In the process of these coat layers being recruited and ultimately forming a vesicle, the protein constituents form a dense network of interactions with each other, with the membrane, and with transmembrane cargo proteins, although there are undoubtedly more interactions to be defined.
Also, the strong depletion of full length, endogenous POT1 in POT1∆OB cells [ 4] does not lead to a disappearance of TRIP6 or LPP from telomeres, suggesting that the OB folds of POT1 are not involved in recruiting TRIP6 or LPP to telomeres, which would then occur through other events or interactions to be defined.
In the case of external interaction calculation, the interactions have to be defined in the comment block of an input file in mol2 format.
While molecular details of these interactions remain to be defined, the peptide map and visual inspection of the structures (PDB codes 1SJJ and 1HML) suggested that HAMLET may potentially fit into the cavity between the actin-binding domain and the central rod domain, linked by the flexible neck domain (Fig. 6A).
Although the function of the IL1RAPL1 RhoGAP2 interaction remains to be defined, we found that RhoGAP2 is recruited to synapses by the PTPδ IL1RAPL1 interaction, as suggested by the finding that endogenous RhoGAP2 staining is increased at synapses when IL1RAPL1 is over-expressed or when the interaction between IL1RAPL1 and PTPδ is inhibited by Fc-IL1RAPL2.
These simulations have enabled the effective interaction volume to be defined, and this has allowed the transmission efficiency of energetic fragment ions, formed through a process which also yielded a threshold electron, to be quantified.
When coupled with chemical crosslinking (XL) strategies (Schmidt and Robinson, 2014), this approach is particularly powerful because it allows not only the stoichiometry but also the interaction interfaces to be defined (Schmidt et al., 2013).
Nor did we test for SNP-SNP or SNP-environment interactions as the number of such interactions is very large – there are over 2000 possible two- and three-way interactions between the 23 genotyped common SNPs – and a clear strategy on how to best approach interactions has yet to be defined (Ritchie et al, 2003; Hunter, 2005).
The contribution of each of the three histone residues in ensuring proper Spt16−chromatin interactions is yet to be defined.
Hence, we propose that Golli-BG21 functions to regulate SOCE via a direct interaction with STIM1, but the exact molecular mechanism underlying this interaction has yet to be defined.
All LEF/TCFs interact with Groucho/TLE family members, but a specific site of interaction has yet to be defined [ 24, 27].
