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The result suggests a possible connection between protein binding and production of uncapped 5′-ends in the nearby region.
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These assumptions do not reduce the generality of the steady-state results as only the ratios of binding and production to dilution appear and no such constraints are imposed on the values of these ratios.
The reaction mechanism is attributed to the replacement of the protons of the O H groups by zinc ion at the binding site and production of fluorescence which is blocked in the photo-induced electron transfer (PET) process.
When searching the CaZy database (http://www.cazy.org/) for enzymes with similar specificities, like binding to raw starch and production of maltotriose, two enzymes were found, both from Gram+ organisms with a high GC content like M. aurum (Cantarel et al. 2009; Doukyu et al. 2008; Yang and Liu 2007).
Treatment of endothelial cells with these lipoproteins stimulates monocyte binding and the production of chemotactic factors that contribute to inflammation and endothelial injury and dysfunction.
Through the monitoring of growth, infection and pathogenesis in Citrus sinensis leaves, we showed the importance of an alkanesulfonate binding protein for the growth, infection and production of xantham gum and the development of the canker citric phenotype [ 2].
Our data showed that in cells expressing a MAVS mutant lacking the TRAF2/5 binding sites (Q145N), activation of IRF3 and production of IFNβ were completely abolished in cells depleted of TRAF6, indicating that other TRAF proteins, including TRAF3, could not substitute the function of TRAF6.
In humans, various mechanisms have been proposed, including the direct production of cobalamin binding proteins (transcobalamins) [ 9], upregulation of folate-centred metabolic pathways and production of cobalamin autoantibodies [ 13],[ 26].
IGF binding initiates production of M-CSF and RANKL by osteoblasts and c-fms and RANK by osteoclasts [ 54].
Possible actions of probiotic bacteria in the oral environment are competition of binding sites, production of antimicrobial substances and activation and regulation of the immune response [ 3].
A recent study has shown that although the PhoP S219L mutation is responsible for loss of synthesis of some cell wall lipids and altered morphology of H37Ra, it did not account for the loss of neutral red binding, the production of virulence lipid PDIM and attenuated virulence since complementation of H37Ra with phoP has failed to confer these phenotypes [56].
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