This promoter construct was subsequently transfected into U2OS cells with a control expression vector, a full-length TIEG1 expression vector or a truncated TIEG1 expression vector in which the DNA binding domain was deleted (TIEG1 1 370) to determine if TIEG1 could regulate its activity.
The study of Yu et al. 17 demonstrated that only long, fully functional TCF-1 isoforms initiate GATA3 1b transcription, whereas over-expression of a mutated TCF-1 construct in which the sequence encoding the β-catenin-binding domain was deleted had the opposite effect.
In contrast, the SNLSB− construct, which contains substitutions of A in the conserved W and N residues of the small NLSB site, and the ΔIBB construct, in which the Imp-β binding domaImp-β binding, restore oogenesis but block embryogenesis undomaine same condisions (Gorjánácz et al. 2006).
In support of this model, KAP1 recruitment to the HCMV genome was lost when the KRAB-binding RBCC domain was deleted (not illustrated).
To measure the affinity of VEGF for the ligand-binding domain of VEGFR2, the binding to a construct in which the kinase domain was deleted (VEGFR2 ΔKD m) was determined.
When the C2A domain was deleted, the remaining C2B motif retained the RBG-1 binding activity.
In all cases the conserved cysteine-rich domain was deleted.
When the BEN domain was deleted from either one or both of the GST-fused Elba1 and Elba2 proteins (∆BEN), DNA-binding activity was completely abolished.
The LoxP sites were inserted into introns flanking the fourth exon of the RXRα gene covering the DNA binding domain, which is deleted after crossing the floxed RXRα allele against a transgenic line in which cre recombinase is expressed under the control of the albumin promoter.
Ohta et al., 2014 demonstrated a reduced binding of STIL to Plk4 when PB1 or PB2 domains were deleted.
