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Because the actin filament-binding repeats are required for activation, it has been hypothesized that cortactin recruits Arp2/3 complex to filaments to stimulate nucleation (Uruno et al., 2001).
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Since postpartum psychosis has been linked to activation of the immune system, it has been hypothesized that infectious agents may be involved in the pathogenesis of this disorder.
Both HB22.7 and rituximab activate the p38 signaling pathway, and it has been hypothesized that p38 activation may mediate cytotoxic effects.
It has been hypothesized that repetitive activation of trigeminovascular neurons and consequently repetitive activation of modulatory pain pathways may lead to impairment of function or partial neuronal cell damage in these areas through the liberation of free radicals [1].
It has been hypothesized that activation of VEGFA may induce pathologic angiogenesis beneath the RPE layer.
It has been hypothesized that immune activation and inflammation may increase HIV-1 susceptibility and that cytokines may be useful biomarkers for risk.
It has been hypothesized that microglial activation and the subsequent increase of pro-inflammatory cytokines play an important role in the pathogenesis of PD.
It has been hypothesized that conditional folding of these activation domains may be a prerequisite for their efficient interaction with specific coregulatory proteins, and subsequent transcriptional activity leading to the regulation of target gene(s).
It has been hypothesized that this may be due to the activation of X-linked genes, or a spreading of inactivation to the autosomes.
It has been hypothesized that hemostatic factors play an important role; altered platelet activation as well as impaired fibrinolysis have been found in diabetics [ 10, 11].
It has been hypothesized that HSPE1 and HSPD1 form a complex with and facilitate the activation of pro-caspase 3 [ 32].
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