Kcnq5 Conditional Knockout mouse models

Encoding Kv7.5, Kcnq5 is the mouse ortholog of human KCNQ5 and contributes a slowly activating, noninactivating potassium conductance that co-assembles with Kv7.3 to form a distinct component of the neuronal M current, with particularly strong expression in hippocampal CA3, dentate gyrus, cortical interneurons, auditory brainstem, and in vascular and airway smooth muscle where it sets resting tone. Kv7.5 activates at more negative potentials than Kv7.2-containing channels and is strongly PIP2 dependent and calmodulin regulated, and it is suppressed by Gq-coupled receptor signaling, which converts muscarinic or purinergic input into increased excitability or vasoconstriction. Human KCNQ5 loss-of-function variants cause intellectual disability with or without epilepsy. Nulls are viable, so conditional alleles serve cell-type attribution rather than lethality rescue, and gating knockins test whether the shifted voltage dependence carries the phenotype. Because Kcnq2 and Kcnq3 supply overlapping M current, compound genetics and retigabine-sensitive current measurement should accompany any single-locus interpretation.

Conditional deletion of Kcnq5 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Kcnq5 floxed stock yields usable cohorts.