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Very low concentrations of NO activate G proteins such as Gs, stimulating adenylyl cyclase, and the L-type calcium current (ICaL) from cardiac voltage-dependent L-type calcium (VDLC) channels and Gi, hence stimulating muscarinic K+ channels [ 31].
In contrast, vasodilators such as atrial natriuretic peptide (ANP) and NO activate a cGMP-dependent kinase that, by interacting with myosin phosphatase, dephosphorylates myosin and thus prevents muscle contraction [ 14].
In addition to the Ras/MEK/ERK/Ets-1 signaling pathway elucidated here, NOS2 and NO activate multiple oncogenic signaling pathways such as EGFR, PI3K/Akt, c-Myc, HIF-1a, NF-kB and Src [ 8].
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We hypothesized that in myocytes and pericytes of ureteric microvessels, NO activates a cGMP/PKG-dependent pathway.
Fum-PD-induced NO activates AMP-activated protein kinase (AMPK), which subsequently modulates macrophage inflammatory response.
But something else happened, too: without Met30, VP16 could no longer activate transcription.
Furthermore, the signaling pathways that are initiated by NO to activate BAX/BAK-induced cell death are also unknown.
Moreover, membrane dissociated Cdc25 can no longer activate Ras2, triggering an increase in Ras ·GDP levels [ 4].
Since NO activates sGC, increasing sGC activity via NO-independent heme-dependent sGC stimulators represents an alternative approach to enhance NO signaling.
Many cells need an active PI3K pathway to grow, and when they have no activating mutation of the pathway, they over-express IGF1 receptors [ 162].
Beyond 25 pfh (transition from threshold to specification level), Otx has no activating effect on endo16 expression even though the site is still in activation.
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