The result indicated that neuronal expression and regulated proteolysis of prion protein are essential for myelin maintenance.
Large fibers we affected in axons when morphometry was used and identical pathologies were detected in the sciatic nerves.
However, when NAIP use baculovirus IAP-repeat (BIR) domains to interact with caspases, they inhibit otherwise automatic formation of procaspase-9, an apoptosis initiator.
[4] The three-dimensional structure of all BIR domains is constructed of two to three NH2-terminus α-helices, a central antiparallel β-sheet, and two to three carboxy-terminus α-¬helices.
The interaction between NAIP and hippocalcin, a neuronal calcium-sensor protein, has been observed to take place in the zinc-binding region along with other specific amino acids.
In sympathetic neurons, the expression of NAIP-BIR3 and hippocalcin did not provide any significant protection from cell death from the withdrawal of nerve growth factor.
This is unexpected because, in nerve growth factor withdrawal, caspase-3 and -9 are activated, causing cell death, which are the very caspases blocked by NAIP.
When overexpressed, XIAP is able to block caspases extremely well and prevents cell death of sympathetic neurons when nerve growth factors are deprived.