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SOD1 mutations remained the only known cause of 'classical' ALS until causative mutations in the gene TARDBP were found (Sreedharan et al., 2008), and therefore have been studied extensively in a variety of animal and cellular models (Ilieva et al., 2009).
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KRAS mutations remain the most frequently observed alteration among MC (64.9 %) and mucinous borderline tumors (MBOT) (92.3%%).
Since SOD1 mutations remain the most common genetic cause of ALS, we explored the possible changes in ELP3 expression in SOD1-mediated ALS.
The most common mutation remained the deletion of a phenylalanine residue at position 508 (ΔF508), which causes inappropriate folding of CFTR, followed by its proteolytic degradation in the endoplasmic reticulum.
The type of sensitizing mutation remained the same for each patient throughout the study period.
Analysis of the reaction mixture after 14 and 21 days at room temperature (data not shown) indicated that protein variants containing one or both of the selected mutations remained in the soluble fraction.
That is, to define the role of high-throughput sequencing in defining the prognosis in our cohort, as TP53 mutations remained as the only independent genomic variable.
This shorter time to incidence of reverse mutations remained in the subsets of in vivo Gag mutations that reached dominance or completeness.
These mutations remained after the sequencing was repeated (and after UDG treatment).
Nonetheless, it is possible that mutations contributing new early alleles arose uniquely in the gene-pool under selection for earliness, and such mutations remained confined in the Northern Flints.
These mutations remained stable throughout the prolonged 15 30 passages in KMB17 cells.
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