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Therefore, it has been postulated that the cells may regulate CaM-mediated signalling through the regulation of the availability of its targets or CaM itself.
There is experimental evidence suggesting that the cell can regulate CaM signalling through regulating local CaM pools (Toutenhoofd and Strehler, 2000).
Lysine 116 trimethylation is believed to be a posttranslational modification that helps regulate CaM activity.
In the proposed model, CaM may regulate its targets with one, two or three Ca2+ ions as well as in the apo- or fully bound states.
Cell adhesion molecules (CAMs) may regulate feather morphogenesis by constraining cell motion and forming borders.
The molecular mechanisms by which CaMs may regulate disease resistance are unknown.
Because nitric oxide (NO) and NOS are ubiquitous in malignant tumors and known to exert pro-tumor effects [ 37, 38], PTPRZ1 may regulate NO production in SCLC cells by changing the tyrosine phosphorylation status of CaM.
Phytophagous insects may regulate primary production.
Alternatively, FruM may regulate dopamine neuronal activities.
Different oncogenic pathways may regulate common genes.
RA may regulate neurogenesis via several mechanisms.
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