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Among TFs families, NAC TFs and their corresponding cis-acting sequences act as molecular switches to regulate temporal and spatial gene expression [ 2, 3].
These sequences act as primers to which the DNA polymerase can add nucleotides in the 5′ → 3′ direction but in the opposite direction in which synthesis is proceeding on the lagging strand.
These signature sequences act as PAR agonists and suggest extensive gene duplication (Figure 6).
Although the Sprouty4 promoter without E-box and N-box was normally activated by bFGF, the inhibition of bFGF-dependent activation by Hes7 was partially canceled (Figure 3F, right), suggesting that E-box and N-box sequences act as the Hes7-responsive elements.
Based on our observations on these genome-scale data, we believe that the dynamical equilibrium hypothesis proposed for mouse [25] could be generalized to human: during the de novo methylation process in the genome, repetitive sequences (such as Alu sequences) act as DNA methylation center.
It seems unlikely that the gene's internal repeat sequences act as genuine CRISPRs.
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Alternatively, occurrence of a DNA double-strand break near short inverted repeat sequences acts as a starting point in the formation of large DNA palindromes [38] [43].
A further possible explanation would be if most conserved sequences acted as CRMs.
Simultaneous amplification of murine Ttn sequences acted as an endogenous 2-copy gene control.
The complementary sequences acted as a decoy, sequestering endogenous miR-146a and other miRNAs with the same seed sequences (see Supplementary material online, Figure S5H ).
This vast array of biochemical decorations of genomic sequences acts as a highly flexible epigenetic code that has the capacity to regulate not only individual genes but also entire networks.
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