Our previous studies using the engineered monomeric 14-3-3ζ 14-3-3ζ 14-3-3ζ 14-3-3ζm 14-3-3ζm 14-3-3ζmained binding activity towardshowedcthatphosphorylated 14-3-3ζ 14-3-3ζ 14-3-3ζon, it prevented heat-induced aggregation of monomersubfretained1.
In a previous study using Ca2+-binding mutants of CaM, we discovered lobe-specific regulation by CaM of AC1 and AC8; no CaM mutant could regulate AC1, while partially liganded CaM could regulate AC8.
In this report there was no effect of the substitutions examined at K305 on 9D12 reactivity, whereas a previous study using rEDIII found significant reductions in 9D12 binding for a K305E mutant [22].
A previous study using bacterially expressed protein domains demonstrated that removal of the extreme C-terminal proline resulted in avid binding of GluA4 CTD to PDZ domains of SAP97 under in vitro conditions with purified proteins [13].
Consistently, the presence of an alternative receptor-binding domain in addition to the CROPs has also been proposed by a previous study using truncated forms of TcdB.
Moreover, although there is a close relationship between the amygdala and the ventrocaudal caudate putamen, previous studies using autoradiography have shown limited binding of CORT [49], due to minimal expression of GR with no appreciable MR in the ventrocaudal caudate putamen [50].
The binding specificity observed using the natural trimer and the expanded synthetic glycan array are consistent with previous studies using earlier versions of the array containing more limited sets of glycans and with competition studies (van Vliet et al. 2005).
Moreover, previous studies using face voice pairs have shown that crossmodal binding of affective information involves the left amygdala (Dolan et al. 2001; Ethofer et al. 2006) and this brain structure receives both visual and auditory inputs (McDonald 1998).
Previous studies using animal-derived, isolated, or recombinant surfactant have demonstrated binding of surfactant proteins to a variety of nanoparticles.
Evidence from previous studies using soluble HSV-1 glycoprotein and UV-inactivated virus suggested that binding of HSV-1 virions to the cell surface might be sufficient to stimulate intracellular signalling pathways.
