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The combined effects of reduced concentrations of substrates for DNA synthesis and downregulation of genes encoding proteins required for DNA replication is expected to produce replication stress in nutrient-depleted cells that failed to enter into or maintain a G1 arrest, and arrest growth in S phase instead.
The parameter set driving our system is not filtered to retain only those that produce replication dynamics consistent with coherent firing just at the G1/S boundary.
A strain lacking Tel1, on the other hand, failed to produce replication intermediates at ARS700.5 even in the presence of cleavage (Fig 2B, bottom left).
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In order to produce replication-deficient retroviral particles genes encoding the structural and envelope proteins, as well as the HNF6 coding plasmid were transfect into the human embryonic kidney 293T packaging cells.
The rcAd26 vector system was produced by cloning the adenovirus E1 region from wild-type Ad26 into pAdApt26, the adaptor plasmid that we had previously made to produce replication-incompetent Ad26 vectors (16).
The idea of a retrovirus as a gene-transfer agent was first seen as dangerously oncogenic, until 1983 and 1984 when Mann, Mulligan and Baltimore [ 8] devised cell lines that would produce replication-defective retroviruses that still exploited the capacity of the viruses to incorporate themselves efficiently in the DNA of dividing cells.
Since the resampling produces replication factors equal or less than M ( M ≥ ∑ i = 1 K N k ), we opted to add the remaining particles to the PE with the largest weight.
Once HIV-1 has infected a cell and integrated its genome into the cellular DNA, that cell may revert to a resting state, only producing replication competent virions when activated at a later date.
In this case, epi-marked Y chromosomes that survive spermatogenesis potentially transmit the epi-mark to embryos in the next generation and contribute to the SK phenotype of SA-ZD by producing replication, mitotic, and/or cell cycle defects, and ultimately the death of sons.
We produced replication-competent Ad serotype 26 (rcAd26) vectors by adding the E1 region back into a replication-incompetent Ad26 vector backbone with the E3 or E3/E4 regions deleted.
We describe a model to quantify the contribution of mutational differences between the leading and lagging strands in producing replication-induced skew.
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