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An inversion effect on persistence-related fMRI activity in the FFA and OFA would suggest that, in addition to LO, these areas mediate a feedback effect on sustained figure-ground processing in early visual areas; this would also suggest that LO is either modulated by the FFA and the OFA, or is itself a primary basis of the face inversion effect on persistence.
The rapid induction of type-A ARRs by exogenous cytokinin has been shown to mediate a feedback mechanism, which decreases the sensitivity of the plant to the hormone, indicating that type-A RRs act as negative regulators of cytokinin-induced responses [ 21, 23, 24].
59 PCDH11X/Y's interactions with β-catenin 67, 71 and PP1α 59 have the potential to mediate a feedback loop regulating levels of cytoplasmic β-catenin, and thereby influence the formation of the D V, A P, and L R axes.
It has been shown that Interleukin-1 alpha (IL1A) and Interleukin-1 beta (IL1B) act via their receptor (IL1R) to induce gene expressions which in term mediate a feedback protein synthesis involved in the later wave of inflammatory responses [ 15, 24].
In the mammalian olfactory receptor (OR) system, the expression of an ectopic OR transgene is sufficient to mediate a feedback inhibition that prevents the expression of the active endogenous OR gene, independent of the receptor signal transduction pathway (Nguyen et al., 2007).
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Thus, the VSG itself mediates a feedback loop that controls the state of monoallelic gene expression.
Additionally, previous work indicated that Ku70 mediates a feedback loop selectively modulating the propensity toward apoptosis or cell cycle progression/survival.
The expressed OR protein mediates a feedback loop that inhibits removal of heterochromatin marks from all other alleles, preventing their transcription (Serizawa et al., 2003; Lyons et al., 2013).
A number of recent reports show that Ser/Thr kinases mTOR, JNK, and PKCζ mediate a negative feedback loop in the insulin signaling cascade by phosphorylating IRS-1 at Ser position 307 [29], [29].
In addition, although the complete role of Tetherin in mammals remains unclear, limited data show that Tetherin can (at least) mediate a specific feedback mechanism to turn off interferon production by plasmacytoid dendritic cells [8], [47].
Thus, it is reasonable to speculate that the proinflammatory cytokines in RA patients may stimulate IL-37 expression, and IL-37 may mediate a negative feedback mechanism to suppress excessive proinflammatory cytokines in RA patients.
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