Author

C. M. Nicolae

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· 3

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 3 Research Focus:drug response / drug discovery· 2 Research Focus:gene regulatory network inference· 2 Approach:genetic perturbation / CRISPR· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

G.-L. Moldovan· 3 shared K. E. Clements· 3 shared A. Dhoonmoon· 2 shared E. M. Schleicher· 2 shared C. L. Stump· 1 shared H.-G. Wang· 1 shared L. M. Jackson· 1 shared T. Thakar· 1 shared

Activity by Year

2018-2020 · peak 2/yr

Co-Author Collaboration Network

9 top collaborators · 24 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

3 shared papersCancer Biology

G.-L. Moldovan

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Dual genome-wide CRISPR knockout and CRISPR activation screens identify common mechanisms that regulate the resistance to multiple ATR inhibitors

E. M. Schleicher, A. Dhoonmoon, K. E. Clements, L. M. Jackson, C. L. Stump, C. M. Nicolae, G.-L. Moldovan

The paper uses dual CRISPR screens to identify genes affecting resistance to ATR inhibitors in cancer cells.

bioRxiv · Apr 8, 2020Cancer Biology

Genome-wide CRISPR synthetic lethality screen identifies a role for the ADP- ribosyltransferase PARP14 in replication fork stability controlled by ATR

A. Dhoonmoon, E. M. Schleicher, C. M. Nicolae, K. E. Clements, G.-L. Moldovan

The paper identifies PARP14's role in replication fork stability through a CRISPR screen, showing its dependence on the ATR-CHK1 pathway.

bioRxiv · Apr 8, 2020Cancer Biology

Loss of E2F7 confers resistance to poly-ADP-ribose polymerase (PARP) inhibitors in BRCA2-deficient cells

K. E. Clements, T. Thakar, C. M. Nicolae, X. Liang, H.-G. Wang, G.-L. Moldovan

This study identifies E2F7 as a regulator of chemoresistance in BRCA2-deficient cells, showing its role in enhancing PARP inhibitor and cisplatin resistance through RAD51 upregulation.

bioRxiv · Apr 3, 2018Cancer Biology