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Jonathan B. Johnnidis

Researcher at University of Pennsylvania

Publications -  7
Citations -  3817

Jonathan B. Johnnidis is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Stem cell & Cytotoxic T cell. The author has an hindex of 7, co-authored 7 publications receiving 3328 citations. Previous affiliations of Jonathan B. Johnnidis include Massachusetts Institute of Technology.

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Regulation of progenitor cell proliferation and granulocyte function by microRNA-223

TL;DR: It is reported here that the myeloid-specific microRNA-223 (miR-223) negatively regulates progenitor proliferation and granulocyte differentiation and activation and that genetic ablation of Mef2c suppresses progenitors expansion and corrects the neutrophilic phenotype in miR- 223 null mice.
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YAP1 Increases Organ Size and Expands Undifferentiated Progenitor Cells

TL;DR: It is reported here that YAP1 increases organ size and causes aberrant tissue expansion in mice and that the Hippo signaling pathway regulates organ size in mammals and can act on stem cell compartments, indicating a potential link between stem/progenitor cells, organ size, and cancer.
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Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection.

TL;DR: It is demonstrated that the T-box transcription factors T-bet and Eomesodermin differentially regulate two phenotypically and functionally distinct subsets of antiviral CD8+ T cells in mice, which may be important for antiviral immunity during chronic viral infections in humans.
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Clonal dynamics of native haematopoiesis

TL;DR: This work has established a novel experimental model in mice where cells can be uniquely and genetically labelled in situ to address the question of how a large number of long-lived progenitors are the main drivers of steady-state haematopoiesis during most of adulthood.
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Cutting Edge: Persistently Open Chromatin at Effector Gene Loci in Resting Memory CD8+ T Cells Independent of Transcriptional Status

TL;DR: It is proposed that these chromatin changes poise effector genes for rapid upregulation, but are insufficient for PolII recruitment and transcription.