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Indeed, we and others could recently show that disease associated mutations in phosphorylation sites or of critical residues constituting their recognition by cognate kinases are found in various signalling molecules, including several docking protein family members [ 57, 59, 60].
In several tumour cell lines, TNF- α induced the expression of several different adhesive molecules including several integrin subunits, ICAM-1 and VCAM-1 (Orosz et al, 1993; Qin et al, 1993; Choo et al, 2005).
Manual approaches have successfully modeled a number of molecules, including several group I introns (Lehnert et al., 1996; Michel and Westhof, 1990) and the yeast phenylalanine tRNA (Levitt, 1969), but require expert knowledge of RNA structure.
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A large number of other non-collagen molecules are present in the interterritorial matrix; these molecules include several small proteoglycans such as biglycan, decorin, fibromodulin, the matrilins, and cartilage oligomeric matrix protein (COMP).
Another set of cluster 2-associated genes that encodes cell adhesion molecules includes several collagen genes plus the laminin B gene (Lama2) and two nidogen genes (Nid1 and Nid2).
These molecules include several inhibitors of the Fanconi anemia (FA) DNA repair pathway (which coordinates HR and TLS for the repair of interstrand crosslinks) and indeed were confirmed to exacerbate the cytostatic/cytotoxic potential of CDDP in FA-proficient but not in FA-deficient ovarian cancer cells.
Sensors for a variety of metal cations, anions and neutral small molecules are highlighted, including several developed by Australian researchers.
A large number of sulfated and sulfonated molecules inhibit EV71, including several antagonists of P2X receptors, suggesting a possible role for P2X receptors in cell entry.
Extensive studies exploiting the potential of ribozymes and RNAi molecules have been carried out, including several clinical trials using these technologies for treating certain human diseases [ 1, 4].
Figure 6 shows a proposed mechanism of action including several key molecules involved in cell proliferation, apoptosis and inflammation based on our microarray study on mastic oil treated LLC cells and the relevant literature.
Multiple therapeutic strategies have been developed to block the MET pathway including several small molecule inhibitors and antibodies [ 14].
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