Splicing of intron 3 of human BACE requires the flanking introns 2 and 4.

Regulation of proteolytic cleavage of the amyloid precursor protein by the aspartic protease BACE may occur by alternative splicing and the generation of enzymatically inactive forms. In fact, the presence of exonic donor and acceptor sites for intron 3 generates the two deficient variants BACE457 and BACE476. In HEK293 cells, when introns are inserted separately in the BACE cDNA, we found that whilst introns 2 and 4 are efficiently spliced out, intron 3 is not removed.

Clustering transmembrane-agrin induces filopodia-like processes on axons and dendrites.

The transmembrane form of agrin (TM-agrin) is primarily expressed in the CNS, particularly on neurites. To analyze its function, we clustered TM-agrin on neurons using anti-agrin antibodies. On axons from the chick CNS and PNS as well as on axons and dendrites from mouse hippocampal neurons anti-agrin antibodies induced the dose- and time-dependent formation of numerous filopodia-like processes.

Isoform pattern and AChR aggregation activity of agrin expressed by embryonic chick retinal ganglion neurons.

Several isoforms of chick agrin, which differ in their activity to aggregate AChRs at the neuromuscular junction, are generated by alternative splicing at splice site B. We analyzed the isoform pattern and the functional properties of agrin in a defined population of CNS neurons. At all developmental stages retinal ganglion cells purified by immunopanning expressed the agrin B0, B11, and B19 isoforms.