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Alu repeats have been implicated in differential methylation states of the genome, in the translation response to cellular stress, and in the regulation of transcription [ 2].
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In addition to genes related to the immune response, those that may be implicated in differential methylation levels were investigated.
For example, sex chromosome complement, independent of hormonal effects, has been implicated in causing differential expression of genes coding for proteins such as calbindin, prodynorphin, and nitric oxide synthase in the brain, and differential expression of two histone demethylases in neurons.
PI3K (III) has been implicated in the differential regulation of vesicle trafficking at apical and basolateral regions.
Previous high-resolution studies have focused on the de novo methylation of the promoter region of Oct-4 [28]–[32], but have not analyzed parameters that influence methylation of the 2000 base pair upstream region that has been implicated in the differential regulation of Oct-4 gene expression in ES cells and the epiblast [33].
Socioeconomic status (SES) differences in attitudes towards cancer have been implicated in the differential screening uptake and the timeliness of symptomatic presentation.
Sex steroids, sexual dimorphism in the renin angiotensin and endothelin systems have been implicated in the differential response to high salt diet [ 39, 40].
For example, in mammals, PABN has been implicated in the differential recognition of weak poly(A) signals that are often associated with promoter-proximal poly(A) sites in genes whose de-regulation is associated with oncogenic transformation [ 26].
In vitro studies have provided evidence for their functional basis, and these polymorphisms have been implicated in the differential response to β1-agonists and antagonists in numerous studies [ 6– 10].
Differences in the activities of several other signaling molecules, including mTOR and Sirtuins, have also been implicated in the differential effects of CR on normal versus tumor cells [ 91].
Although various signaling molecules, including cytokines [ 11], reactive oxygen species [ 12], nitric oxide [ 13], calcium [ 14], cyclooxygenase-2 (PTGS2) [ 15] and MAP kinases [ 16] have been implicated in the bystander process, the differential signal transduction pathways regulating the responses to bystander damage are not completely understood.
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