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Several predicted target genes, such as mitogen-activated protein kinase kinase 2 (MAKT32), AKT3 or BAD, are implicated in multiple pathways, demonstrating the potential for miRNAs to influence cellular processes such as proliferation, migration and apoptosis.
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Over expression of DAB2 resulted in alterations of multiple pathways as demonstrated by expression profiling and functional network analysis, which confirmed the role of DAB2 as an adaptor molecule involved in multiple receptor-mediated signalling pathways.
The functional variability of genes within multiple pathways was also demonstrated.
Thus, our data demonstrate multiple pathways for L1 integration in cultured cells, and show that L1 is not simply an insertional mutagen, but that its retrotransposition can result in significant deletions of genomic sequence.
Taken together with the mutations found in telomerase subunits and in the Shelterin component Tin2, this work demonstrates that multiple pathways can contribute to a telomere dysfunction disease.
Taken with evidence for early establishment of NPC architecture, these data demonstrate that multiple pathways for nucleocytoplasmic transport were established prior to the radiation of modern eukaryotes but that selective pressure continues to sculpt the KAP-β family.
Further studies demonstrated that multiple pathways mediated the preventive effect of AST.
The presence of multiple pathways to mediate cell contractility demonstrates the importance of this generated force in FN-matrix assembly.
As previously demonstrated, targeting multiple pathways is likely to be more efficacious for eradicating tumor cells than targeting EGFR alone (Müller et al., 2014).
The pathway network demonstrates the cooperation of multiple pathways to perform biological processes and organises pathways into functionally related clusters with interdependent outcomes.
Our analyses demonstrate that genomic alterations may affect multiple pathways, which could be classified as drug effector and non-effector pathways by the way they target the two cancer hallmarks 'sustaining proliferative signaling' and 'evading growth suppressors' [21].
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