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Alan Wells

Researcher at University of Pittsburgh

Publications -  375
Citations -  24434

Alan Wells is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Epidermal growth factor & Signal transduction. The author has an hindex of 83, co-authored 348 publications receiving 21405 citations. Previous affiliations of Alan Wells include Tuskegee University & United States Department of Veterans Affairs.

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Migration of tumor cells in 3D matrices is governed by matrix stiffness along with cell-matrix adhesion and proteolysis.

TL;DR: The experimental findings here represent, to the knowledge, discovery of a previously undescribed set of balances of cell and matrix properties that govern the ability of tumor cells to migration in 3D environments.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Cell adhesion and motility depend on nanoscale RGD clustering.

TL;DR: It is found that NR6 cells can migrate on substrata where adhesion is mediated solely by the YGRGD peptide, and the variation of cell speed with spatial presentation of Y GRGD is mediated via its effect on cell adhesion.
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Localized biphasic changes in phosphatidylinositol-4,5-bisphosphate at sites of phagocytosis

TL;DR: The temporal sequence of phosphoinositide metabolism suggests that accumulation of 4,5-PIP2 is involved in the initial recruitment of actin to the phagocytic cup, while its degradation contributes to the subsequent cytoskeletal remodeling.
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Ligand-induced transformation by a noninternalizing epidermal growth factor receptor

TL;DR: Findings imply that activation of the protein tyrosine kinase activity at the cell membrane is sufficient for the growth-enhancing effects of EGF, suggesting that downregulation can serve as an attenuation mechanism, without which transformation ensues.