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It has also been reported that chromothripsis, a massive genomic rearrangement in a single catastrophic event, at the RB1 locus may cause gene inactivation [13].
Genetic drift may cause gene variants to disappear completely and thereby reduce genetic variation.
Perturbations in any of these proteins due to loss of D4Z4 repeats resulting in increased chromatin accessibility may cause gene deregulation in trans and play a role in the pathogenesis of FSHD.
On the basis of these observations, one would conclude that the VEGF promoter G4 is a site of G to OG oxidation in cells that may cause gene transcription to go awry, particularly when the damage is not repaired.
The different processes that occur during this transient period may cause gene expression patterns to differ between normal and cloned embryos, which may then affect the regulation of later development.
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Moreover, mutual clustering is sensitive to small data variations which may easily cause gene membership change.
Vitamin B12 and folate deficiency in general cause the global hypomethylation [ 36] and may also cause gene specific hypermethylation [ 37].
Intragenic insertions may also cause gene inactivation, either through premature termination of transcription or by disrupting gene splicing (see [164]).
The experiments that showed that changing genes' positions may cause aberrant gene regulation also support this hypothesis [ 15, 16].
Our data suggest that the white gene has an unusual intrinsic affinity for heterochromatin, which may cause this gene to be more sensitive to PEV than most other genes.
However, complex regulatory network may cause differential gene expression among functional neighbors of the mutated gene.
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