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We explored the genetic interactions between the Src42A and Ben/dUev1a complex and found that ptc>Src42A-triggered migration phenotype and MMP1 expression were suppressed strongly by RNAi downregulation of either Ben or dUev1a alone, and completely by both, suggesting that the Ben/dUev1a complex is necessary for Src42A-induced cell migration.
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We considered that testing of specific risk factors requires a more rigorous comparison, namely of offspring of BEN and non-BEN patients from BEN villages.
Friend of Israel, benefactor of Ben Gurion University of the Negev and other worthy causes.
The concept of multifactorial etiology of BEN anticipates that a combination of polymorphic gene variants and various environmental factors causes an increased risk for the disease.
There was no statistically significant effect of a paternal history of BEN.
We report the results of the methylation profiling of BEN patients.
The standardized questionnaire included their family history of BEN and of other kidney diseases.
In 5 of BEN patients none of these variants were found.
(D ) Sequence alignment of Drosophila and mammalian (human) orthologs of BEN domain proteins.
In addition, the influence of bentonite (ben).
The hypothesis implicating the multifactorial nature of the BEN aetiology assumes that genetic factors create a predisposition to BEN [ 76].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com