We also show that the DNA binding activity can be inhibited by the tumour suppressor p53 and suggest that this may prevent genome destabilizing events such as HR between non-homologous sequences.
While 15d-PGJ2 is able to directly bind to Keap1 thiol residues and induce Nrf2, without the depletion of GSH [18,33], NF-κB binding activity can be inhibited by 15d-PGJ2 theough the direct modification of the p65 subunit [32].
Firstly, methylation of CpG dinucleotides within transcription factor binding sites can inhibit transcription factor binding and, therefore, directly influence gene activity (Hark et al. 2000).
First, methylation of CpG dinucleotides within transcription-factor binding sites can inhibit transcription-factor binding and, therefore, directly influence gene activity.
Our observation that ATP or ADP binding can inhibit sarDinG nuclease activity, and that a mutation targeted to the ATP-binding site increases the exonuclease activity, suggests that the 'helicase' domain of sarDinG functions to modulate the activity of the nuclease, perhaps targeting it to suitable nucleic acid substrates.
While direct binding can inhibit caspase enzyme activity, subtle caspase-3 modifications can also have a significant effect on enzyme activity, intracellular location and its lifespan (Choi et al., 2009; Jiang et al., 2009; Dunne et al., 2013).
Most of the G-quadruplex binding Phen-Ni complexes can inhibit telomerase activity in vitro as indicated by the telomeric repeat amplification protocol (TRAP) assay and such inhibition is clearly concentration dependent.
The eIF4E-binding region within eIF4G can inhibit eIF4A helicase activity when not bound to eIF4E.
The data suggest that either ATP or ADP binding at the nucleotide-binding cleft of the helicase can inhibit the exonuclease activity of sarDinG, presumably due to conformational changes transmitted from the helicase to the nuclease domain.
TFPI-2 can inhibit activity of these enzyme, but also can directly inhibit the activity of MMPs [ 10, 29].
ER has been shown to block NF-κB activity at several steps: (a) it can inhibit the IKK activity; (b) it can inhibit degradation of I κB; (c) it can block DNA binding by NF-κB; (d) it can bind coactivators and compete with NF-κB for coactivators binding; and (e) it can directly bind to DNA-bound NF-κB to inhibit NF-κB-mediated transcriptional activation.
