Activity

Filter

Cancel
Date Panel Item Activity
7 actions
Mendeliome v1.3915 PRMT1 Zornitza Stark Marked gene: PRMT1 as ready
Mendeliome v1.3915 PRMT1 Zornitza Stark Gene: prmt1 has been classified as Green List (High Evidence).
Mendeliome v1.3915 PRMT1 Zornitza Stark Phenotypes for gene: PRMT1 were changed from Neurodevelopmental disorder, MONDO:0700092 to Neurodevelopmental disorder, MONDO:0700092, PRMT1-related
Mendeliome v1.3914 PRMT1 Zornitza Stark Classified gene: PRMT1 as Green List (high evidence)
Mendeliome v1.3914 PRMT1 Zornitza Stark Gene: prmt1 has been classified as Green List (High Evidence).
Mendeliome v1.3913 PRMT1 Zornitza Stark changed review comment from: PMID 39937650 reports four individuals from four unrelated families with heterozygous de novo missense PRMT1 variants presenting with neurodevelopmental disorder and dystonia. Functional studies demonstrated reduced protein stability and enzymatic activity, supporting a loss‑of‑function mechanism.
Sources: Literature; to: PMID 39937650 reports four individuals from four unrelated families with heterozygous de novo missense PRMT1 variants presenting with neurodevelopmental disorder and dystonia (in two). Functional studies demonstrated reduced protein stability and enzymatic activity, supporting a loss‑of‑function mechanism.

Two of the individuals had the same variant, p.Glu291Lys.

Sources: Literature
Mendeliome v1.3913 PRMT1 Zornitza Stark gene: PRMT1 was added
gene: PRMT1 was added to Mendeliome. Sources: Literature
Mode of inheritance for gene: PRMT1 was set to MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown
Publications for gene: PRMT1 were set to 39937650
Phenotypes for gene: PRMT1 were set to Neurodevelopmental disorder, MONDO:0700092
Review for gene: PRMT1 was set to GREEN
Added comment: PMID 39937650 reports four individuals from four unrelated families with heterozygous de novo missense PRMT1 variants presenting with neurodevelopmental disorder and dystonia. Functional studies demonstrated reduced protein stability and enzymatic activity, supporting a loss‑of‑function mechanism.
Sources: Literature