TGFβ1 and renin-angiotensin system have been suggested as the common pathway leading to CAN, an unknown disease characterized by fibrosis and inflammation.
As the 2002 2012 hiatus is included in the 2001 2013 or 2002 2014 or 2002 2012 periods, the last can be suggested as the common hiatus duration in the all GMSTs/GMATs of the nine time series included in this study.
Circuit level brain dysfunction has been suggested as a common mechanism through which diverse genetic risk factors and neurobiological sequelae lead to the core features of autism spectrum disorder (Geschwind 2009; Port et al. 2014).
Chronic inflammation was suggested as a common denominator in the induction of nearly all age-associated chronic diseases or site-specific cancers [4 9].
Nevertheless, virion exclusion has been suggested as a common strategy of vif-deficient retroviruses to circumvent Apobec restriction, and exclusion of mA3 from MLV virions has been demonstrated by some groups [35] although not by others [23], [29], [36].
This form of genetic variation has been suggested as a common cause of both normal and disease-related inter-individual variation in complex phenotypes [ 7].
The event-driven method does not account for HGT, which is suggested as a common mechanism for transferring neighboring genes (Lawrence and Roth, 1996).
Among factors such as obesity, hypercholesterolemia, hyperlipidemia, increased formation of advanced glycation end-products [ 13] and increased oxidative stress [ 14], a dysfunction in angiogenesis also has been suggested as a common origin for diabetic vascular complications [ 15].
Several studies using FISH have demonstrated that the TMPRSS2-ERG fusion can result from both translocations and interstitial deletions between TMPRSS2 and ERG [ 5, 11- 14], with deletion being suggested as a common mechanism for fusion formation [ 11, 15, 16].
A negatively charged residue close to the CXXC motif appears to be conserved in ATPases for metals (divalent) other than copper, and repulsion has been suggested as a common mechanism to prevent the binding of Cu(I).
