Sentence examples for binding of the zinc from inspiring English sources

For this TFZF, rational design was used to optimize the binding of the zinc finger protein to its DNA element and the resulting TFZF demonstrated a direct correlation between increased affinity and efficiency of target gene regulation.

On type 1 promoters, the initial binding of the zinc protein TFIIIA allows the successive recruitment of the multisubunit complex TFIIIC and the Brf1-TFIIIB activity, composed of the TATA box binding protein TBP, the TFIIB-related factor Brf1, and the SANT domain protein Bdp1.

In yeast Zap1, interaction between the two ZF where the tCWCH2 motif is located is required for the high-affinity binding of the zinc ion [ 45].

Many single amino acid substitutions are predicted to significantly impair DNA binding of the zinc fingers potentially making them functionally inactive (Dickinson et al, 2011).

In addition, Zap1, a yeast zinc-sensing transcription factor, also possesses a tandem CWCH2 structure in its zinc-responsive domain, where the interaction between the two ZF is required for the high affinity binding of the zinc ion (43).

Methylation of cytosines at the ICR inhibits binding of the zinc finger protein CTCF to the paternal allele, preventing its role as an insulator and allowing long-range interactions of the IGF2 promoter with enhancer elements downstream of the H19 gene [ 9- 11].

The cis-acting E-box element is found in the E-cadherin promoter region and binding of the zinc-finger protein, SNAIL or SIP1, represses gene expression.

Heterochromatin boundaries are normally limited by binding of the zinc-finger insulator protein CTCF; CTCF binding, however, is lost at the CAG boundaries in myotonic dystrophy (Cho et al. 2005; Filippova et al. 2001).

In contrast, binding of the Zinc-finger transcription factor CTCF in the mouse liver [ 22, 23], while also generally enriched near CREB binding sites, did not correlate with the inducibility of CREB target genes after fasting.

The most common mechanism of action is binding to the zinc site of the MMP enzyme, thereby blocking its activity.

Given that SBP can act as a potent metal chelator, inhibition of DNA repair via binding to the zinc finger domain of PARP-1 is a plausible antitumor mechanism for this drug.