With these results we demonstrate that the stochasticity and discreteness of the Ca2+ signaling in the dyadic cleft, determined by single binding events, can be described using a deterministic model of Ca2+ diffusion together with a stochastic model of the binding events, for a specific range of physiological relevant parameters.
Consequently, it is likely that stochastic binding events instead of consistent cell culture sub-populations explain most of the observed cell-type specific binding events for the low and isolated peaks.
LINE- and LTR-embedded human-specific TF-binding sites constitute 64%, 5%, and 18% of all human-specific binding events for NANOG, OCT4, and CTCF, respectively.
This analysis identified 826, 2,386, and 591 human-specific binding events for the NANOG, OCT4, and CTCF TFs, respectively (supplementary data sets S4 S6, Supplementary Material online).
Similarly, 90.5%, 65.1%, and 94.6% of human-specific binding events for CTCF, NANOG, and OCT4, respectively, are located within the PMDs (P < 0.0001 in all instances; fig. 2).
These binding events are highly specific yet occur with micromolar affinity.
Discrete Aβ binding events correlate to specific membrane permeation events.
All human-specific binding events identified for five different regulatory proteins (SOX2, RNAPII [RNA polymerase II], TAF1, KLF4, and p300) mapped within repeat-derived sequences in the reference human genome database (table 1 and fig. 1).
However, the issue of specific versus non-specific binding to chromatin/DNA was extensively addressed in our previous Cell paper (Chen et al, 2014b) and the relevant results that provide strong evidence for the long-lived binding events to represent site specific interactions are listed below: 1) We deleted the Sox2 DNA binding domain and tracked its movement.
This resulted in 7, 314 MCF-7-specific CTCF binding events, 2, 730 ZR75-1-specific CTCF binding events, and 1, 037 MCF10A-specific CTCF binding events.
