Furthermore, neurabin binds to actin [76] and this binding is required for its localization in dendritic spines [39].
To further investigate whether the C-terminal domain of UNC-116 can bind to MTs and whether this binding is required for its function in establishing dendritic MTs, we first examined the amino acid sequence of the C-terminal region of UNC-116.
However, while ORC binding is required for replication licensing, ORC also binds to regions where initiation does not take place.
MLL2 binding is required for changes in chromosome architecture around developmental genes and establishes promoter-enhancer looping interactions in a cell-cycle-dependent manner.
Wilson and al. [48] suggested that CTCF binding is required for MyoD-induced IGF-2 gene activity in muscle.
Previous studies showed that this BMP binding is required for the anti-, but not for the pro-BMP effect of CV2.
Combined, these data confirm that synphilin-1 is a lipid binding protein and suggest that lipid binding is required for inclusion formation.
It appears that heterodimerization in response to chemokine binding is required for the termination or alteration of signaling by an increasing number of chemokine receptors [13].
Rather, we find here that NF-Y binding is required for recruitment of key components of the MLL methylating complex –MLL1 and Menin- and for deposition of H3K4me3 and H3K79me2.
Interestingly, the interaction of hTTP with MEKK4 in the absence of CIN85 did not appear to lead to the same enhanced phosphorylation of hTTP, suggesting that CIN85 binding is required for these phosphorylation events to occur.
While high-affinity ligand binding is sufficient for activation of most canonical signaling pathways, low-affinity binding is required for the activation of the Signal transducers and activators of transcription (Stats) and Phospholipase C-gamma 1 (PLCγ1).
