M
Martin Prlic
Researcher at Fred Hutchinson Cancer Research Center
Publications - 78
Citations - 5272
Martin Prlic is an academic researcher from Fred Hutchinson Cancer Research Center. The author has contributed to research in topics: T cell & Cytotoxic T cell. The author has an hindex of 24, co-authored 68 publications receiving 3531 citations. Previous affiliations of Martin Prlic include University of Washington & University of Minnesota.
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Journal ArticleDOI
MAST: a flexible statistical framework for assessing transcriptional changes and characterizing heterogeneity in single-cell RNA sequencing data
Greg Finak,Andrew McDavid,Masanao Yajima,Jingyuan Deng,Vivian H. Gersuk,Alex K. Shalek,Chloe K. Slichter,Hannah W. Miller,M. Juliana McElrath,Martin Prlic,Peter S. Linsley,Raphael Gottardo +11 more
TL;DR: This work argues that the cellular detection rate, the fraction of genes expressed in a cell, should be adjusted for as a source of nuisance variation and provides gene set enrichment analysis tailored to single-cell data.
Posted ContentDOI
MAST: A flexible statistical framework for assessing transcriptional changes and characterizing heterogeneity in single-cell RNA-seq data
Greg Finak,Andrew McDavid,Masanao Yajima,Jingyuan Deng,Vivian H. Gersuk,Alex K. Shalek,Chloe K. Slichter,Hannah W. Miller,M. Juliana McElrath,Martin Prlic,Peter S. Linsley,Raphael Gottardo +11 more
TL;DR: A new methodology to analyze single-cell transcriptomic data is presented that models this bimodality within a coherent generalized linear modeling framework, and the cellular detection rate, the fraction of genes turned on in a cell, is introduced.
Journal ArticleDOI
In vivo survival and homeostatic proliferation of natural killer cells.
TL;DR: It is shown that mouse NK cells undergo homeostatic proliferation when transferred into NK-deficient Rag+/− γC−/− hosts, and that mature NK survival is critically dependent on interleukin (IL)-15, implying that IL-15 responsiveness by bystander cells is critical for NK maintenance.
Journal ArticleDOI
Duration of the initial TCR stimulus controls the magnitude but not functionality of the CD8+ T cell response
TL;DR: The results indicate that the duration of initial antigen encounter influences the magnitude of the primary response, but does not program responsiveness during the secondary challenge.
Journal ArticleDOI
Distinct Effects of STAT5 Activation on CD4+ and CD8+ T Cell Homeostasis: Development of CD4+CD25+ Regulatory T Cells versus CD8+ Memory T Cells
Matthew A. Burchill,Christine A. Goetz,Martin Prlic,Jennifer J. O’Neil,Ian R. Harmon,Steven J. Bensinger,Laurence A. Turka,Laurence A. Turka,T. Paul Brennan,Stephen C. Jameson,Michael A. Farrar +10 more
TL;DR: It is established that activation of STAT5 is the primary mechanism underlying both IL-7/IL-15-dependent homeostatic proliferation of naive and memory CD8+ T cells and IL-2-dependent development of CD4+CD25+ regulatory T cells.