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Jan Cerny

Researcher at University of Massachusetts Medical School

Publications -  189
Citations -  3804

Jan Cerny is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Transplantation & Medicine. The author has an hindex of 30, co-authored 170 publications receiving 3181 citations. Previous affiliations of Jan Cerny include Charles University in Prague & Memorial Medical Center.

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T-cell engagement of dendritic cells rapidly rearranges MHC class II transport

TL;DR: It is proposed that tubular endosomes extend intracellularly and polarize towards the interacting T cell, but only when antigen-laden dendritic cells encounter T cells of the appropriate specificity, and serves to facilitate the ensuing T-cell response.
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Sustained Small Interfering RNA-Mediated Human Immunodeficiency Virus Type 1 Inhibition in Primary Macrophages

TL;DR: In this paper, the authors investigated if sustained siRNA-mediated silencing of human immunodeficiency virus type 1 (HIV-1) is possible in terminally differentiated macrophages, which constitute an important reservoir of HIV in vivo.
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The small chemical vacuolin-1 inhibits Ca2+-dependent lysosomal exocytosis but not cell resealing

TL;DR: It is suggested that lysosomes are dispensable for resealing after wounding because cells heal normally in the presence of vacuolin‐1, the most potent compound.
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A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.

TL;DR: A large-scale RNA interference screen reveals a new mechanism of imatinib resistance in chronic myeloid leukemia that can be therapeutically targeted and demonstrates that a U.S. Food and Drug Administration–approved drug can overcome this resistance and kill leukemia stem cells without harming the nonmalignant precursors that give rise to normal blood cells.
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T Cells Induce Extended Class II MHC Compartments in Dendritic Cells in a Toll-Like Receptor-Dependent Manner

TL;DR: A Toll-like receptor-dependent signal is required to allow Ag-loaded dendritic cells to respond to T cell contact by formation of extended endosomal compartments, which does not result in massive translocation of class II MHC molecules to the cell surface.