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Mitochondrial malfunction has been implicated to be responsible for increased glycolysis [ 16].
C-terminal sequences of the upstream gene were implicated to be responsible for these lower levels of cleavage [ 33].
The residual telomere length, rather than reduced telomerase activity, has been implicated to be responsible for the phenotype in telomerase deficient mice (Hao et al., 2005b).
Widespread distributions of transposable DNAs, such as IS elements, have been implicated to be responsible for large genomic changes, and also provide a rich source of repetitive sequences to apply our method.
A wide number of molecules such as cytokines, chemokines and their receptors, and growth factors have been implicated to be responsible for the metastatic property of breast cancer cells [ 3- 9].
The activation of PAR-4 has been implicated to be responsible for leukocyte recruitment, modulation of rolling and adherence of leukocytes, such as neutrophils and eosinophils, as well as regulation of vascular endothelial cell activity (Gomides et al. 2012; Kataoka et al. 2003; Leger et al. 2006; Vergnolle et al. 2002).
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As only high ATP concentrations induced SC death, P2X7R is implicated to be the receptor responsible for SC death.
However, the one electron reductases implicated in MMC activation are unlikely to be responsible for NQO1 independent activation of MMC in tumours in an aerobic environment.
Pro-inflammatory immune responses are thought to be responsible for the tissue damage that occurs in severe sepsis, while anti-inflammatory responses are implicated in the enhanced susceptibility to secondary infections [7].
Of these four variants, 2 were discarded since within genes already reported to be responsible for phenotypically divergent recessive diseases: KANK2, implicated in palmoplantar keratoderma and woolly hair (MIM 616099) and CHRNG, implicated in multiple pterygium syndrome (MIM 253290).
However, despite the initially encouraging data implicating hepatic TNF α, ultimately it does not appear to be responsible for altering intestinal permeability through an MLCK-dependent mechanism.
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