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Several factors have already been identified that either drive or depress entrepreneurial activities.
Furthermore, genetic alleles have been identified that either enhance or suppress oxygen deprivation survival [28], [29], [30].
In the case of C1q, several receptors have been identified that either recognize the globular heads (e.g. gC1qR) or the collagenous portion (e.g. cC1qR) [28], [29], [29].
A number of mechanisms have been identified that either promote or suppress RHAMM expression.
Several spindle proteins, including XKCM1 and XMAP215 family members have been identified that either stabilize or destabilize MTs by mediating the rapid changes between polymerization and depolymerization [ 8, 15].
-wrap> In addition to the genes mentioned above, several proteins and pathways have been identified that either promote or suppress PDAC progression, and their effects on tumour development have been studied, some of which are summarized in Table 2.
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Several classes of protein domains have been identified that are either designed for or are capable of interacting with protein C-termini – these include PDZ and TPR domains.
With non-adherence to imatinib, the concerns are: what factors have been identified that may either enhance adherence or engender non-adherence behaviour?
Although numerous AKAP disruptors have previously been identified that can inhibit either RI- or RII-selective AKAPs, no AKAP disruptors have been identified that have isoform specificity for RIα versus RIβ or RIIα versus RIIβ.
Numerous genetic and environmental factors have been identified that can modulate either replicative aging, or chronological aging, or both.
Although DSBs are induced by the evolutionarily conserved topoisomerase-like protein Spo11 (Keeney et al., 1997), many poorly conserved accessory proteins have been identified that are required either to facilitate the formation of the DSBs themselves or position the DSBs within the euchromatin (de Massy, 2013).
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