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Andreas Ludwig

Researcher at University of Leoben

Publications -  357
Citations -  7732

Andreas Ludwig is an academic researcher from University of Leoben. The author has contributed to research in topics: Equiaxed crystals & Continuous casting. The author has an hindex of 40, co-authored 335 publications receiving 6580 citations. Previous affiliations of Andreas Ludwig include RWTH Aachen University & École Polytechnique Fédérale de Lausanne.

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The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion.

TL;DR: It is demonstrated that ADAM10 is involved in the constitutive cleavage of CX3CL1 and thereby may regulate the recruitment of monocytic cells to CX2CL1-expressing cell layers and prevent de-adhesion of bound THP-1 cells.
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The hyperpolarization-activated channel HCN4 is required for the generation of pacemaker action potentials in the embryonic heart

TL;DR: It is shown that HCN4 is essential for the proper function of the developing cardiac conduction system and the proper generation of pacemaker potentials in the emerging sinoatrial node.
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Selective loss of cone function in mice lacking the cyclic nucleotide-gated channel CNG3

TL;DR: CNG3-deficient mice provide an animal model to dissect unequivocally the contribution of rod and cone pathways for normal retinal function and the functional loss of cone function correlates with a progressive degeneration of cone photoreceptors but not of other retinal cell types.
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Chemokine Receptor CXCR6-Dependent Hepatic NK T Cell Accumulation Promotes Inflammation and Liver Fibrosis

TL;DR: It is demonstrated that hepatic NKT cells accumulate CXCR6-dependent early upon injury, thereby accentuating the inflammatory response in the liver and promoting hepatic fibrogenesis.
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Loss of the Timp gene family is sufficient for the acquisition of the CAF-like cell state

TL;DR: Generating quadruple TIMP knockout (TIMPless) fibroblasts is generated to unleash metalloproteinase activity within the tumour-stromal compartment and it is shown that complete Timp loss is sufficient for the acquisition of hallmark CAF functions.