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Incidentalome v1.11 TTN Sarah Milton Source Victorian Clinical Genetics Services was removed from TTN.
Source Victorian Clinical Genetics Services was removed from TTN.
Source ClinGen was added to TTN.
Phenotypes for gene: TTN were changed from to Dilated cardiomyopathy 1G, MONDO:0011400; TTN-related myopathy, MONDO:0100175; Myopathy, myofibrillar, 9, with early respiratory failure, MONDO:0011362; Tibial muscular dystrophy, MONDO:0010870; TTN-related myopathy, dominant-negative TTNsv, MONDO:1060225
Incidentalome v1.10 TTN Sarah Milton changed review comment from: Summary of phenotypes as per Clingen:

Dilated cardiomyopathy 1G, MONDO:0011400
- Definitive association
- AD
- Molecular mechanism - truncating variants in exon with sufficiently high PSI, exact mechanism remains unclear - haploinsufficiency on it's own unlikely to be the only contributing factor, some papers postulate accumulation of truncated poison peptides contribute.

TTN-related myopathy, MONDO:0100175
- Definitive association
- AR
- Lumped: limb-girdle muscular dystrophy, (MIM #608807), centronuclear myopathy, Salih myopathy (MIM #611705), Emery-Dreifuss-like muscular dystrophy (not an OMIM entity), titinopathy with congenital contractures (not an OMIM entity), minicore myopathy (not an OMIM entity), distal titinopathy
- Presumably loss of function molecular mechanism, frameshift, deletion, missense, splice site variants have been called LP/P for this phenotype, PSI less relevant

Myopathy, myofibrillar, 9, with early respiratory failure MONDO:0011362
- Definitive association
- AD
- Missense variants in exon 344 A band

Tibial muscular dystrophy, MONDO:0010870
- Moderate association
- AD
- Variants in M line – missense and truncating exon 363

TTN-related myopathy, dominant-negative TTNsv, MONDO:1060225
- Moderate association
- AD
- Multiexon in frame deletion/CNV escape NMD, expressed
- Located in Z disk, A,I or A/M band deletions
- Phenotype ranges from arthrogryposis to adult onset distal myopathy

Hypertrophic cardiomyopathy, MONDO:0005045, AD
- Limited association
- AD

Arrhythmogenic right ventricular cardiomyopathy, MONDO:0016587
- Disputed association
- AD; to: Summary of phenotypes as per Clingen:

Dilated cardiomyopathy 1G, MONDO:0011400
- Definitive association
- AD
- Molecular mechanism - truncating variants in exon with sufficiently high PSI, exact mechanism remains unclear - haploinsufficiency on it's own unlikely to be the only contributing factor, some papers postulate accumulation of truncated poison peptides contribute.


TTN-related myopathy, MONDO:0100175
- Definitive association
- AR
- Lumped: limb-girdle muscular dystrophy, (MIM #608807), centronuclear myopathy, Salih myopathy (MIM #611705), Emery-Dreifuss-like muscular dystrophy (not an OMIM entity), titinopathy with congenital contractures (not an OMIM entity), minicore myopathy (not an OMIM entity), distal titinopathy
- Presumably loss of function molecular mechanism, frameshift, deletion, missense, splice site variants have been called LP/P for this phenotype, PSI less relevant


Myopathy, myofibrillar, 9, with early respiratory failure MONDO:0011362
- Definitive association
- AD
- Missense variants in exon 344 A band

Tibial muscular dystrophy, MONDO:0010870
- Moderate association
- AD
- Variants in M line – missense and truncating exon 363


TTN-related myopathy, dominant-negative TTNsv, MONDO:1060225
- Moderate association
- AD
- Multiexon in frame deletion/CNV escape NMD, expressed
- Located in Z disk, A,I or A/M band deletions
- Phenotype ranges from arthrogryposis to adult onset distal myopathy


Hypertrophic cardiomyopathy, MONDO:0005045, AD
- Limited association
- AD


Arrhythmogenic right ventricular cardiomyopathy, MONDO:0016587
- Disputed association
- AD
Incidentalome v1.10 TTN Sarah Milton reviewed gene: TTN: Rating: GREEN; Mode of pathogenicity: None; Publications: ; Phenotypes: ; Mode of inheritance: BOTH monoallelic and biallelic (but BIALLELIC mutations cause a more SEVERE disease form), autosomal or pseudoautosomal
Incidentalome v1.0 TTN Gene migrated from ENSG00000155657 to ENSG00000155657 (gene set migration)
Incidentalome v0.168 TTN Zornitza Stark Marked gene: TTN as ready
Incidentalome v0.168 TTN Zornitza Stark Gene: ttn has been classified as Green List (High Evidence).
Incidentalome v0.168 TTN Zornitza Stark Publications for gene: TTN were set to
Incidentalome v0.167 TTN Zornitza Stark Mode of inheritance for gene: TTN was changed from Unknown to BOTH monoallelic and biallelic, autosomal or pseudoautosomal
Incidentalome v0.166 TTN Zornitza Stark Tag cardiac tag was added to gene: TTN.
Incidentalome v0.166 TTN Zornitza Stark changed review comment from: DEFINITIVE by ClinGen.; to: DEFINITIVE by ClinGen for DCM and myopathy.

MODERATE for tibial muscular dystrophy and myofibrillar myopathy.

LIMITED for HCM and ARVC.
Incidentalome v0.166 TTN Zornitza Stark edited their review of gene: TTN: Changed phenotypes: Cardiomyopathy, dilated, 1G, MIM#604145, Cardiomyopathy, familial hypertrophic, 9, MIM# 613765, Tibial muscular dystrophy, tardive, MIM#600334, Salih myopathy (MIM#611705), Muscular dystrophy, limb-girdle, type 2J, 608807; Changed mode of inheritance: BOTH monoallelic and biallelic, autosomal or pseudoautosomal
Incidentalome v0.0 TTN Zornitza Stark gene: TTN was added
gene: TTN was added to Incidentalome_VCGS. Sources: Expert Review Green,Victorian Clinical Genetics Services
Mode of inheritance for gene: TTN was set to Unknown