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It is difficult to establish the role of a single factor because the cause of a defect is believed to be multifactorial in many cases; for example, some cases may result from a combination of environmental teratogens with genetic and chromosomal abnormalities3.
These results were unchanged after H2O2 treatment, suggesting that oxidative stress observed in the absence of TP53INP1 was the consequence and not the cause of a defect in mitochondria degradation.
Considering the essential function of SYP-1 in crossover formation (MacQueen et al. 2002), these results strongly support the possibility that impaired SYP-1 loading is the cause of a defect in crossover formation and consequent failure in bivalent formation in both the wild type and pgl-1 mutants at temperatures ≥26.5° and 25°, respectively.
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In 1959, lack of muscle GP was identified as the cause of a glycogenolytic defect confined to the skeletal muscles [3], [4].
To assess the feasibility of segregant-pool-based mapping of phenotype-causing genes in natural strains of fission yeast, we investigated the cause of a maltose utilization defect (Mal-) of the S. pombe strain CBS5557 (originally known as Schizosaccharomyces malidevorans).
The gene, known as FOXP2, was identified in 1998 as the cause of a subtle speech defect in a large London family, half of whose members have difficulties with articulation and grammar.
The gene, FOXP2, was identified in 1998 as the cause of a subtle speech defect in a large London family, half of whose members have difficulties with articulation and grammar.
Moreover, the observation that deletion of arn1+ caused a defect of Cat1 internalization from the PM induced by cycloheximide was comparable to the endocytosis defect of the Cat1-a mutant, which was probably deficient in ubiquitination on lysine residues from Lys18 to Lys35 (Fig. 3E, Fig. 8D).
We have shown that knockdown or inhibition of aPKC cause a defect in PrE sorting.
The CFU assays indicate that there are significantly more early progenitors in the TIEG1−/− marrow cultures also eliminating this as a cause of the defect as well.
If amino acid limitation is indeed a cause of the defect in starvation induced-SQSTM1 synthesis in Baf-treated cells, exogenous amino acid supplementation should increase the SQSTM1 level.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com