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Through an initial series of experiments, we confirmed that PLX4720 had good selectivity for BRAF-mutated melanoma cell lines over those harbouring NRAS mutations and also demonstrated that PLX4720 was able to induce significant levels of apoptosis.
Firstly, our modestly sized cohort may under- or overestimate the frequency of certain genetic mutations and also limits our ability to identify a mutational signature, epigenetic or not, that is typical of primary or metastatic melanoma tumors or those that correlate with key histologic parameters that confer a defined level of metastatic potential (i.e., depth, mitotic rate).
Phenotypic resistance testing remains important for the identification of human cytomegalovirus (HCMV) strains possibly harboring novel mutations and also for the determination of foscarnet and cidofovir resistance.
Mutations in PCSK9 can cause severe autosomal dominant hypercholesterolemia [4], [8] [14] (i.e., 'gain-of-function' mutations), and also low circulating levels of LDL cholesterol [15] [19] (i.e., 'loss-of-function' mutations).
The results of this study provide molecular information in drug selection for patients with specific tubulin mutations and also have important implications for the development of future anti-mitotic compounds that are able to target drug-resistant cancer cells.
Moreover, the level of resistance was not only linked to the amino acid found in position 143, but was highly modulated by the combination with secondary mutations and also by the back-ground integrase sequence present in patient at baseline [28].
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In addition, we propose a diversity operator to be used instead of mutation and also maintain an archive of good solutions.
However, expressed transcripts from the tammar wallaby show no evidence of this mutation and also include the leader peptide.
Two substitutions (I343T and E368K) were isolated twice, in each case both as a single mutation and also in combination with additional mutations.
The transgene is a minigene containing APP with the Arctic mutation and also the Swedish and Indiana mutations, under the control of the PDGF promoter [ 54].
As noted above, given the frequency and penetrance of VWS and PPS, it is unlikely that one of these controls would have a mutation and also be unaffected.
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