Author

A. C. Neininger

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· 3

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:differential expression· 2 Organism:human· 2 Assay:scRNA-seq· 2 Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1

Frequent Co-Authors

D. T. Burnette· 3 shared A. L. Means· 1 shared B. C. Knollmann· 1 shared B. Chen· 1 shared C. J. Cho· 1 shared C. Ramos· 1 shared E. A. Patterson· 1 shared G. Wahl· 1 shared

Activity by Year

2019-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersCell Biology

D. T. Burnette

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3 papers

Recent·Most cited

The Hippo pathway regulates density-dependent proliferation of iPSC-derived cardiac myocytes

A. C. Neininger, X. Dai, Q. Liu, D. T. Burnette

This study shows that the Hippo pathway regulates density-dependent proliferation of iPSC-derived cardiac myocytes by modulating YAP/TAZ activity, with small molecules enhancing proliferation in low-density conditions.

bioRxiv · Apr 12, 2021Cell Biology

Single-cell transcriptomics reveals a conserved metaplasia program in pancreatic injury

Z. Ma, N. K. Lytle, B. Chen, N. Jyotsana, S. Weiser Novak, C. J. Cho, L. Caplan, O. Ben-Levy, A. C. Neininger, D. T. Burnette, V. Q. Trinh, M. C. B. Tan, E. A. Patterson, R. Arrojo e Drigo, R. R. Giraddi, , K. E. DelGiorno

The paper uses single-cell RNA sequencing to identify a conserved metaplasia program in pancreatic injury, revealing mucin/ductal populations and neoplastic transformation potential.

bioRxiv · Apr 9, 2021Cell Biology

MCL-1 inhibition by selective BH3 mimetics disrupts mitochondrial dynamics in iPSC-derived cardiomyocytes

M. L. Rasmussen, N. Taneja, A. C. Neininger, L. Wang, L. Shi, B. C. Knollmann, D. T. Burnette, V. Gama

This study shows that MCL-1 inhibition by BH3 mimetics disrupts mitochondrial dynamics and function in iPSC-derived cardiomyocytes, suggesting a non-apoptotic role for MCL-1 in cardiac health.

bioRxiv · Aug 22, 2019 · PreprintCell Biology