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In this way, a recent study reported p-Akt2 phosphorylation of nNOS at Ser1412 in synaptosomes, suggesting the functioning of this mechanism in different organs and subcellular fractions [24].
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In this regard, it is worth noting that Yap1 and Pap1 form different disulfide bonds depending on conditions and/or to alter the longevity of the response [43], [44] but also that a single cysteine pair could be sufficient for function of this mechanism although in this case there would be only one level of response.
The function of this mechanism is to facilitate communication across regions.
While the function of this mechanism remains to be fully resolved, it is clear that genetic heterogeneity can contribute to fitness, especially for pathogens which must perform various tasks simultaneously in hostile environments.
As nuclear translocation of angiogenin is critical for the angiogenic function of angiogenin, this mechanism could play a significant role in the anti-angiogenic activity of pU2.
Many chemical agents, the chemosensitizers, may after the function of this fragile mechanism.
The authors show that the Shh-promoted proliferation of granule cell progenitors requires Smurf1 and Smurf2, suggesting an important function of this regulatory mechanism in a well-characterized physiological context dependent on Hedgehog ligands.
The finding that ENVOY is at least in some cases – as exemplified by the influence on phr1 and tre39031 – not able to execute its light-dependent function in darkness suggests that the presence of its putative interaction partners is required for a proper function of this regulatory mechanism.
The numbers of teeth in the gears dictated the functions of the mechanism.
The identification of deleterious missense mutations in bladder tumours indicates a causative role of loss of TSC1 function via this mechanism in bladder tumorigenesis.
Taken together, these results suggest that FMRP repression of synaptic HSPG co-receptors normally regulates trans-synaptic signaling to modulate synaptic structure and function, and that disruption of this mechanism is causal in synaptogenesis defects in the Drosophila disease model of fragile X syndrome.
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CEO of Professional Science Editing for Scientists @ prosciediting.com