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We next determined the capacity of these human IRAK-M variants to activate NF-κB spontaneously when overexpressed in 293T cells as had been described for WT IRAK-M [ 1].
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The evaluation of the in vitro capacity of the L75P variant to activate LCAT is far beyond the scope of the present paper; however, it is likely that the L75P apoA-I has impaired LCAT activation ability, despite the mutation being far from the apoA-I central region involved in LCAT activation.
A variant predicted to activate a pre-existing splice site, while also reducing the natural splice site strength, was demonstrated experimentally to result in cryptic splicing, regardless of whether it was predicted it to be the predominant isoform; e.
All variants were able to activate allergen-specific T cells in PBMC, as well as Art v 1-specific T cell lines and clones.
The model for the complex structure provides a working model for rationalizing available biochemical data on this important interaction and can form the basis for the design of Fc variants with a greater capacity to activate the complement system for example on binding to cancer cells or other target structures.
Phospho-mimetic variants have a reduced ability to activate clients in vivo and different affinity for Hsp70.
The best studied example of a balanced polymorphism is in serum mannose-binding protein, in which several variants that have reduced capacity to activate complement have been identified [ 57].
Namely, the Cys variant of Nematostella NF-κB has a more avid binding affinity for a κB site from the promoter of the Nv-IκB gene (Figure 6A); however, the Cys variant has a lesser ability to activate a multimeric κB-site promoter in transient transfection assays in human A293 cells (Figure 6B).
A read is only said to corroborate cryptic splicing if and only if the variant under consideration is expected to activate cryptic splicing.
The AabZIP1 variant with C1 domain deletion lost the ability to activate ADS and CYP71AV1 promoters regardless of ABA treatment.
Second, do compounds that transcriptionally reactivate mutant p53 variants, such as thiosemicarbazone derivatives, also restore its ability to activate SERCA?
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