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Albrecht Schwab

Researcher at University of Münster

Publications -  123
Citations -  5818

Albrecht Schwab is an academic researcher from University of Münster. The author has contributed to research in topics: Cell migration & Transient receptor potential channel. The author has an hindex of 43, co-authored 107 publications receiving 5116 citations. Previous affiliations of Albrecht Schwab include Queen Mary University of London.

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Role of Ion Channels and Transporters in Cell Migration

TL;DR: After presenting general principles by which transport proteins affect cell migration, the role of channels and transporters involved in cell migration is discussed systematically.
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Anomalous dynamics of cell migration

TL;DR: By analyzing the trajectories of wild-type and mutated epithelial (transformed Madin–Darby canine kidney) cells, it is shown experimentally that anomalous dynamics characterizes cell migration.
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Directional cell migration and chemotaxis in wound healing response to PDGF-AA are coordinated by the primary cilium in fibroblasts.

TL;DR: Micropipette analysis is used to show that a normal chemosensory response to PDGF-AA in fibroblasts requires the primary cilium, and suggests that in coordination with cytoskeletal reorganization, the fibroblast primary cILium functions via ciliary PDGFRα signaling to monitor directional movement during wound healing.
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Autocrine purinergic receptor signaling is essential for macrophage chemotaxis.

TL;DR: The authors found that more than one type of ATP receptor type as well as metabolites of ATP contributed to the migratory responses of macrophages; furthermore, ATP was not released through pannexin-1 proteins, as has been suggested for neutrophils, suggesting that autocrine purinergic receptor signaling may play a general role in regulating the chemotactic responses of immune cells.
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Protons make tumor cells move like clockwork.

TL;DR: In this paper, a review on how this characteristic, acidic tumor micro-and nano-environment controls tumor cell migration is presented, where the authors show that tumor cells cope with hypoxia and the resulting glycolysis by overexpressing the Na+/H+ exchanger NHE1, monocarboxylate transporters MCT1 and/or MCT4, and the carbonic anhydrase CA IX.