Author

R. P. Hobbs

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· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Research Focus:chromatin & epigenetic regulation· 2 Organism:human· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Assay:ChIP-seq· 1

Frequent Co-Authors

A. V. Kossenkov· 1 shared B. G. Poll· 1 shared B. M. Ward· 1 shared C. C. Norbury· 1 shared C. M. Pineda· 1 shared C.-W. Chen· 1 shared E. Lesko· 1 shared E. S. Dahl· 1 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 12 mutual co-author links

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1 shared paperCell Biology

A. V. Kossenkov

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

K. E. Leon, R. Buj, E. Lesko, E. S. Dahl, C.-W. Chen, Y. Imamura Kawasawa, A. V. Kossenkov, R. P. Hobbs, K. M. Aird

This study shows that DOT1L regulates the senescence-associated secretory phenotype (SASP) through epigenetic control of IL1A expression in oncogene-induced senescence.

bioRxiv · Aug 21, 2020Cell Biology

Keratin 17 regulates nuclear morphology and chromatin organization

J. T. Jacob, R. R. Nair, B. G. Poll, C. M. Pineda, R. P. Hobbs, M. J. Matunis, P. A. Coulombe

This study shows that Keratin 17 regulates nuclear morphology, chromatin organization, and cell proliferation in epithelial cells.

bioRxiv · Jul 16, 2020Cell Biology

Type I interferon-dependent CCL4 is induced by a cGAS/STING pathway that bypasses viral inhibition and protects infected tissue, independent of viral burden

N. J. Parekh, T. E. Krouse, I. E. Reider, R. P. Hobbs, B. M. Ward, C. C. Norbury

The paper shows that T1-IFN produced by a subset of VACV-infected cells via the cGAS/STING pathway protects mice by recruiting inflammatory monocytes, independent of viral replication.

bioRxiv · May 2, 2019Immunology