Paralytic (gene)

[6] Channel kinetics are influenced by splicing, that not only changes protein structure but can allow for varying modifications, like differential binding of cofactors.

[6] The voltage sensor 4 in HD III is partially formed by exon L and K.[7] The alternative splicing at this locus causes a difference in the charged current at this channel.

[7] Paralytic encodes a protein channel which transfers sodium ions into neurons and is activated in response to changes in the voltage across a membrane[1] to propagate an action potential.

Some of these, such as bss1 and bss2 can be caused by a single point mutation in the paralytic gene which makes the channel less able to inactivate itself after being activated.

[7] Insect species have only one a single sodium channel gene which encodes the mammalian equivalent of α subunit.

Insects like D. melanogaster take advantage of alternative splicing and RNA editing to generate distinct gating properties of sodium channels.

[9] Fly models can be used to study branches of human epilepsy, by using GEFS+ mutations at SCN1A gene for knock-in's at the para locus in D.