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The second factor that might have contributed to the variation in BD PRO recovery was tissue-specific expression of some putative BD PROs coupled with the transient expression system that involved use of embryos to assess BD PRO function.
Most importantly, removing pros function in trx mutant type II neuroblasts leads to the formation of supernumerary type I neuroblasts.
In the next step, we determined those genes affected by loss of pros function for each organ with the DS.
To determine those genes affected by loss of pros function, we calculated a discriminating score reflecting the differential expression between V1 mutant and other pros alleles.
As previously described, loss of pros function in the AMC induced several alterations including axon pathfinding defects and abnormal growth and taste responses.
Interestingly, we also found that loss of pros function induced the misregulation of a subset of genes important for growth, and autophagy.
The observation that NETs express pro-thrombotic and pro-coagulant functions has attracted much attention.
Overall, phosphorylation of Bid can serve as a switch between the pro-apoptotic and pro-survival functions of the protein.
Depending on the context, autophagy has been shown to have either pro-survival or pro-death functions.
Besides these pro-death functions, BNIP3 also mediates pro-survival autophagy induction.
This effort is further complicated if the pro-death gene also has essential pro-survival functions (e.g., calpain).
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