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To assess whether Aβ could realistically localise to living retinas to mediate such effects, we subretinally injected nanomolar levels of oligomeric Aβ1-42 into wildtype mice.
However, specific c-Src partners that might mediate such effects remain unidentified.
However, various signaling intermediates and protein substrates that mediate such effects remain to be identified.
The anti-inflammatory effects of PPAR activation, occurring through genomic and non-genomic PPAR-dependent mechanisms, may mediate such effects.
Increased levels of cortisol in the mother could potentially mediate such effects of depression and anxiety on the development of the foetal HPA system.
Since growth regulatory and apoptotic mechanisms are largely interdependent and complexed further by cross talk among signaling pathways, the attribution of one or the other event to mediate such effects may be premature.
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To test whether altered cell contractility mediated such effects, we analyzed cells for changes in shape using F-actin labeling.
The association of IL-1β release by astrocytes and microglia prompts the investigation of how exactly is hyperglycemia mediating such effects.
There is evidence that TIP60/KAT5 mediates such effects by regulating gene expression, especially of genes linked to apoptotic cell death (Pirooznia et al, 2012) and axonal transport (Johnson et al, 2013).
This study was carried out to investigate the effect of rapid eye movement sleep (REMS) deprivation (REMSD) on the cytomorphology of the dorsal raphe (DR) neurons and to evaluate the possible role of REMSD-induced increased noradrenalin (NA) in mediating such effects.
However, the specific downstream events by which PLAB mediates such effect remain to be determined.
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mediate such talks
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mediate antiviral effects
mediate such relationships
mediate estrogenic effects
mediate such interactions
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mediate such differences
mediate cellular effects
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