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Serge Haan

Researcher at University of Luxembourg

Publications -  74
Citations -  7010

Serge Haan is an academic researcher from University of Luxembourg. The author has contributed to research in topics: Janus kinase & Signal transduction. The author has an hindex of 33, co-authored 69 publications receiving 6025 citations. Previous affiliations of Serge Haan include RWTH Aachen University & Queen's University Belfast.

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Principles of interleukin (IL)-6-type cytokine signalling and its regulation.

TL;DR: This review focuses on recent progress in the understanding of the molecular mechanisms of IL-6-type cytokine signal transduction, with emphasis on the termination and modulation of the JAK/STAT signalling pathway mediated by tyrosine phosphatases, the SOCS (suppressor of cytokine signalling) feedback inhibitors and PIAS (protein inhibitor of activated STAT) proteins.
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SOCS3 exerts its inhibitory function on interleukin-6 signal transduction through the SHP2 recruitment site of gp130.

TL;DR: The interplay of two inhibitors in the signal transduction pathway of interleukin-6 is analyzed and it is demonstrated that the tyrosine phosphatase SHP2 and SOCS3 do not act independently but are functionally linked.
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Activation of STAT3 by IL-6 and IL-10 in Primary Human Macrophages Is Differentially Modulated by Suppressor of Cytokine Signaling 3

TL;DR: Different sensitivities of IL-10 and IL-6 signaling toward mechanisms that inhibit the Janus kinase/STAT pathway define an important mechanism that contributes to the different anti-inflammatory potencies of these two cytokines.
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In search of definitions: Cancer-associated fibroblasts and their markers.

TL;DR: The aim of this review is to give a thorough overview of the commonly used fibroblast markers in the field and their various strengths and, more importantly, their weaknesses, as well as to highlight potential future avenues for CAF identification and targeting.
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Sustained IL-6/STAT-3 signaling in cholangiocarcinoma cells due to SOCS-3 epigenetic silencing.

TL;DR: SOCS-3 epigenetic silencing is responsible for sustained IL-6/STAT-3 signaling and enhanced Mcl-1 expression in cholangiocarcinoma.