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In summary, cell death following integrin inhibition is detachment mediated, represents an atypical form of anoikis involving necrosis as well as autophagy, and is modulated by TGF- β pathway activity.
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Selectin mediated tethering represents one of the earliest steps in T cell extravasation into lymph nodes via high endothelial venules and is dependent on the biosynthesis of sialyl Lewis X sLexx) ligands by several glycosyltransferases, including two fucosyltransferases, fucosyltransferase-IV and –VII.
It can be hypothesized that miRNA mediated control represents an ancient major mechanism of cellular control providing small versatile molecules at comparably less metabolic effort for respective synthesis compared to protein translation.
This according to the journal Atherosclerosis and a University of Wisconsin study published in journal Circulation that concluded: "The suppression of platelet-mediated thrombosis represents a potential mechanism for the beneficial effects of purple grape products, independent of alcohol consumption, in cardiovascular disease".
We speculate that this Unc119-mediated inhibition represents a non-immunologic recovery mechanism in certain infections.
If active, the above deletion mechanism through repeat-mediated recombination represents a novel route for the variation of sequence recognition by Type I RM systems.
Compared to some other protein interactions, this would be rather weak, but among SH3-mediated interactions represents a perfectly respectable value.
As this number approximates the number of GAS transcription factors this raises the possibility that sRNA-mediated regulation represents a major mechanism of regulation in this pathogen.
This transporter-mediated interplay represents a direct link between inhibitory and excitatory neurotransmission and may function as a negative feedback combating intense excitation in pathological conditions such as epilepsy or ischemia.
It is interesting that BaF3 cells, expressing a mutated EPOR unable to bind beta-Trcp, are hypersensitive to EPO, suggesting beta-Trcp-mediated ubiquitination represents a negative modulator of EPO-induced cellular proliferation [35].
EDHF-mediated vasodilation represents a considerable proportion of total vasodilation, which is resistant to inhibitors of nitric oxide- and prostacyclin synthesis, and is caused by endothelium-dependent hyperpolarization of smooth muscle and subsequent closure of voltage-gated Ca2+-channels leading to relaxation [3] [5].
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