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Udgivet

Intracellular collagen degradation mediated by uPARAP/Endo180 is a major pathway of extracellular matrix turnover during malignancy

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  1. Regulation of ETAA1-mediated ATR activation couples DNA replication fidelity and genome stability

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  2. Immune regulation by fibroblasts in tissue injury depends on uPARAP-mediated uptake of collectins

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  3. Comparison of two different culture conditions for derivation of early hiPSC

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  4. M2-like macrophages are responsible for collagen degradation through a mannose receptor-mediated pathway

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  5. Human embryonic stem cells in culture possess primary cilia with hedgehog signaling machinery

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  1. TAFI deficiency causes maladaptive vascular remodeling after hemophilic joint bleeding

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Collagen density regulates the activity of tumor-infiltrating T cells

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  3. CCL2/MCP-1 signaling drives extracellular matrix turnover by diverse macrophage subsets

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  4. Immune regulation by fibroblasts in tissue injury depends on uPARAP-mediated uptake of collectins

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. uPARAP/Endo180 receptor is a gatekeeper of VEGFR-2/VEGFR-3 heterodimerisation during pathological lymphangiogenesis

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Vis graf over relationer

We recently reported that uPARAP/Endo180 can mediate the cellular uptake and lysosomal degradation of collagen by cultured fibroblasts. Here, we show that uPARAP/Endo180 has a key role in the degradation of collagen during mammary carcinoma progression. In the normal murine mammary gland, uPARAP/Endo180 is widely expressed in periductal fibroblast-like mesenchymal cells that line mammary epithelial cells. This pattern of uPARAP/Endo180 expression is preserved during polyomavirus middle T-induced mammary carcinogenesis, with strong uPARAP/Endo180 expression by mesenchymal cells embedded within the collagenous stroma surrounding nests of uPARAP/Endo180-negative tumor cells. Genetic ablation of uPARAP/Endo180 impaired collagen turnover that is critical to tumor expansion, as evidenced by the abrogation of cellular collagen uptake, tumor fibrosis, and blunted tumor growth. These studies identify uPARAP/Endo180 as a key mediator of collagen turnover in a pathophysiological context.

OriginalsprogEngelsk
TidsskriftJournal of Cell Biology
Vol/bind169
Udgave nummer6
Sider (fra-til)977-85
Antal sider9
ISSN0021-9525
DOI
StatusUdgivet - 20 jun. 2005

ID: 46435744