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Jonas Larsson

Researcher at Lund University

Publications -  134
Citations -  7929

Jonas Larsson is an academic researcher from Lund University. The author has contributed to research in topics: Stem cell & Haematopoiesis. The author has an hindex of 40, co-authored 122 publications receiving 7228 citations. Previous affiliations of Jonas Larsson include Center for Neural Science & Karolinska Institutet.

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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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Two different areas within the primary motor cortex of man

TL;DR: It is shown that area 4 in man can be subdivided into areas '4 anterior' and '4 posterior' (4p) on the basis of both quantitative cytoarchitecture and quantitative distributions of transmitter-binding sites and by positron emission tomography that two representations of the fingers exist.
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Activation by Attention of the Human Reticular Formation and Thalamic Intralaminar Nuclei

TL;DR: In this paper, a positron emission tomographic study showed activation of the midbrain reticular formation and of thalamic intralaminar nuclei when human participants went from a relaxed awake state to an attention-demanding reaction-time task.
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Two Retinotopic Visual Areas in Human Lateral Occipital Cortex

TL;DR: The retinotopy and functional properties of LO1 and LO2 suggest that they correspond to two new human visual areas, which lack exact homologues in macaque visual cortex.
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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.