It is widely accepted that 3D-Cry toxins exert their toxic effect by the sequential binding to insect gut proteins named cadherins and glycosyl-phosphatidyl-inositol (GPI) anchored proteins such as aminopeptidase-N (APN) or alkaline phosphatase (ALP) resulting in toxin oligomerization and pore formation that finally cause cell lysis and disruption of the insect gut (Pardo-López et al. 2013).
While many of the RNA-binding proteins dimerize exclusively in the cytosol, the LexA repressor [ 17], the leucine-zipper activator [ 18, 19], and the Arc repressor [ 20] have been shown to form an oligomer either in the cytosol ("dimer path") or on the DNA by sequential binding ("monomer path").
Eukaryotic cells coordinate chromosome duplication by the assembly of protein complexes at origins of DNA replication by sequential binding of member proteins of the origin recognition complex (ORC), CDC6, and minichromosome maintenance (MCM) proteins.
The enzyme is activated by sequential binding of product molecules with dissociation constant K P = (k P − / k P + ) for each binding step.
The spliceosome is a highly dynamic structure, assembled by sequential binding and release of the small nuclear RNAs and protein factors.
Quinupristin/dalfopristin is a synthetic, parenteral, streptogramin antibiotic that acts by sequential ribosomal binding to inhibit protein synthesis and is effective in vitro against Enterococcus faecium, MRSA, Streptococcus pneumoniae, and other Gram-positive cocci.
HIV-1 entry into host cells is mediated by the sequential binding of the envelope glycoprotein gp120 to CD4 and a chemokine receptor.
Signal transduction of IL-4 is mediated by a sequential binding process, initiated first by binding of IL-4 to its high-affinity single membrane spanning receptor chain IL-4Rα (Fig. 1a).
The pre-RCs are formed by the sequential binding of the origin recognition complex (ORC1 to ORC6), cell division cycle 6 (Cdt1), Cdt1 and minichromosome maintenance (MCM2 to MCM7) proteins to DNA [ 1].
During the differentiation of 3T3-L1 preadipocytos to adipocytes, the SWI/SNF (for 'SWItch/Sucrose NonFermentable') chromatin remodeling complex and histone modifying enzymes lead to chromatin remodeling that is followed by the sequential binding of PolII, TATA binding protein (TBP) and other transcription factors to activate the transcription of PPARγ [ 20].
