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The characterization of SOX9 dimerization mutants identified in some CD patients, suggests that SOX9 binds to an inverted repeat of the heptameric sequence and that this dimeric binding is necessary for the SOX9-dependent expression of chondrocyte-related genes [13].
The closure of the active site cavity by the loop between TMHs 5 and 6 (loop 5 6) upon substrate binding is necessary for directional pumping12.
Finally, human disease-causing mutations in NPC1 domain 2 decrease NPC2 binding, suggesting that NPC2 binding is necessary for NPC1 function in humans.
Unlike the wild-type ING1, the W235A mutant, overexpressed in the stable clones of melanoma cells or in HT1080 cells, was unable to stimulate DNA repair after UV irradiation or promote DNA-damage-induced apoptosis, indicating that H3K4me3 binding is necessary for these biological functions of ING1.
These results demonstrate that Mad3p binding is necessary for Cdc20 turnover, and suggest the intriguing possibility that the N-terminal Mad3 KEN box acts in trans as a Cdc20p destruction signal during early mitosis.
Nested deletions and site-specific point mutations of the CRE located at nucleotide −224 resulted in a significant loss of induction by cAMP, demonstrating that CREB binding is necessary for the stimulation of the gene [13].
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If DNA binding were necessary for PARP-dependent mADPR accumulation, the PARP-dZF1 mutant, which has little or no detectable DNA binding capacity, would be expected to show little or no ability to reconstitute O/N stress-induced NAD degradation or TRPM2 activation in the DT40 system.
This indicated that while ATP binding was necessary for oligomerization, ATP hydrolysis was not.
7. Oxidation of the enzyme (Fe2+ → Fe3+ transition) is influenced by Ca2+ ions [ 25]. 8. Endogenously generated 5-HP is the preferential substrate for the 5-LO mediated LTA-synthase reaction [ 26]. 9. ATP and membrane binding are necessary for 5-LO activation [ 13].
Our results also suggest that receptor binding is necessary but not sufficient for cytotoxicity.
These data suggest that Myb domain binding is necessary but not sufficient for inhibition of Rad51-mediated D-loop formation.
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