Disease relevance of Irx5

• Thus, an Irx5 repressor gradient negatively regulates potassium-channel-gene expression in the heart, forming an inverse I(to,f) gradient that ensures coordinated cardiac repolarization while also preventing arrhythmias [1].

High impact information on Irx5

• The homeodomain transcription factor Irx5 establishes the mouse cardiac ventricular repolarization gradient [1].
• We show that, in mice lacking the homeodomain transcription factor Irx5, the cardiac repolarization gradient is abolished due to increased Kv4.2 potassium-channel expression in endocardial myocardium, resulting in a selective increase of the major cardiac repolarization current, I(to,f), and increased susceptibility to arrhythmias [1].
• The Iroquois homeobox gene, Irx5, is required for retinal cone bipolar cell development [2].
• These results indicate that there are at least two distinct genetic pathways (Irx5-dependent and Vsx1-dependent) regulating the development of Type 2 and Type 3 cone bipolar cells [2].
• In Irx5-deficient mice, defects were observed in the expression of some, but not all, immunohistological markers that define mature Type 2 and Type 3 OFF cone bipolar cells, indicating a role for Irx5 in bipolar cell differentiation [2].

Anatomical context of Irx5

• The spatiodevelopmental pattern of Irx5 matched that of ANF, a marker for the forming working myocardium of the chambers [3].

Other interactions of Irx5

• We report here the cloning and expression analysis of two novel mouse Irx genes, Irx5 and Irx6 [4].
• Transcripts for Irx5 were detected specifically in the endocardium lining the ventricular and atrial working myocardium that also expressed von Willebrand factor, but were absent from the endocardium of the endocardial cushions, i.e., the atrioventricular canal, inner curvature, and outflow tract [3].

References