Author

J.-C. Jean

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

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:human· 2 Assay:scRNA-seq· 2 Approach:experimental assay· 1 Research Focus:protein folding & dynamics· 1 Approach:statistical model· 1

Frequent Co-Authors

D. N. Kotton· 2 shared A. A. Wilson· 1 shared A. Emili· 1 shared A. Hamvas· 1 shared A. Petcherski· 1 shared B. C. Blum· 1 shared C. Torres-Arancivia· 1 shared C. Villacorta-Martin· 1 shared

Activity by Year

2019-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 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

D. N. Kotton

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Patient-specific iPSCs carrying an SFTPC mutation reveal the intrinsic alveolar epithelial dysfunction at the inception of interstitial lung disease

K.-D. Alysandratos, S. J. Russo, A. Petcherski, E. P. Taddeo, R. Acin-Perez, C. Villacorta-Martin, J.-C. Jean, S. Mulugeta, B. C. Blum, R. M. Hekman, M. Vedaie, S. Kook, J. A. Wambach, F. S. Cole, A. Hamvas, , D. N. Kotton

This study uses patient-derived iPSCs with an SFTPC mutation to model early alveolar epithelial dysfunction in interstitial lung disease, revealing proteostasis, metabolic, and inflammatory changes.

bioRxiv · Nov 13, 2020Cell Biology

Amyloidogenic Proteins Drive Hepatic Proteostasis Remodeling in an Induced Pluripotent Stem Cell Model of Systemic Amyloid Disease

R. M. Giadone, D. C. Liberti, T. M. Matte, J. D. Rosarda, C. Torres-Arancivia, S. Ghosh, J. K. Diedrich, S. Pankow, N. Skvir, J.-C. Jean, J. R. Yates, A. A. Wilson, L. H. Connors, D. N. Kotton, R. L. Wiseman, G. J. Murphy

This study uses iPSC-derived hepatic cells to show that liver proteostasis factors and UPR signaling correlate with TTR amyloid production and can reduce amyloid secretion through ER stress-independent activation.

bioRxiv · Nov 10, 2019 · PreprintCell Biology