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TEs can be divided into two classes (I and II) based on their replication mechanism.
TEs can be divided into two classes based on their replication mechanism: retrotransposons (class I) and DNA transposons (class II) [ 1].
Based on their replication mechanism prions can transmit misfolding and aggregation of PrP (i) at the molecular level, (ii) within or at the surface of cells, (iii) from one cell to another, (iv) in and between tissues [e.g., along neuroanatomical pathways in the peripheral and central nervous system (PNS, CNS), or between the lymphoreticular system and the PNS], and (v) also between individuals.
A speculative approach would be to organize viruses according to their "age", i.e., their suspected time of appearance during evolution, based on their replication rates, in the following putative timeline: viroids, RNA viruses, retro- and para-retroviruses, giant viruses, DNA viruses.
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Therefore, a SAGA-based mechanism to discriminate between chromosomal and non-chromosomal DNA would primarily target non-chromosomal DNA molecules of internal or foreign origin based on their expression and replication potential, i.e. on their potential toxicity.
TEs can be divided into two main categories based on their mode of replication: Class I TEs or Retrotransposons; and Class II TEs or DNA transposons that also include the Miniature Inverted-repeat Transposable Elements (MITEs).
The seven cell lines used in this study were selected solely based on their ability to support replication of both viruses.
As noted, the seven cell lines used in this study were selected solely based on their ability to support replication of VSV and SeV.
Throughout the manuscript we will refer to parental NYVAC as replication-restricted and NYVAC-C7L as replication-competent, based on their different abilities to produce progeny virus in cultured human cells, with limited virus replication cycle for the former and complete replication cycle for the latter.
This information was used to rank-order combinations of DAAs based on their ability to inhibit replicon replication against genotype 1a and 1b HCV.
Based on replication theory, inversion of replication origin located in the A+T-rich region would lead to reversal of strand asymmetry [9], [10], [18].
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