High impact information on Bis1

• Overexpression of Bis1 results in a cell elongation phenotype, whereas bis1(-) cells exhibit a reduced viability in stationary phase similar to that seen in ish1(-) cells [1].
• Bis-1 prevented 5-HT-evoked sensory LTF [2].
• The murine Bis1 seizure gene and the Kcnab2 gene encoding the beta2-subunit of the K+ channel are different [3].
• Chromosomes 4 and 13 in beta-carboline-induced seizures in mice: benzodiazepine binding [4].
• For two of these strains, we obtained significant results showing that genes located on chromosomes 4 and 13, provisionally termed respectively Bis1 and Bis2, were involved in the regulation of beta-carboline-induced seizures [5].

Biological context of Bis1

• We tested the hypothesis that Bis1, a gene involved in seizure regulation in mice which has been localized to the distal part of chromosome 4, was the same as the gene Kcnab2, encoding the beta2-subunit for voltage-dependent K+ channels [3].

Other interactions of Bis1

• Two facts suggested this hypothesis: Kcnab2 is located in the 3.1-cM confidence interval containing Bis1 and many studies have shown an involvement of K+ channels in the genesis of seizures [3].

References