They focused on the possibility that defects of the midline and laterality defects (situs inversus) are etiologically related.
Not mutually exclusive to this explanation is the interesting possibility that defects in the timing of CENP-A expression, or promiscuous binding of CENP-A to other chaperones, coupled to defects in proteolysis, might cumulatively conspire to permit increased CENP-A accumulation at transcription factor binding sites in cells.
Previous reports [36], [37] showed that neurexin is not essential for NMJ formation in larvae and adults, but cannot rule out the possibility of defects or delays early in development, for which the animal might compensate later.
Additionally, our observations also raise the possibility that defects in signaling pathways that result in increased expression of the IFI16 gene in certain individuals contributes to premature ageing and ageing-dependent diseases.
To rule out the possibility that defects in the processing or secretion of the killer toxin [32] were responsible for the observed killer phenotypes, double-stranded viral RNA was extracted from wild-type and mutant cells and visualized (Fig. 3B).
These results raise the possibility that defects associated with BECN1 activity in CF may not impact S. aureus induced autophagy.
But the work reported here suggests the possibility that defects in the function of p53 could lead to cancer via dysregulation (specifically upregulation) of the Alu elements themselves.
75– 77 Such results highlight the possibility of defects in adipose tissue metabolism in South Asians that extend beyond elevated total abdominal fat.
This study raises the possibility that defects in the establishment of brain lateralization could indeed be causative of cognitive or other symptoms of brain dysfunction.
However, in the afore-mentioned study, other mechanisms potentially impairing AB clearance were not investigated, leaving open the possibility of defects in other dead cell clearance effectors, such as phagocytes.
