Author

A. Calderon

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

Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Organism:human· 1

Frequent Co-Authors

G. David· 2 shared A. Sachan· 1 shared D. Solouk· 1 shared F. Boccalatte· 1 shared J. Koch· 1 shared J. Morales-Valencia· 1 shared K. Ruggles· 1 shared L. Dehmelt· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 19 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

2 shared papersCell Biology

G. David

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Crosstalk between Rac and Rho GTPase activity mediated by Arhgef11 and Arhgef12 coordinates cell protrusion-retraction cycles.

S. Nanda, A. Calderon, T.-T. Duong, J. Koch, A. Sachan, X. Xin, D. Solouk, Y.-W. Wu, P. Nalbant, L. Dehmelt

The paper investigates Rac and Rho GTPase crosstalk mediated by Arhgef11 and Arhgef12, showing they coordinate cell protrusion-retraction cycles during migration.

bioRxiv · Feb 20, 2023Cell Biology

The Sin3B chromatin modifier restricts cell cycle progression to dictate hematopoietic stem cell differentiation

A. Calderon, T. Mestvirishvili, F. Boccalatte, K. Ruggles, G. David

This study identifies Sin3B as a regulator linking cell cycle progression to hematopoietic stem cell differentiation by modulating chromatin accessibility and gene expression.

bioRxiv · Jan 23, 2023 · PreprintCell Biology

The chromatin associated Sin3B is a critical regulator of DNA damage repair through the engagement of the Non-Homologous End Joining.

J. Morales-Valencia, A. Calderon, S. Saini, G. David

This study shows Sin3B is critical for DNA damage repair by promoting non-homologous end joining through MDC1 recruitment, highlighting its role in genomic integrity and potential as a cancer therapeutic target.

bioRxiv · Mar 9, 2022 · PreprintCancer Biology