Author

J. Schertzer

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· 1 Microbiology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

B. D. Henriksbo· 2 shared A. Yang· 1 shared C. L. K. Hung· 1 shared F. F. Anhe· 1 shared H. Harvey· 1 shared J. F. Cavallari· 1 shared J. Magolan· 1 shared J. V. Giordano· 1 shared

Activity by Year

2018-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 15 mutual co-author links

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2 shared papersMicrobiology

B. D. Henriksbo

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Exploration of BAY 11-7082 as a novel antibiotic

V. E. Coles, P. Darveau, X. Zhang, H. Harvey, B. D. Henriksbo, A. Yang, J. Schertzer, J. Magolan, L. L. Burrows

The paper identifies BAY 11-7082 as a molecule that stimulates biofilm formation in Pseudomonas aeruginosa and inhibits growth of MRSA and other pathogens, with analogues showing enhanced anti-Staphylococcal activity.

bioRxiv · Sep 28, 2021 · PreprintMicrobiology

Metabolic endotoxemia is dictated by the type of lipopolysaccharide

F. F. Anhe, N. G. Barra, J. F. Cavallari, B. D. Henriksbo, J. Schertzer

The paper shows that the type of lipopolysaccharide (LPS) determines metabolic endotoxemia effects, with E. coli LPS causing dysglycemia and inflammation while R. sphaeroides LPS has beneficial effects.

bioRxiv · Jul 13, 2021Physiology

A Patient-Derived Cellular Model for Huntington Disease Reveals Phenotypes at Clinically Relevant CAG Lengths

C. L. K. Hung, T. Maiuri, L. E. Bowie, R. Gotesman, S. Son, M. Falcone, J. V. Giordano, V. Mattis, T. Lau, V. Kwan, V. Wheeler, J. Schertzer, K. Singh, R. Truant

This paper develops a patient-derived cellular model for Huntington Disease that maintains TP53 function and exhibits HD phenotypes at clinically relevant CAG lengths.

bioRxiv · Apr 12, 2018Cell Biology