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Heterozygous AKAP9 variants have been reported in three unrelated LQTS type 11 probands: a 3-year-old male with c.4021C>A (p.Gln1341Lys) (PMID:36395689), a 10-year-old female and two unaffected relatives carrying c.11487_11489del (p.Thr3830ValfsTer12) (PMID:38585551), and a 47-year-old male with a novel frameshift c.7252_7255del (p.Glu2418ProfsTer5) (PMID:36421840). Segregation was demonstrated in two affected relatives. However, a recent evidence-based reappraisal classified AKAP9 as a limited/disputed LQTS gene based on sparse case numbers and variable pathogenicity assertions (PMID:31983240).
Functional assays of the p.Ser1570Leu variant show disrupted binding of AKAP9 (Yotiao) to the KCNQ1 channel, loss of cAMP-induced phosphorylation of IKs, and prolonged simulated ventricular action potentials, consistent with delayed repolarization (PMID:18093912).
Key Take-home: AKAP9 currently has limited clinical validity for LQTS and should be interpreted with caution in diagnostic testing.
Gene–Disease AssociationLimitedThree unrelated probands, two small pedigrees, limited segregation, and a disputed classification in a recent reappraisal Genetic EvidenceLimited3 probands with heterozygous AKAP9 variants, segregation in 2 relatives, variant classes include missense and frameshift ([PMID:36395689], [PMID:38585551]) Functional EvidenceModerateCellular assays demonstrate disrupted Yotiao–KCNQ1 interaction and loss of I(Ks) response for p.Ser1570Leu consistent with delayed repolarization ([PMID:18093912]) |