Fgf11 Conditional Knockout mouse models

Fgf11, the mouse ortholog of human FGF11, belongs to the intracellular FGF homologous factor subfamily and, despite the name, encodes no secreted mitogen: the protein lacks a signal peptide, does not engage FGFR ectodomains, and instead functions within the cytosol through a beta-trefoil core that docks onto the C-terminal tails of voltage-gated sodium channels and interacts with hypoxia-responsive machinery, having been described as a HIF-1alpha modulator in T cells and tumor contexts. This intracellular mechanism dictates allele strategy: secreted-ligand logic such as ligand traps or neutralizing antibodies is inapplicable, and interpretation should center on channel gating, cytoskeletal, and transcriptional readouts. Nulls are viable, so constitutive deletion is feasible, while domain-swap or interaction-surface point knockins are far more informative than whole-gene ablation for separating channel binding from other partners. The closely related paralogs Fgf12, Fgf13, and Fgf14 occupy overlapping neuronal and cardiac territory, so compound genetics is often required before assigning an excitability or arrhythmia endpoint to this locus.

A floxed Fgf11 allele paired with Cre gives spatial control that whole body knockouts cannot offer. People use it to separate developmental roles from adult homeostasis, to model somatic mutations, and to match disease that begins in one organ.