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It is not currently known if specific DAF-16 targets may regulate translation.
In addition, the circadian clock may regulate translation more broadly, because the activity of the translation initiation complex, including the eukaryotic translational initiation factor 4E-binding protein 1 (4E-BP1) as well as the mTORC1 pathway (both of which are indispensable for protein synthesis), is under circadian control in both SCN and liver.
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The enrichment of target genes in the ribosome-related pathway indicates that miRNAs may directly regulate translation.
Since the 3'-UTR of CLOCK gene may contain sequences that regulate translation efficiency, mRNA stability, and polyadenylation signals, the rs1801260 polymorphism may be associated with other functional polymorphisms in 3'-UTR regions, which act as regulatory domains of the gene, and may influence the circadian rhythms [ 34, 40].
Since the majority of the transcription start sites of the protein coding genes were unknown in Xoo, these clones may represent partial mRNAs, riboswitches, or independent non-coding RNAs which may attenuate transcription or regulate translation initiation.
The high expression of ABCF1 may regulate the translation of inflammatory cytokines and thus affect the development of gout.
ABCF1 protein has been reported to both regulate and be regulated by TNF and may regulate the translation of inflammatory cytokines (Powell et al., 2013).
Many miRNAs may regulate the translation of proteins that act in tissue proliferation and tissue patterning such as mir-200a (which may target integrin) and mir-145 (which may interact with ERBB4 mRNA).
However, it is possible that rps7 may regulate the translation initiation of specific gene(s).
Recently, there has been intriguing evidence that AKT may regulate IRES-mediated tratslathen at the level of ITAFs.
These highly conserved proteins may regulate the translation of RNA, and post-transcriptional events, such as RNA splicing and editing, nucleolytic cleavages and chromosome packaging among other functions.
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