Author

S. N. Brun

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

Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

R. J. Shaw· 3 shared A. H. Pham· 1 shared A. Ianniciello· 1 shared A. Limpert· 1 shared A. M. Blessing· 1 shared C. Lin· 1 shared D. D. Engle· 1 shared D. E. Frigo· 1 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 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

R. J. Shaw

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The autophagy initiating kinase ULK1 is required for pancreatic cancer cell growth and survival

R. J. Shaw, S. N. Brun, J. Lumibao, A. Limpert, H. Ren, A. Ianniciello, N. Cosford, H. Tiriac, M. Downes, R. Evans, D. D. Engle

This study shows ULK1 is essential for pancreatic cancer cell growth and survival, and ULK1 inhibitors can enhance immunotherapy by increasing MHC Class I expression.

bioRxiv · May 15, 2021 · PreprintCancer Biology

HDAC3 regulates senescence and lineage-specific transcriptional programs in non-small cell lung cancer

L. J. Eichner, S. D. Curtis, S. N. Brun, J. T. Baumgart, D. S. Ross, T. J. Rymoff, R. J. Shaw

This study identifies HDAC3's role in regulating senescence and lineage-specific transcription in NSCLC, revealing therapeutic implications for HDAC3 inhibitors.

bioRxiv · Oct 14, 2020 · PreprintCancer Biology

Inhibition of CAMKK2 impairs autophagy and castration-resistant prostate cancer via suppression of AMPK-ULK1 signaling

C. Lin, A. M. Blessing, T. L. Pulliam, Y. Shi, S. R. Wilkenfeld, J. J. Han, M. M. Murray, A. H. Pham, K. Duong, S. N. Brun, R. J. Shaw, M. M. Ittmann, D. E. Frigo

This study shows that inhibiting CAMKK2 blocks autophagy and slows castration-resistant prostate cancer by disrupting AMPK-ULK1 signaling.

bioRxiv · Jun 2, 2020Cancer Biology