Psychiatry related information on Kcnab1

• Mice with a null mutation of the K+ channel regulatory subunit Kv beta 1.1 have altered excitability in hippocampal neurons and are impaired in the social transmission of food preferences (STFP) task [1].

High impact information on Kcnab1

• Pattern of Kv beta subunit expression in macrophages depends upon proliferation and the mode of activation [2].
• In addition, long-term potentiation (LTP) was more readily induced in aged Kvbeta1.1 knockout mice [3].
• Among them, a group of ion channels show specific regulation in CB: the potassium channels Kir6.1 and Kcnn4 are up-regulated, while the modulatory subunit Kcnab1 is down-regulated by low PO2 levels [4].
• Ibotenic acid lesions of the hippocampus in the 12-month-old Kv beta 1.1 mutants caused an impairment in the STFP task [1].
• This suggests that Kvbeta1.1-dependent A-type K+ channels contribute to frequency-dependent spike broadening and may regulate the sAHP by controlling Ca2+ influx during action potentials [5].

Biological context of Kcnab1

• Genetic mapping of the voltage-gated shaker potassium channel beta subunit Kcnab1 to mouse chromosome 3 [6].
• To specifically test whether Kv beta1 is a genetic modifier of the Kv beta2-null phenotype, we generated Kv beta1.1-deficient mice by gene targeting and bred them to Kv beta2-null mice [7].

Other interactions of Kcnab1

• Kv beta2 is the predominant Kv beta subunit in the mammalian nervous system, but its functions in vivo are not clear [7].
• Coimmunoprecipitation experiments showed that Kv1.2 and Kvbeta1.1 interact in these tissues [8].

Analytical, diagnostic and therapeutic context of Kcnab1

• RESULTS: The presence of Kvalpha1.2 and Kvbeta1.1 was confirmed in adult mouse crista ampullaris by Western blotting [8].

References