Reverse query / human → dog
dilated cardiomyopathy 1A.
Familial dilated cardiomyopathy with conduction defect due to LMNA mutation is a rare familial dilated cardiomyopathy characterized by left ventricular enlargement and/or reduced systolic function preceded or accompanied by significant conduction system disease and/or arrhythmias including bradyarrhythmias, supraventricular or ventricular arrhythmias. Disease onset is usually in early to mid-adulthood. Sudden cardiac death may occur and may be the presenting symptom. In some cases, it is associated with skeletal myopathy and elevated serum creatine kinase.
Which dogs are a natural model of this human disease. Each row is a distinct gene pathway with a canine model, ranked by evidence strength. We assert the canine disease models the human one (gene-level), never that a dog allele equals a human variant.
| Canine model pathway | Evidence | Ortholog | Human anchor | Canine variant · assembly |
|---|---|---|---|---|
| — OMIA model-of | OMIA-anchored | one2one | — | gene-level (no single variant) |
Established genes without a canine model yet
Of the 1 genes GenCC calls an established (Definitive / Strong / Moderate) cause of dilated cardiomyopathy 1A, these 1 do not have a canine natural model in our substrate yet. Not "no dog carries this", a stated gap in what we hold, the honest frontier of the reverse query.
Gene-disease validity from GenCC (thegencc.org, CC0), the established tail across ClinGen, OMIM, Orphanet, and others. Each gene links to its Sniff lookup, where the human ortholog and any canine evidence we hold are shown, gene-level (INV-57).