Activity

Filter

Cancel
Date Panel Item Activity
15 actions
Intellectual disability syndromic and non-syndromic v1.592 ATP9A Zornitza Stark Publications for gene: ATP9A were set to 34379057; 34764295
Intellectual disability syndromic and non-syndromic v1.591 ATP9A Zornitza Stark Mode of inheritance for gene: ATP9A was changed from BIALLELIC, autosomal or pseudoautosomal to BOTH monoallelic and biallelic, autosomal or pseudoautosomal
Intellectual disability syndromic and non-syndromic v1.590 ATP9A Zornitza Stark edited their review of gene: ATP9A: Added comment: PMIDs 34379057, 34764295, 36604604 and 40226306 report 12 unrelated families with ATP9A variants. Six families carry biallelic loss‑of‑function variants causing an autosomal recessive neurodevelopmental disorder with post‑natal microcephaly, failure‑to‑thrive and behavioural abnormalities; five families carry de novo heterozygous missense variants causing autosomal dominant nonsyndromic intellectual disability with seizures and autism‑like features. Multiple functional studies in patient cells, mouse knock‑out models and rescue assays provide strong loss‑of‑function evidence.; Changed publications: 34379057, 34764295, 36604604, 40226306; Changed mode of inheritance: BOTH monoallelic and biallelic, autosomal or pseudoautosomal
Intellectual disability syndromic and non-syndromic v0.5168 ATP9A Zornitza Stark Phenotypes for gene: ATP9A were changed from Neurodevelopmental delay; Postnatal microcephaly; Failure to thrive; Gastrointestinal symptoms to Neurodevelopmental disorder with poor growth and behavioural abnormalities, MIM# 620242
Intellectual disability syndromic and non-syndromic v0.5167 ATP9A Zornitza Stark edited their review of gene: ATP9A: Changed phenotypes: Neurodevelopmental disorder with poor growth and behavioural abnormalities, MIM# 620242
Intellectual disability syndromic and non-syndromic v0.4333 ATP9A Zornitza Stark Publications for gene: ATP9A were set to http://dx.doi.org/10.1136/jmedgenet-2021-107843
Intellectual disability syndromic and non-syndromic v0.4332 ATP9A Zornitza Stark Classified gene: ATP9A as Green List (high evidence)
Intellectual disability syndromic and non-syndromic v0.4332 ATP9A Zornitza Stark Gene: atp9a has been classified as Green List (High Evidence).
Intellectual disability syndromic and non-syndromic v0.4331 ATP9A Zornitza Stark edited their review of gene: ATP9A: Changed rating: GREEN
Intellectual disability syndromic and non-syndromic v0.4331 ATP9A Zornitza Stark edited their review of gene: ATP9A: Added comment: Four unrelated families and mouse model.; Changed publications: 34379057, 34764295
Intellectual disability syndromic and non-syndromic v0.3930 ATP9A Zornitza Stark Marked gene: ATP9A as ready
Intellectual disability syndromic and non-syndromic v0.3930 ATP9A Zornitza Stark Gene: atp9a has been classified as Amber List (Moderate Evidence).
Intellectual disability syndromic and non-syndromic v0.3930 ATP9A Zornitza Stark Classified gene: ATP9A as Amber List (moderate evidence)
Intellectual disability syndromic and non-syndromic v0.3930 ATP9A Zornitza Stark Gene: atp9a has been classified as Amber List (Moderate Evidence).
Intellectual disability syndromic and non-syndromic v0.3929 ATP9A Zornitza Stark gene: ATP9A was added
gene: ATP9A was added to Intellectual disability syndromic and non-syndromic. Sources: Literature
Mode of inheritance for gene: ATP9A was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: ATP9A were set to http://dx.doi.org/10.1136/jmedgenet-2021-107843
Phenotypes for gene: ATP9A were set to Neurodevelopmental delay; Postnatal microcephaly; Failure to thrive; Gastrointestinal symptoms
Review for gene: ATP9A was set to AMBER
Added comment: Vogt et al. 2021 report on 3 individuals from 2 unrelated consanguineous families with different homozygous truncating variants in ATP9A, presenting with DD/ID of variable degree (2 mild, 1 severe), postnatal microcephaly (OFC range: −2.33 SD to −3.58 SD), failure to thrive, and gastrointestinal symptoms. Patient-derived fibroblasts showed reduced expression of ATP9A, and consistent with previous findings also overexpression of interacting partners, ARPC3 and SNX3.
Sources: Literature