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ANKS1B haploinsufficiency has emerged as a candidate cause of neurodevelopmental disorders based on a genome-wide a-CGH study of 1,800 Italian patients, in which pathogenic CNVs encompassing ANKS1B were identified, although the number of affected probands is unspecified (PMID:38674362). To date, no familial segregation beyond de novo occurrence has been reported, and specific variant-level data are lacking, limiting genetic resolution.
Functional models support a haploinsufficiency mechanism: Anks1b haploinsufficiency in mice recapitulates white matter and social behavior deficits analogous to those in patients, with rescue by clemastine (PMID:38129387). Comparative proteomic analysis of Anks1b-haploinsufficient synapses reveals altered Rac1 signaling within oligodendrocytes (PMID:37255534), while biochemical and structural studies elucidate high-affinity interactions between AIDA-1 and SynGAP, linking ANKS1B to synaptic Ras-GAP regulation (PMID:38759928). Together, these data provide moderate functional evidence for ANKS1B involvement in neurodevelopmental pathology.
Key Take-home: ANKS1B haploinsufficiency likely contributes to neurodevelopmental disorders via disrupted synaptic and oligodendrocyte pathways, supporting its consideration in diagnostic genetic testing.
Gene–Disease AssociationLimitedSingle CNV cohort identified ANKS1B alterations without specific proband counts ([PMID:38674362]); limited segregation data Genetic EvidenceLimitedOne a-CGH study reports pathogenic CNVs in ANKS1B ([PMID:38674362]); no detailed variant-level or segregation data Functional EvidenceModerateAnks1b haploinsufficiency models recapitulate neurodevelopmental phenotypes with rescue experiments; structural and biochemical assays define pathogenic mechanism ([PMID:38129387]; [PMID:37255534]; [PMID:38759928]) |