The lack of full rescue indicates that additional light-induced pathways are involved.
When these controls establish that the rescue construct is functional, the absence of RNAi rescue indicates that the observed phenotype is caused by an off-target knock-down.
Although an improvement of light-induced retinal degeneration was observed in the Trα−/− background, the lack of complete rescue indicate that additional pathways are also involved.
Rescue indicates the miR-124 RMCE allele with miR-124 reintegrated at the endogenous locus (34).
Despite their extensive sequence divergence, both transgenes suppressed rescue, indicating that hybrid lethal activity is an ancestral function of Lhr (Maheshwari and Barbash 2012).
First, the kinetics of endogenous EPSCs were unaltered in UNC-13L and UNC-13S rescue, indicating that the intrinsic kinetics of muscle ACh responses were not affected.
Again, the stem cells from Rps27l −/− fetal livers failed to rescue sterilized recipient mice with 100% death within 12 days post reconstitution, whereas those from wild type or heterozygous fetal liver caused a 100% rescue, indicating an intrinsic defect.
By contrast, partial silencing of c-Cbl did not affect the abundance of the partially glycosylated or band B of ∆F508-CFTR after temperature rescue, indicating that c-Cbl does not affect ∆F508-CFTR protein translation (Fig. 1).
A similar construct that contained the putative feelgood (N301K) mutation in creb3l2 failed to rescue, indicating that the N301K substitution disturbs creb3l2 function and accounts for the feelgood mutant phenotype (Fig. 5G,I,J).
Furthermore, the observation that suppressing Derlin-1 function did not completely abolish torsinA rescue indicates that torsinA might be working in conjunction with other unknown factors to mediate a neuroprotective role.
