In the case of PLCB3, discordant results have been reported when the gene is knocked out in mice producing both embryonic lethality and normal development in different studies [ 23, 24]; however, it has been found that the knockout of a related gene, the PLCB1, developed epilepsy in mice [ 25].
Deletions of α-Neurexin result in increased lethality, normal synapse number and gross anatomy but severely impaired synaptic functioning, a pattern strikingly similar to neuroligin gene knockouts [ 16, 66, 67].
Since knockout of genes essential for autophagy, Atg5 or Atg7, results in normal embryonic development and postnatal lethality [55], [56], autophagy alone is unlikely to contribute to the phenotypes observed in Pik3c3 mutant embryos.
LC50, defined as concentration in normal fly media causing 50% lethality in seven days, was determined for PTZ and the AEDs (results not presented).
However, the exact function of Trx1 in normal tissues remains unclear because of the early lethality of the Trx1-deficient embryo.
The exact function of Trx1 in normal tissues remains unclear, however; Trx1-deficient embryos exhibit early lethality, suggesting that Trx1 is essential for normal development.
All together, these findings suggested that oxidative injury plays a significant functional role in the enhanced lethality induced by the panobinostat/ZOL combination in PCa and MM cells, but not in normal prostate epithelial cells.
It was previously reported that ubiquitous dZip2 knockdown resulted in lethality [ 17]We did not see this lethality under normal culturing conditions.
The lethality associated with UAS-endoAA66W was observed both in the absence of endogenous EndoA (in endoA nulls), and in the presence of EndoA in normal dosage (overexpression paradigm).
