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ITGB1BP2 – Dilated Cardiomyopathy

The association between ITGB1BP2 and dilated cardiomyopathy (MONDO_0005021) is currently classified as Limited. In a case report, a missense variant, c.938C>G (p.Ala313Gly), was identified in a 45-year-old male with familial dilated cardiomyopathy, suggesting a possible role for ITGB1BP2 in disease pathogenesis (PMID:23124043). In a larger multi‐patient study screening 928 individuals, only a very low number of ITGB1BP2 variations were detected among hypertensive and cardiopathic patients, and no clear genotype/phenotype correlation was established (PMID:20017903).

Functional assessment studies have not provided definitive evidence that the identified variants disrupt melusin function in a way that contributes to the development of dilated cardiomyopathy. Despite the biological plausibility of melusin in myocardial stress signaling, the experimental data remain inconclusive. Key take‑home sentence: While ITGB1BP2 is a candidate gene for dilated cardiomyopathy, further genetic and functional studies are needed before it can be reliably used in diagnostic or commercial applications.

References

  • Gene • 2013 • Identification of a missense mutation in the melusin-encoding ITGB1BP2 gene in a patient with dilated cardiomyopathy PMID:23124043
  • BMC Medical Genetics • 2009 • Melusin gene (ITGB1BP2) nucleotide variations study in hypertensive and cardiopathic patients PMID:20017903

Evidence Based Scoring (AI generated)

Gene–Disease Association

Limited

Only one familial case with the missense variant c.938C>G (p.Ala313Gly) was identified (PMID:23124043), supported by a larger cohort study showing an extremely low number of variants without a clear phenotype correlation (PMID:20017903).

Genetic Evidence

Limited

Genetic evidence is restricted to a single candidate missense mutation among 255 patients and a few additional rare variants from a cohort study, none of which have demonstrated robust segregation.

Functional Evidence

Limited

Functional studies have not confirmed a clear mechanistic effect of ITGB1BP2 variants on heart muscle function, leaving the pathogenicity unresolved.