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Skeletal dysplasia v0.405 ATR Chirag Patel Marked gene: ATR as ready
Skeletal dysplasia v0.405 ATR Chirag Patel Gene: atr has been classified as Green List (High Evidence).
Skeletal dysplasia v0.404 Chirag Patel Copied gene ATR from panel Mendeliome
Skeletal dysplasia v0.404 ATR Chirag Patel gene: ATR was added
gene: ATR was added to Skeletal dysplasia. Sources: Expert Review Green,Victorian Clinical Genetics Services
Mode of inheritance for gene: ATR was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: ATR were set to 12640452; 19620979; 30199583; 23111928
Phenotypes for gene: ATR were set to Seckel syndrome 1, MIM# 210600
Skeletal dysplasia v0.372 HOXD13_SPD1_GCG Bryony Thompson STR: HOXD13_SPD1_GCG was added
STR: HOXD13_SPD1_GCG was added to Skeletal dysplasia. Sources: Expert Review Green,Expert list
paediatric-onset tags were added to STR: HOXD13_SPD1_GCG.
Mode of inheritance for STR: HOXD13_SPD1_GCG was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted
Publications for STR: HOXD13_SPD1_GCG were set to 8817328; 33811808; 33533119
Phenotypes for STR: HOXD13_SPD1_GCG were set to Synpolydactyly 1 MIM#186000
Skeletal dysplasia v0.371 HOXA13_HFGS_GCN3 Bryony Thompson STR: HOXA13_HFGS_GCN3 was added
STR: HOXA13_HFGS_GCN3 was added to Skeletal dysplasia. Sources: Expert Review Green,Expert list
paediatric-onset tags were added to STR: HOXA13_HFGS_GCN3.
Mode of inheritance for STR: HOXA13_HFGS_GCN3 was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted
Publications for STR: HOXA13_HFGS_GCN3 were set to 10839976; 12073020; 33811808
Phenotypes for STR: HOXA13_HFGS_GCN3 were set to Hand-foot-uterus syndrome MIM#140000
Skeletal dysplasia v0.370 COMP_MEDPSACH_GAC Bryony Thompson STR: COMP_MEDPSACH_GAC was added
STR: COMP_MEDPSACH_GAC was added to Skeletal dysplasia. Sources: Expert Review Green,Literature
paediatric-onset tags were added to STR: COMP_MEDPSACH_GAC.
Mode of inheritance for STR: COMP_MEDPSACH_GAC was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted
Publications for STR: COMP_MEDPSACH_GAC were set to 9887340; 17133256; 21922596
Phenotypes for STR: COMP_MEDPSACH_GAC were set to Epiphyseal dysplasia, multiple, 1 MIM#132400; Pseudoachondroplasia MIM#177170
Skeletal dysplasia v0.365 ISCA-37418-Loss Zornitza Stark Phenotypes for Region: ISCA-37418-Loss were changed from Potocki-Lupski syndrome; Smith-Magenis syndrome; moderate intellectual disability, delayed speech and language skills, distinctive facial features, sleep disturbances, and behavioral problems; 182290; Structural cardiovascular anomalies (dilated aortic root, bicommissural aortic valve, atrial/ventricular and septal defects) and sleep disturbance; hypotonia, failure to thrive, mental retardation, pervasive developmental disorders, congenital anomalies; Dental abnormalities; hypotonia, poor feeding, failure to thrive, developmental delay particularly cognitive and language deficity, mild-moderate intellectual deficit, and neuropsychiatric disorders to Smith-Magenis syndrome, MIM#182290
Skeletal dysplasia v0.288 BMP5 Zornitza Stark Phenotypes for gene: BMP5 were changed from Skeletal dysostosis and atrioventricular septal defect to Skeletal dysplasia, MONDO:0018230, BMP5-related; Skeletal dysostosis and atrioventricular septal defect
Skeletal dysplasia v0.287 BMP5 Chirag Patel changed review comment from: 1 patient with skeletal dysostosis, atrioventricular septal defect, hypermobility, laryngo-tracheo-bronchomalacia and dysmorphic features (malar hypoplasia, short palpebral fissures, short nose, low nasal bridge, anteverted nares, long philtrum, small ears with abnormally folded antihelix). Skeletal survey showed mild thoracolumbar scoliosis, four sacral segments, absent ossification of the inferior pubic rami, and patellar aplasia. Trio WGS identified compound heterozygous loss of function variants in BMP5 (c.88_89del, p.(Gly30Argfs*11) and c.1104+2del, p.(?). Abnormal splicing was proven on the suspected splice variant using maternal fibroblasts. BMP5 expression is confined to specific parts of the skeleton and cartilage in mice and is tightly regulated by different enhancers. Previous studies of chicken embryonic heart development showed BMP5 expression in the endoderm underlying the precardiac mesoderm, the myocardium of the atrioventricular canal and outflow tract regions. Other bone morphogenetic proteins are linked to several genetic skeletal disorders.
Sources: Literature; to: 1 patient with skeletal dysostosis, atrioventricular septal defect, hypermobility, laryngo-tracheo-bronchomalacia and dysmorphic features (malar hypoplasia, short palpebral fissures, short nose, low nasal bridge, anteverted nares, long philtrum, small ears with abnormally folded antihelix). Skeletal survey showed mild thoracolumbar scoliosis, four sacral segments, absent ossification of the inferior pubic rami, and patellar aplasia. Trio WGS identified compound heterozygous loss of function variants in BMP5 (c.88_89del, p.(Gly30Argfs*11) and c.1104+2del, p.(?). Abnormal splicing was proven on the suspected splice variant using maternal fibroblasts. BMP5 expression is confined to specific parts of the skeleton and cartilage in mice and is tightly regulated by different enhancers. Previous studies of chicken embryonic heart development showed BMP5 expression in the endoderm underlying the precardiac mesoderm, the myocardium of the atrioventricular canal and outflow tract regions. Other bone morphogenetic proteins are linked to several genetic skeletal disorders.
Sources: Literature
Skeletal dysplasia v0.287 BMP5 Chirag Patel gene: BMP5 was added
gene: BMP5 was added to Skeletal dysplasia. Sources: Literature
Mode of inheritance for gene: BMP5 was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: BMP5 were set to PMID: 39239663
Phenotypes for gene: BMP5 were set to Skeletal dysostosis and atrioventricular septal defect
Review for gene: BMP5 was set to RED
Added comment: 1 patient with skeletal dysostosis, atrioventricular septal defect, hypermobility, laryngo-tracheo-bronchomalacia and dysmorphic features (malar hypoplasia, short palpebral fissures, short nose, low nasal bridge, anteverted nares, long philtrum, small ears with abnormally folded antihelix). Skeletal survey showed mild thoracolumbar scoliosis, four sacral segments, absent ossification of the inferior pubic rami, and patellar aplasia. Trio WGS identified compound heterozygous loss of function variants in BMP5 (c.88_89del, p.(Gly30Argfs*11) and c.1104+2del, p.(?). Abnormal splicing was proven on the suspected splice variant using maternal fibroblasts. BMP5 expression is confined to specific parts of the skeleton and cartilage in mice and is tightly regulated by different enhancers. Previous studies of chicken embryonic heart development showed BMP5 expression in the endoderm underlying the precardiac mesoderm, the myocardium of the atrioventricular canal and outflow tract regions. Other bone morphogenetic proteins are linked to several genetic skeletal disorders.
Sources: Literature
Skeletal dysplasia v0.109 GSC Zornitza Stark Phenotypes for gene: GSC were changed from Foundation Trust) Short stature, auditory canal atresia, mandibular hypoplasia, skeletal abnormalities 602471; Foundation Trust) Short stature, auditory canal atresia, mandibular hypoplasia, skeletal abnormalities 602471 to Short stature, auditory canal atresia, mandibular hypoplasia, skeletal abnormalities, MIM# 602471
Skeletal dysplasia v0.107 GSC Zornitza Stark reviewed gene: GSC: Rating: GREEN; Mode of pathogenicity: None; Publications: 24290375; Phenotypes: Short stature, auditory canal atresia, mandibular hypoplasia, skeletal abnormalities, MIM# 602471; Mode of inheritance: BIALLELIC, autosomal or pseudoautosomal
Skeletal dysplasia v0.70 FBLN1 Zornitza Stark changed review comment from: Single association to disease published in literature - reciprocal translocation region t(12;22)(p11.2;q13.3) found in the family. The breakpoint was located in the intron between the last 2 exons of the FBLN1-D splice variant isoform (exons 19-20). Additional pathogenic missense in ClinVar, but a research finding and inherited; to: Single association of mono-allelic variants to disease published in literature - reciprocal translocation region t(12;22)(p11.2;q13.3) found in the family. The breakpoint was located in the intron between the last 2 exons of the FBLN1-D splice variant isoform (exons 19-20). Additional pathogenic missense in ClinVar, but a research finding and inherited.

Single report of homozygous missense in a family with syndactyly, undescended testes, delayed motor milestones, mental retardation and signs of brain atrophy.
Skeletal dysplasia v0.0 ISCA-37418-Loss Zornitza Stark Region: ISCA-37418-Loss was added
Region: ISCA-37418-Loss was added to Skeletal dysplasia. Sources: NHS GMS,ClinGen,Expert Review Green
Mode of inheritance for Region: ISCA-37418-Loss was set to MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown
Phenotypes for Region: ISCA-37418-Loss were set to Potocki-Lupski syndrome; Smith-Magenis syndrome; moderate intellectual disability, delayed speech and language skills, distinctive facial features, sleep disturbances, and behavioral problems; 182290; Structural cardiovascular anomalies (dilated aortic root, bicommissural aortic valve, atrial/ventricular and septal defects) and sleep disturbance; hypotonia, failure to thrive, mental retardation, pervasive developmental disorders, congenital anomalies; Dental abnormalities; hypotonia, poor feeding, failure to thrive, developmental delay particularly cognitive and language deficity, mild-moderate intellectual deficit, and neuropsychiatric disorders
Skeletal dysplasia v0.0 OAT Zornitza Stark gene: OAT was added
gene: OAT was added to Skeletal dysplasia. Sources: Expert Review Red,NHS GMS
Mode of inheritance for gene: OAT was set to
Phenotypes for gene: OAT were set to Gyrate atrophy of choroid and retina with or without ornithinemia 258870
Skeletal dysplasia v0.0 TRPV4 Zornitza Stark gene: TRPV4 was added
gene: TRPV4 was added to Skeletal dysplasia. Sources: NHS GMS,Expert Review Green
Mode of inheritance for gene: TRPV4 was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted
Phenotypes for gene: TRPV4 were set to Digital arthropathy-brachydactyly, familial 606835; Parastremmatic dwarfism 168400; Scapuloperoneal spinal muscular atrophy 181405; SED, Maroteaux type 184095; Brachyolmia type 3 113500; Hereditary motor and sensory neuropathy, type IIc 606071; Spinal muscular atrophy, distal, congenital nonprogressive 600175; Metatropic dysplasia 156530; Spondylometaphyseal dysplasia, Kozlowski type 184252
Skeletal dysplasia v0.0 NBAS Zornitza Stark gene: NBAS was added
gene: NBAS was added to Skeletal dysplasia. Sources: Radboud University Medical Center, Nijmegen,Expert Review Green
Mode of inheritance for gene: NBAS was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: NBAS were set to 27789416
Phenotypes for gene: NBAS were set to Short stature, optic nerve atrophy, and Pelger-Huet anomaly, 614800
Skeletal dysplasia v0.0 GSC Zornitza Stark gene: GSC was added
gene: GSC was added to Skeletal dysplasia. Sources: NHS GMS,Radboud University Medical Center, Nijmegen,Expert list,Expert Review Green
Mode of inheritance for gene: GSC was set to BIALLELIC, autosomal or pseudoautosomal
Phenotypes for gene: GSC were set to Foundation Trust) Short stature, auditory canal atresia, mandibular hypoplasia, skeletal abnormalities 602471; Foundation Trust) Short stature, auditory canal atresia, mandibular hypoplasia, skeletal abnormalities 602471
Skeletal dysplasia v0.0 ATP7A Zornitza Stark gene: ATP7A was added
gene: ATP7A was added to Skeletal dysplasia. Sources: Emory Genetics Laboratory,Expert list,NHS GMS,Radboud University Medical Center, Nijmegen,Expert Review Green,UKGTN
Mode of inheritance for gene: ATP7A was set to X-LINKED: hemizygous mutation in males, biallelic mutations in females
Phenotypes for gene: ATP7A were set to Spinal muscular atrophy, distal, 300489; Menkes disease 309400; Occipital horn syndrome 304150