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| Childhood onset dystonia, chorea or related movement disorder v8.2 | NTN1 |
Ida Ertmanska gene: NTN1 was added gene: NTN1 was added to Childhood onset dystonia, chorea or related movement disorder. Sources: Literature Q2_26_promote_green tags were added to gene: NTN1. Mode of inheritance for gene: NTN1 was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted Publications for gene: NTN1 were set to 28945198; 33472083 Phenotypes for gene: NTN1 were set to Mirror movements 4, OMIM:618264; mirror movements 4, MONDO:0032641 Review for gene: NTN1 was set to GREEN Added comment: PMID: 28945198 Meneret et al., 2017 NTN1 c.1801T>C/p.Cys601Arg variant of NTN1 segregated in a dominant manner with congenital mirror movements (CMM) in three affected members of a French family - though there were 2 asymptomatic carriers as well. Heterozygous variant c.1552_1554del/p.Ile518del in NTN1 segregated with CMM in all 3 affected members of a family from the United Kingdom. NTN1 variant c.1802G>C/p.Cys601Ser found in a sporadic case with CMM. PMID: 33472083 Pourchet et al., 2021 Mouse model - a conditional ntn1 knockout in the brainstem impairs midline crossing of corticospinal axons and leads to mirror movements. Sources: Literature |
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| Childhood onset dystonia, chorea or related movement disorder v7.20 | PTPN1 | Ida Ertmanska Added comment: Comment on list classification: There are 11 unrelated individuals reported with heterozygous PTPN1 variants, presenting in childhood with loss of previously acquired skills, spasticity/dystonia, cerebral atrophy, and white matter changes. There is a high degree of non-penetrance, as 9/12 reported patients have inherited the PTPN1 variants from their asymptomatic parents. Hence, this gene is recommended for Green with expert review to determine if the non-penetrance is in scope of testing. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Childhood onset dystonia, chorea or related movement disorder v7.19 | PTPN1 |
Ida Ertmanska gene: PTPN1 was added gene: PTPN1 was added to Childhood onset dystonia, chorea or related movement disorder. Sources: Literature Q1_26_promote_green tags were added to gene: PTPN1. Mode of inheritance for gene: PTPN1 was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted Publications for gene: PTPN1 were set to 10066179; 39986310 Phenotypes for gene: PTPN1 were set to Encephalopathy, HP:0001298; dystonia, early-onset, and/or spastic paraplegia, MONDO:0859215 Review for gene: PTPN1 was set to GREEN Added comment: PMID: 39986310 Zhu et al., 2025 Reported heterozygous PTPN1 variants in 12 patients from 11 families. 2/10 were canonical splice variants, 2 were missense variants, and 6 were STOP-gain. 3 cases were de novo, 9 individuals inherited the variant from an asymptomatic parent. Sequencing method: WES + Sanger. Phenotype: 12/12 individuals experienced subacute loss of skills (age range 15 months to 8 years) after initial normal development in 11 of 12 (one patient had mild motor delay); weakness (12/12), spasticity (initially manifesting as a hemiparesis in seven patients and then becoming bilateral) +/- dystonia, bulbar involvement (dysphagia and/or dysphasia) in 11/12 patients; absence of seizures. In 4/12 patients, fever and raised liver enzymes were noted around the time of presentation. Brain MRI findings: Cerebral atrophy (9/12 patients), non-specific white matter changes (8/12), intracranial calcification (2/12). In 8 cases, the brain abnormalities resolved.Some patients demonstrated stabilisation / recovery of neurological function in the absence of treatment, while in others the disease appeared to respond to immune suppression. Functional evidence: PMID: 10066179 Elchebly et al., 1999 - Ptpn1 knock-out (KO) mice are both viable and healthy, demonstrating enhanced insulin sensitivity and resistance to metabolic syndrome. PTPN1 is associated with {Insulin resistance, susceptibility to}, MIM:1258539 in OMIM. It is not associated with disease in ClinGen or Gene2Phenotype (resources accessed 24 Mar 2026). Probability of loss-of-function intolerance (pLI) score = 1.00 (predicted to be highly intolerant to LoF). Sources: Literature |
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| Childhood onset dystonia, chorea or related movement disorder v6.2 | NUS1 |
Achchuthan Shanmugasundram gene: NUS1 was added gene: NUS1 was added to Childhood onset dystonia, chorea or related movement disorder. Sources: Literature Mode of inheritance for gene: NUS1 was set to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted Publications for gene: NUS1 were set to 32334381; 32959737; 38291835 Phenotypes for gene: NUS1 were set to movement disorder, MONDO:0005395 Review for gene: NUS1 was set to GREEN Added comment: PMID:32334381 reported a patient with childhood onset static and focal upper limb dystonia and was diagnosed with a monoallelic NUS1 variant via WES. PMID:32959737 reported a 34-year-old patient with autosomal dominant NUS1 variant and with a prominent and progressive generalised dystonia. PMID:38291835 reported five unrelated patients ranging from 13 to 53 years of age with monoallelic NUS1 variant. They presented with movement disorder and its onset ranged from birth to 13 years of age. Three of them had dystonia. Sources: Literature |
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| Childhood onset dystonia, chorea or related movement disorder v4.10 | DCC |
Achchuthan Shanmugasundram changed review comment from: PMID:20431009 reported the identification of a splice site variant in DCC gene in a 4-generation French Canadian family and 1 bp insertion in a five-generation large Iranian family with congenital mirror movements. Incomplete penetrance was observed in these two families (PMIDs: 19127048 & 19720981). PMID:21242494 reported the identification of a truncating variant in DCC gene in a 3-generation Italian family with in which 4 individuals had mirror movements of the arms and hands with onset in infancy or early childhood. PMID:28250454 reported the identification of heterozygous DCC variants in individuals from four unrelated multigenerational families with congenital mirror movements and/or agenesis of the corpus callosum. PMID:31697046 reported the identification of heterozygous frameshift variant in five members of an Ethiopian Jewish family. Monoallelic variants of DCC gene has been associated with relevant phenotypes in OMIM (MIM #157600), but not yet in Gene2Phenotype.; to: PMID:20431009 reported the identification of a splice site variant in DCC gene in a 4-generation French Canadian family and 1 bp insertion in a five-generation large Iranian family with congenital mirror movements. Incomplete penetrance was observed in these two families (PMIDs: 19127048 & 19720981). PMID:21242494 reported the identification of a truncating variant in DCC gene in a 3-generation Italian family with in which 4 individuals had mirror movements of the arms and hands with onset in infancy or early childhood. PMID:28250454 reported the identification of heterozygous DCC variants in individuals from four unrelated multigenerational families with congenital mirror movements and/or agenesis of the corpus callosum. PMID:31697046 reported the identification of heterozygous frameshift variant in five members of an Ethiopian Jewish family, of which four members were symptomatic, showing reduced penetrance of the variant. Two pregnancies in this family were terminated due to prenatal detection of agenesis of the corpus callosum and dilated lateral ventricles. Only one of these foetuses were tested and carried the variant. Monoallelic variants of DCC gene has been associated with relevant phenotypes in OMIM (MIM #157600), but not yet in Gene2Phenotype. |
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| Childhood onset dystonia, chorea or related movement disorder v3.33 | SLC18A2 |
Achchuthan Shanmugasundram changed review comment from: PMID:23363473 - Eight children from an extended consanguineous Saudi Arabian family had a complex neurological disorder apparent since infancy. This disorder is characterised by abnormal movements, including parkinsonism, dystonia, and poor fine motor skills, as well as autonomic dysfunction, including abnormal sweating, cold extremities, and poor sleep. They were identified with a homozygous SLC18A2 variant (p.Pro387Leu). Functional evaluation showed that protein harbouring this variant has dramatically reduced activity than wild type protein, suggesting severe, but not complete loss of function as mechanism of action. PMID:26497564 - Two male siblings from a consanguineous fancy was reported with a disorder comprising truncal hypotonia, a general paucity of movements, extrapyramidal signs and cognitive delay. They were identified with a homozygous SLC18A2 variant (p.Pro237His).; to: PMID:23363473 - Eight children from an extended consanguineous Saudi Arabian family had a complex neurological disorder apparent since infancy. This disorder is characterised by abnormal movements, including parkinsonism, dystonia, and poor fine motor skills, as well as autonomic dysfunction, including abnormal sweating, cold extremities, and poor sleep. They were identified with a homozygous SLC18A2 variant (p.Pro387Leu). Functional evaluation showed that protein harbouring this variant has dramatically reduced activity than wild type protein, suggesting severe, but not complete loss of function as mechanism of action. PMID:26497564 - Two male siblings from a consanguineous family was reported with a disorder comprising truncal hypotonia, a general paucity of movements, extrapyramidal signs and cognitive delay. They were identified with a homozygous SLC18A2 variant (p.Pro237His). PMID:31240161 - A child from a consanguineous family presented with hypotonia, mental disability, epilepsy, uncontrolled movements, and gastrointestinal problems and was identified with a homozygous SLC18A2 variant (p.Pro316Ala). PMID:34078222 - A 6-month-old male infant who presented with developmental delay and suspected cerebral palsy was also diagnosed with infantile parkinsonism-dystonia-2 and was identified with the homozygous variant (p.Pro237His) reported in PMID:26497564. This gene has been associated with relevant phenotypes in OMIM (PMID:618049), but not in Gene2Phenotype. |
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| Childhood onset dystonia, chorea or related movement disorder v3.33 | SLC18A2 |
Achchuthan Shanmugasundram commented on gene: SLC18A2: PMID:23363473 - Eight children from an extended consanguineous Saudi Arabian family had a complex neurological disorder apparent since infancy. This disorder is characterised by abnormal movements, including parkinsonism, dystonia, and poor fine motor skills, as well as autonomic dysfunction, including abnormal sweating, cold extremities, and poor sleep. They were identified with a homozygous SLC18A2 variant (p.Pro387Leu). Functional evaluation showed that protein harbouring this variant has dramatically reduced activity than wild type protein, suggesting severe, but not complete loss of function as mechanism of action. PMID:26497564 - Two male siblings from a consanguineous fancy was reported with a disorder comprising truncal hypotonia, a general paucity of movements, extrapyramidal signs and cognitive delay. They were identified with a homozygous SLC18A2 variant (p.Pro237His). |
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| Childhood onset dystonia, chorea or related movement disorder v1.63 | DDC | Arina Puzriakova Phenotypes for gene: DDC were changed from Aromatic L-amino acid decarboxylase deficiency, 608643; Dystonia to Aromatic L-amino acid decarboxylase deficiency, OMIM:608643; Aromatic L-amino acid decarboxylase deficiency, MONDO:0012084 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Childhood onset dystonia, chorea or related movement disorder v1.3 | DDC | Lothar Schlueter reviewed gene: DDC: Rating: GREEN; Mode of pathogenicity: None; Publications: 28100251, 30952622; Phenotypes: Aromatic L-amino acid decarboxylase deficiency 608643, floppy child, dystonia, hypotonia, developmental delay, oculogyric crisis; Mode of inheritance: BIALLELIC, autosomal or pseudoautosomal | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Childhood onset dystonia, chorea or related movement disorder v0.7 | NPHP3 |
Ellen McDonagh Source PanelApp was added to NPHP3. Mode of inheritance for gene NPHP3 was changed from to BIALLELIC, autosomal or pseudoautosomal Added phenotypes Nephronophthisis 3, 604387; Senior-Loken syndrome; Renal-hepatic-pancreatic dysplasia 1, 208540; Nephronophthisis; Meckel syndrome 7, 267010; Renal-hepatic-pancreatic dysplasia for gene: NPHP3 |
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| Childhood onset dystonia, chorea or related movement disorder v0.7 | DDC |
Ellen McDonagh Source PanelApp was added to DDC. Mode of inheritance for gene DDC was changed from to BIALLELIC, autosomal or pseudoautosomal Added phenotypes Aromatic L-amino acid decarboxylase deficiency, 608643; Dystonia for gene: DDC Publications for gene DDC were changed from to 27830117; 27604308; 24816252 |
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| Childhood onset dystonia, chorea or related movement disorder v0.1 | PDX1 |
Ellen McDonagh gene: PDX1 was added gene: PDX1 was added to Childhood onset dystonia or chorea or related movement disorder. Sources: South West GLH Mode of inheritance for gene: PDX1 was set to BIALLELIC, autosomal or pseudoautosomal Phenotypes for gene: PDX1 were set to Pancreatic agenesis 1 260370; MODY, type IV 606392 |
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| Childhood onset dystonia, chorea or related movement disorder v0.1 | ARSA |
Ellen McDonagh Source South West GLH was added to ARSA. Mode of inheritance for gene ARSA was changed from to BIALLELIC, autosomal or pseudoautosomal Added phenotypes Metachromatic leukodystrophy, 250100 for gene: ARSA |
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| Childhood onset dystonia, chorea or related movement disorder v0.0 | ATIC |
Ellen McDonagh gene: ATIC was added gene: ATIC was added to Childhood onset dystonia or chorea or related movement disorder. Sources: London North GLH,Expert Review Red Mode of inheritance for gene: ATIC was set to |
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