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This consecutive extravasation is regulated by the sequential interaction of adhesion molecules and their cognate ligands, expressed by leukocytes, platelets, and endothelial cells.
The recruitment of T cells across the inflamed blood brain barrier during EAE is mediated by the sequential interaction of different adhesion and/or signalling molecules on the immune cell and the blood brain barrier endothelium.
Extravasation of circulating immune cells is a multi-step process that is regulated by the sequential interaction of different adhesion and signaling molecules on the immune cells and on the endothelium.
The fidelity of this process from protein sorting to endosomal-lysosomal fusion is maintained by the sequential interaction of four complexes termed the endosomal sorting complexes required for transport (ESCRT complexes).
Thus, the kinetics and molecular interactions occurring between circulating immune cells with the BBB are crucial in the pathogenesis of EAE and MS. In general, the multi-step recruitment of circulating immune cells across the BBB is regulated by the sequential interaction of various adhesion or signaling molecules on the leukocyte and on the endothelial cell surfaces [ 3, 4].
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Activation of naive CD4 T cells by dendritic cells requires the sequential interaction of many TCR molecules with peptide-class II complexes of the appropriate specificity.
They are pore-forming toxins with a complex mechanism that involves the sequential interaction with receptors.
When the enzyme functions as ATP synthase, the ion current through FO causes the rotation of the γ1ε1 complexcomplex relative to the other subunits, and the catalysis of ATP synthesis is mediated by sequential interaction of the rotating γ subunit with the three catalytic β subunits [ 3, 13, 17, 24].
Autophagy is initiated by sequential interactions between the nutrient-sensing MTOR kinase and ULK1 protein complex (UKC).
Background: The processes of osteogenesis, bone remodelling, fracture repair and metastasis to bone are determined by complex sequential interactions involving cellular and microcirculatory parameters.
They are classically activated following ligand receptor interaction by the sequential activation of a linear cascade of protein kinases, including Ras, Raf-1, MEK, and the MAPKs ERK-1 and ERK-2 (Puri and Siegel, 1993; Smerz-Bertling and Duschl, 1995) on the one hand and PI 3-kinase and Akt on the other hand (Franke et al, 1997; Fahy et al, 2003).
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by the sequential fraction
by the sequential arrangement
by the sequential dehydrogenation
by the sequential removal
by the sequential measurement
by the sequential chemical
by the sequential culture
by the sequential replacement
by the sequential binding
by the sequential balancing
by the sequential approximation
by the sequential selection
by the sequential expression
by the sequential migration
by the sequential recovery
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