High impact information on Kcna6

• Using the oocyte heterologous expression system, pl14a was shown to inhibit both a K+ channel subtype (Kv1.6, IC50 = 1.59 microM) and neuronal (IC50 = 8.7 microM for alpha3beta4) and neuromuscular (IC50 = 0.54 microM for alpha1beta1 epsilondelta) subtypes of the nicotinic acetylcholine receptor (nAChR) [1].
• The IKL remaining in -/- neurons was blocked by DTX, suggesting the underlying channels contained subunits Kv1.2 and/or Kv1.6 (also DTX-sensitive) [2].
• Identification of the delayed rectifier potassium channel, Kv1.6, in cultured astrocytes [3].
• Immunocytochemical staining showed double-labeling of glial fibrillary acidic protein-positive cells with antibody specific for the Kv1.6 channel [3].
• Methylamine, but not ammonia, is hypophagic in mouse by interaction with brain Kv1.6 channel subtype [4].

Biological context of Kcna6

• This study establishes the gene order cen-opt-dfw-Rho (D6Mit44)-Kcna1, Kcna5, Kcna6 on distal mouse Chr 6 and suggests that the neurological mutants opt and dfw affect two different genes, neither of which is caused by a mutation in any one of the three clustered K channels [5].

Analytical, diagnostic and therapeutic context of Kcna6

• Reverse transcription-polymerase chain reaction, Western blot and immunohistochemical results indicate that a full expression in the brain of Kv1.6 is required only for the activity of MET, and confirms the different action mechanism of ammonia and MET [4].
• A relatively high level of Kv1.6 transcript was identified by RT-PCR and then confirmed and quantitated by ribonuclease protection assays using a Kv1.6-specific riboprobe [3].

References