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Analysing the specificity of cell matrix interaction by antibody blocking experiments suggests an integrin α5β1 -specific adhesintegrin α5β1 -specificle adhesion on heparin was shown to be mediated by selectins (CD62L).
The initial step of leukocyte rolling is mediated by selectins, which bind to their respective ligands such as P-selectin glycoprotein ligand 1 (PSGL-1), CD44, or E-selectin ligand 1 (ESL-1) [14] 14].
The interaction of ECs with leukocytes, such as activated NK cells, involves attachment and rolling which are predominantly mediated by selectins and carbohydrate-rich ligands, such as mucins [1] [3].
The adhesion of platelets to endothelial cells is also mediated by selectins [ 10].
Leukocyte rolling along inflamed blood vessels is mediated by selectins [ 4- 6].
Neutrophil rolling, also mediated by selectins, follows, enabling the leukocyte to interact with chemokines exposed on the endothelium.
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Specifically, catch bond nature of a selectin molecule, first visualized in the forced dissociation of P- [22] or L-selectin [23] from PSGL-1, was correlated biologically with a shear-threshold feature for leukocyte tethering and rolling adhesion mediated by selectin-ligand interactions [24], [25].
Interactions between leukocytes and endothelial cells are largely mediated by selectin family of receptors and integrins.
Numerous studies have shown that the initial interaction between leucocytes and the vascular endothelial cell surface is mediated by selectin adhesion systems (Alon and Feigelson, 2002; Rosen, 2004).
In addition to the steps mediated by selectin and adhesion molecules, chemokine receptors support the selective recruitment of differentiated T cells into tissues through interaction with endothelial and tissue-expressed chemokines [ 6- 8].
The interaction between human prostate cancer (PCa) cells and bone marrow (BM) endothelium follows a rolling-and-adhesion cascade mediated by E-selectin ligand (ESL): E-selectin.
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