Author

D. R. Iyer

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

Biology Disciplines

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Cell Biology· 3

Signature Assays, Organisms & Methods

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Research Focus:chromatin & epigenetic regulation· 3 Approach:experimental assay· 3 Assay:DNA methylation· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:clustering· 1

Frequent Co-Authors

N. Rhind· 2 shared A. E. Tijhuis· 1 shared C. Soriani· 1 shared D. C. Spierings· 1 shared D. Fachinetti· 1 shared F. Foijer· 1 shared G. De Feudis· 1 shared L. Garribba· 1 shared

Activity by Year

2017-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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2 shared papersCell Biology

N. Rhind

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Author profile →

3 papers

Recent·Most cited

Short-term molecular consequences of chromosome mis-segregation for genome stability

L. Garribba, G. De Feudis, V. Martis, M. Galli, M. Dumont, Y. Eliezer, R. Wardenaar, M. R. Ippolito, D. R. Iyer, A. E. Tijhuis, D. C. Spierings, M. Schubert, S. Taglietti, C. Soriani, S. Gemble, , S. Santaguida

This study shows that aneuploidy can trigger chromosome instability (CIN) by causing DNA replication stress and continuous CIN, leading to genetically diverse cells with varying proliferation abilities.

bioRxiv · Jun 19, 2022Cell Biology

The chromatin-binding domain of Ki-67 together with p53 protects human chromosomes from mitotic damage

O. Garwain, X. Sun, D. R. Iyer, R. Li, L. J. Zhu, P. D. Kaufman

This study shows that the C-terminal chromatin-binding domain of Ki-67, along with p53, prevents mitotic chromosome damage in human cells.

bioRxiv · Oct 16, 2020Cell Biology

Replication Fork Slowing And Stalling are Distinct, Checkpoint-Independent Consequences of Replicating Damaged DNA

D. R. Iyer, N. Rhind

This paper investigates how DNA damage affects replication fork behavior in fission yeast, finding that the intra-S checkpoint slows replication by inhibiting origin firing but not fork speed, and facilitates lesion bypass while preventing fork stalling.

bioRxiv · Mar 31, 2017Cell Biology