Author

W.-T. Lu

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 1 Cell Biology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Assay:DNA methylation· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Nagano· 1 shared A. R. Davidson· 1 shared A. Rowan· 1 shared A. S. Bader· 1 shared A. Suarez-Bonnet· 1 shared Argyr· 1 shared B. Almeida· 1 shared B. Bakker· 1 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperCancer Biology

A. Nagano

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci

A. S. Bader, J. Luessing, B. R. Hawley, G. L. Skalka, W.-T. Lu, N. F. Lowndes, M. Bushell

This study identifies DDX17 as essential for DNA repair at loci deficient in DNA:RNA hybrids by promoting hybrid formation at DSB sites.

bioRxiv · Oct 14, 2021Cell Biology

Targeted cancer therapy induces APOBEC fuelling the evolution of drug resistance

D. R. Caswell, M. K. Mayekar, P. Gui, E. K. Law, N. I. Vokes, C. M. Ruiz, M. Dietzen, M. Angelova, C. Bailey, O. Pich, B. Bakker, W. Wu, T. J. Humpton, D. L. Kerr, W. Hill, , Argyr

This study shows that targeted cancer therapy induces APOBEC-mediated mutagenesis, promoting drug resistance by increasing genetic diversity through mechanisms involving NF-κB activation and reduced DNA repair.

bioRxiv · Dec 18, 2020Cancer Biology

An anti-CRISPR protein induces strong non-specific DNA binding activity in a CRISPR-Cas complex

W.-T. Lu, C. N. Trost, H. Muller-Esparza, L. Randau, A. R. Davidson

This study shows that AcrIF9 enhances non-specific DNA binding in a CRISPR-Cas complex, which is conserved across homologues and suggests a new mechanism for Acr function.

bioRxiv · May 28, 2020 · PreprintMicrobiology