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In vitro, the MUC1 mucin can mediate breast cancer cell migration by binding to intercellular adhesion molecule-1 (ICAM-1).
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Inflammatory cells may adhere to and injure lung parenchymal cells through binding to intercellular adhesion molecule 1.
Vinculin is a cytoskeleton protein involved in extracellular matrix adhesion and intercellular junctions by binding to actin filaments.
In addition to providing structural support to tissues, the ECM has evolved to regulate intercellular signaling pathways, for example by binding to growth factors and regulating their distribution or activity in the extracellular space (Hynes, 2009).
Furthermore, many statins directly block the interaction between intercellular adhesion molecule (ICAM -1 and leukocyte functICAM -1ociandd antigen (leukocyte binding to a site within Lfunction-associated
Antibodies attack antigens by binding to them.
By binding to AT-1 receptors, angiotensin II enhances the expression of proinflammatory mediators, increases vascular permeability by inducing vascular endothelial growth factor (VEGF), and stimulates the expression of endothelial adhesion molecules (P-selectin and E-selectin), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) [ 6].
The β2 (CD18) family of integrins includes CD11a/CD18 (LFA-1), CD11b/CD18 (Mac-1 or complement receptor [CR] 3), CD11c/CD18 (CR4, p150,95), and CD11d/CD18 and is crucial in transendothelial migration by the binding of CD11a/CD18 to intercellular adhesion molecule 1 (ICAM-1) [ 10, 11].
The firm arrest of leukocytes to the endothelium during inflammation is known to be mediated by endothelial intercellular adhesion molecules (ICAMs) binding to activated integrins displayed on leukocyte surface.
Different strength in their binding to GL3 is also likely to change the intercellular movement of TRY and CPC [ 14].
In cell assays, AD- and PD-associated protein aggregates show similarities to prions in terms of (i) binding to or uptake by cells of Aβ [ 96], tau [ 28, 63] or α-synuclein aggregates [ 63, 91], (ii) seeding in or on cells of Aβ [ 96], tau [ 63, 80] or α-synuclein aggregates [ 54, 63, 91], and (iii) intercellular spread of tau [ 28] and α-synuclein deposition [ 34].
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