The extrinsic pathway is triggered by members of the tumor necrosis factor (TNF) superfamily, which bind and activate their corresponding DRs. For example, binding of TNF-related apoptosis-inducing ligand (TRAIL) to the extracellular domains of the DR4 and DR5 promotes clustering of these receptors, and then induces apoptosis.
For example, binding of GRD to sprouty-related EVH1 domain-containing protein 1 (Spred1) inhibits Spred1 function and localizes GRD to the membrane to inactivate membrane-anchored Ras.
For example, binding of opiate agonists and antagonists is differentially affected by sodium ion11, and Na+ conductance is altered by opiate agonists12.
For example, binding of Mmi1 to the ssm4 transcript triggers pre-mature pre-mRNA 3′-end formation near regions containing DSR elements34.
Changes in conformation subsequently initiate a biochemical response by alterations in, for example, binding affinity to another protein or enzymatic activity.
For example, binding of TRAF2 to TNFR induces signaling, leading to the activation of NF-κB and MAPKs for the regulation of inflammatory responses and cell death and survival.
For example, binding of silver ions with fungal cell wall during [19, 22] synthesis.
An example binding site patch is shown in Fig. 1 for the cofactor binding site of CDK2 [14].
For example, binding to metabolites, such as fructose-1,6-bisphosphate (FBP), can forge PKM2 into more active tetramer (Dombrauckas et al., 2005).
For example, binding sites might be able to modulate gene expression as a consequence of differences in affinity (Bain et al., 2012), where high affinity binding sites induce a higher level of transcriptional activation than low affinity binding sites.
We used three different methods to determine an energy matrix from the set of example binding sites.
