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The LP is activated by binding of microbial polysaccharides to circulating lectins, such as mannose-binding lectin (MBL), and requires Ca2+ [7]–[10].
The LP is activated by binding of microbial polysaccharides to circulating lectins, such as mannose-binding lectin (MBL), and requires Ca2+ [10] [13].
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By contrast, binding of microbial constituents to the CRD region of SP-D would lead to a pro-inflammatory response [ 47].
Our results suggest that binding of microbial ligands to TLRs is one of the mechanisms that mediate interactions between coinfected microbes and HIV-1 in human tissues.
MBL directly mediates opsonophagocytosis and acvation of the C-type lectin complement pathway by binding microbial mannose and N-acetylglucosamine surface residues.
Additional insights into microbial degradation processes have been generated by studies of microbial communities using metagenomics.
The innate immune system provides the first line of defence against microbial attack, and is induced by recognition of microbial components, known as pathogen-associated molecular patterns (PAMPs) or microbial-associated molecular patterns (MAMPs), by pattern recognition receptors (PRRs).
In conclusion, it should be stressed that binding of selenium by microbial cells largely depends on the culture conditions, the concentration of selenium in experimental medium, and the organisms used.
These observed differences may partially be explained by the binding of FISH probes to non-target microbial groups within complex environmental samples.
Host-pathogen interactions are generally initiated by host recognition of microbial components or danger signals triggered by microbial invasion.
Molecular docking studies indicated that the synthesized compounds could occupy both p-amino benzoic acid (PABA) and pterin binding pockets of the dihydropteroate synthase (DHPS), suggesting that the target compounds could act by the inhibition of microbial DHPS enzyme.
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