Anja Bielinsky

Professor and Chair

University of Virginia

United States

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Professor Anja Bielinsky is the Chair at the University of Virginia, USA. Her research focuses on DNA damage response, genome stability, and the mechanisms of DNA replication and repair, as reflected in her recent articles. She has explored topics such as the role of RAD18 in hyper-recombination suppression and the implications of MCM10 in genome stability during cell differentiation.

Articles (18)

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2025

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2024

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2024

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2024

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2021

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2021

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2021

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2020

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2020

Collaborators (19)

Maximilian Billmann

Assistant Professor

University Hospital Bonn

GERMANY

Anja Bielinsky

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Articles (18)

Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination

A scalable platform for efficient CRISPR-Cas9 chemical-genetic screens of DNA damage-inducing compounds

Improved detection of DNA replication fork-associated proteins

RNF4 prevents genomic instability caused by chronic DNA under-replication

A critical threshold of MCM10 is required to maintain genome stability during differentiation of induced pluripotent stem cells into natural killer cells

RNF4 and USP7 cooperate in ubiquitin-regulated steps of DNA replication

Fanconi anemia-associated chromosomal radial formation is dependent on POLθ-mediated alternative end joining

Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo

FANCD2-dependent mitotic DNA synthesis relies on PCNA K164 ubiquitination

Scalable CRISPR-Cas9 chemical genetic screens in non-transformed human cells

Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy

BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage.

Bi-allelic MCM10 variants associated with immune dysfunction and cardiomyopathy cause telomere shortening

SUMO-Targeted Ubiquitin Ligases and Their Functions in Maintaining Genome Stability

Congenital Diseases of DNA Replication: Clinical Phenotypes and Molecular Mechanisms

Functional cross talk between the Fanconi anemia and ATRX/DAXX histone chaperone pathways promotes replication fork recovery

SLFN11 promotes stalled fork degradation that underlies the phenotype in Fanconi anemia cells

Human NK cell deficiency as a result of biallelic mutations in MCM10

Collaborators (19)

Maximilian Billmann

John Joseph Reynolds

Silke Paust

Antony W Oliver

Anfeng Mu

Kevin Lin

Elizabeth Ormondroyd

Satpal Singh Jhujh

Anil Ganesh

Ezequiel Marron Fernandez de Velasco

Robert Shearer

Minoru Takata

Masato Kanemaki

Michael Simpson

Lata Balakrishnan

Advaitha Madireddy

David Largaespada

Emily M Mace

Luke Erber

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