para Antibody

1. Study identified Shu, a Drosophila mutation causing severe behavioral defects, as a novel hypermorphic allele of the Nav channel gene para. Results suggest that the Shu Nav channels cause an increase in sodium currents, and that this defect is compensated by reduced para function, leading to a more balanced neuronal output. PMID: 27844061
2. analysis revealed that 2 variant-specific amino acid changes, I260T in the S4-S5 linker of domain I (ILS4-S5) and A1731V in the voltage sensor S4 of domain IV (IVS4), contribute to the persistent sodium current (INaP) PMID: 24662849
3. Trp404 and His405 as a putative point of Av3 interaction with DmNav1. PMID: 25055135
4. The para(bss1) has not responded to seizure suppressor mutations identified in screens based on the Drosophila mutants eas protein and sda protein. PMID: 23797108
5. results indicate that increased synaptic activity influences the decision to splice in exon L, which, in turn, may promote seizure. PMID: 22623672
6. 3-dimensional structure modeling of ANEPII and site-4 of the insect sodium channel were carried out by homology modeling, and these models were used as the starting point for nanosecond-duration molecular dynamics simulations. PMID: 20816643
7. Chromosome fusions from patterns of polymorphism at the X-linked para gene were studied. PMID: 12930752
8. The structure of the scorpion alpha-toxin LqhalphaIT binding site in the para sodium channel of Drosophila melanogaster was characterized using NMR Spectroscopy. PMID: 18154318
9. Drosomycin interacts with the voltage-gated sodium channel, DmNa(v)1. PMID: 19574227

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KEGG: dme:Dmel_CG9907

STRING: 7227.FBpp0303597

UniGene: Dm.22809