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Stefan Karlsson

Researcher at Lund University

Publications -  303
Citations -  20537

Stefan Karlsson is an academic researcher from Lund University. The author has contributed to research in topics: Stem cell & Haematopoiesis. The author has an hindex of 70, co-authored 292 publications receiving 19180 citations. Previous affiliations of Stefan Karlsson include deCODE genetics & Netherlands Cancer Institute.

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Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death.

TL;DR: Pathological examination revealed an excessive inflammatory response with massive infiltration of lymphocytes and macrophages in many organs, but primarily in heart and lungs, which suggests a prominent role for TGF-beta 1 in homeostatic regulation of immune cell proliferation and extravasation into tissues.
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Defective haematopoiesis and vasculogenesis in transforming growth factor-beta 1 knock out mice

TL;DR: The data indicate that the primary effect of loss of TGF beta 1 function in vivo is not increased haematopoietic or endothelial cell proliferation, which might have been expected by deletion of a negative growth regulator, but defective haem atopoiesis and endothelial differentiation.
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Nonmyelinating Schwann Cells Maintain Hematopoietic Stem Cell Hibernation in the Bone Marrow Niche

TL;DR: It is proposed that glial cells are components of a BM niche and maintain HSC hibernation by regulating activation of latent TGF-β, which is produced as a latent form by a variety of cells.
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Activin Receptor-like Kinase (ALK)1 Is an Antagonistic Mediator of Lateral TGFβ/ALK5 Signaling

TL;DR: It is reported that ALK5 is important for TGFbeta/ALK1 signaling; endothelial cells lacking AlK5 are deficient in TGF beta/ALK 1-induced responses and that theALK5 kinase activity is required for optimal ALK1 activation.
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Abnormal angiogenesis but intact hematopoietic potential in TGF-beta type I receptor-deficient mice.

TL;DR: It is demonstrated here that, while TβRI is crucial for the function of TGF‐β during vascular development and can not be compensated for by the activin receptor‐like kinase‐1 (ALK‐1), functional hematopoiesis and development of he matopoietic progenitors is not dependent on T GF‐β signaling via T βRI.