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Increasing L-carnitine levels lead to enhanced binding affinity of nuclear extracts.
The TNF-308A allele leads to high binding affinity of nuclear factors to the TNF promoter and gives a high level of gene transcription (Kroeger et al. 1997).
Our data suggested that the polymorphism in the Bax promoter was sufficient to cause a difference in binding affinity of nuclear proteins.
Promoter analysis also identified a single nucleotide polymorphism in the Bax promoter of each strain, which can significantly alter the level of expression of this gene, and affect the binding affinity of nuclear proteins.
The minor G allele at rs7528684 is associated with risk of rheumatoid arthritis and systemic lupus erythematosus [ 30], protection from autoimmune Addison disease [ 31] and multiple sclerosis [ 29], and has been found to alter the binding affinity of nuclear factor-κΒ [ 30], making it a good functional candidate SNP.
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To gain more insight into the binding affinities of nuclear extracts to different probes representing the putative transcription factor binding sites we performed several EMSAs.
Because p53 was ruled out as a transcription factor that affected the difference in expression, we determined if the polymorphism affected the binding affinity of other nuclear proteins.
RXRs have been reported to form heterodimers with RARs, TRs and VDR and enhance the binding affinities of these nuclear hormone receptors to DNA SREs [34], [35].
It inhibits glucocorticoid receptor (GR) activity by lowering hormone binding affinity of the receptor and delaying nuclear translocation [20], [21], and also inhibits the mineralocorticoid receptor [22].
Thus, the binding affinity of the Tub4 complex to the nuclear receptor Spc110 may be increased in tub4-S74E cells.
To estimate the binding affinity of CLOCK BMAL1, CLOCKΔ19 BMAL1, and USF, liver nuclear extracts from ZT8 were incubated with increasing amounts of P labeled Dbp EP, Dbp EI2, Per2 E′ or Per1 EP1 E-box doublE-boxanded oligonucleotide proligonucleotide
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