, John F. Tisdale, Yang Du

This study identifies the MLL1 complex as a regulator of fetal hemoglobin repression and shows that targeting MEN1 or KMT2A increases fetal hemoglobin expression in erythroid cells.

bioRxiv · Mar 24, 2025 · PreprintDevelopmental Biology

Pogz deficiency leads to abnormal behavior, transcription dysregulation and impaired cerebellar physiology

Reut Suliman-Lavie, Ben Title, Yahel Cohen, Nanako Hamada, Maayan Tal, Nitzan Tal, Galya Monderer‐Rothkoff, Bjorg Gudmundsdottir, Kristbjorn O. Gudmundsson, Jonathan R. Keller, Guo‐Jen Huang, Koh‐ichi Nagata, Yosef Yarom, Sagiv Shifman

This study shows that Pogz deficiency in mice causes brain abnormalities, transcription dysregulation, and cerebellar dysfunction resembling ASD features in humans.

Nature Communications · Nov 17, 2020Peer-reviewedGenetics