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Teresa Frisan

Researcher at Umeå University

Publications -  76
Citations -  3537

Teresa Frisan is an academic researcher from Umeå University. The author has contributed to research in topics: DNA damage & Cytolethal distending toxin. The author has an hindex of 29, co-authored 75 publications receiving 3202 citations. Previous affiliations of Teresa Frisan include Karolinska University Hospital & Karolinska Institutet.

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Toll-like Receptor 4 Resides in the Golgi Apparatus and Colocalizes with Internalized Lipopolysaccharide in Intestinal Epithelial Cells

TL;DR: It is shown that the murine small intestinal epithelial cell line m-ICcl2 is highly responsive to LPS and expresses both CD14 and TLR4, which indicates an important role of cellular internalization and cytoplasmic traffic in the process of innate immune recognition.
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Epstein-Barr virus (EBV) load in bone marrow transplant recipients at risk to develop posttransplant lymphoproliferative disease: prophylactic infusion of EBV-specific cytotoxic T cells.

TL;DR: The results suggest that prophylactic administration of EBV-CTLs early after BMT appears to provide the most effective protection against the development ofEBV-associated lymphoproliferative disease.
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Local suppression of Epstein-Barr virus (EBV)-specific cytotoxicity in biopsies of EBV-positive Hodgkin's disease

TL;DR: The results suggest that a tumor-associated suppression ofEBV-specific T-cell responses may play an important role in the pathogenesis of EBV+ HD.
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The Haemophilus ducreyi Cytolethal Distending Toxin Induces Cell Cycle Arrest and Apoptosis via the DNA Damage Checkpoint Pathways

TL;DR: It is demonstrated that the effect of the Haemophilus ducreyiCDT is cell type-specific: B cell lines underwent apoptosis, epithelial cells and keratinocytes arrested exclusively in G2, whereas normal fibroblasts arrested both in G1 and G2.
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The Haemophilus ducreyi cytolethal distending toxin induces DNA double-strand breaks and promotes ATM-dependent activation of RhoA

TL;DR: It is shown that a member of the CDT family causes DNA double‐strand breaks in naturally intoxicated cells, acting as a true genotoxic agent, and the existence of a novel signalling pathway for intracellularly triggered activation of the RhoA GTPase via the ATM kinase in response to DNA damage is disclosed.