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One of the large genes driving replication, for instance, bears a single mutation that is found not only in the 1918 virus, but also in all human flus.
Similarly, grants specifically designated for research integrity are vital for driving replication (http://www.arnoldfoundation.org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies .org/reproducibility-initiative-receives-13m-grant-validate-50-landmark-cancer-studies
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Since already small amounts of E1A gene products are sufficient to initiate adenoviral replication resulting in the accumulation of E1A gene products and thus driving viral replication [ 14], leaky replication is frequently observed with this strategy.
This study establishes a robust model of the processes driving DNA replication initiation.
LANA functions to maintain KSHV latency by driving viral replication [46,47], promoting dysregulated cell growth [48] and dynamically regulating both viral and cell gene transcription [49 51].
The major factor driving this replication appears to be glucose, which through its metabolism in beta cells turns on signals for growth [ 41].
This would be expected to set up a positive feedback loop, with premature and thus excessive loss of adult cells driving excessive replication and differentiation in the stem cell compartment.
In keeping with a role for KDM4A activity in controlling DNA replication, overexpression of KDM4A leads to genomic instability in a demethylase-dependent manner, through driving re-replication and site-specific copy gain in genomic regions implicated in cancer [ 177].
The fork-shift model, which does not require origin relocation, is influenced by cis-elements and trans-factors associated with driving and maintaining replication forks.
A future avenue for our work will also be to implement our modeling approach to better understand the mechanistic differences driving the differential replication of human and avian IAV at those temperatures.
L1 RNP could be another example of an enzyme-RNA molecular machinery driving genome-wide replication of L1 sequences.
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