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Mendeliome v1.4850 CHCHD4 Zornitza Stark Marked gene: CHCHD4 as ready
Mendeliome v1.4850 CHCHD4 Zornitza Stark Gene: chchd4 has been classified as Red List (Low Evidence).
Mendeliome v1.4850 CHCHD4 Zornitza Stark Phenotypes for gene: CHCHD4 were changed from IUGR; lactic acidosis; liver disease; hypoglycaemia; dystonia; hypertonia; regression to Mitochondrial disease, MONDO:0044970, CHCHD4-related
Mendeliome v1.4849 CHCHD4 Zornitza Stark Classified gene: CHCHD4 as Red List (low evidence)
Mendeliome v1.4849 CHCHD4 Zornitza Stark Gene: chchd4 has been classified as Red List (Low Evidence).
Mendeliome v1.4848 CHCHD4 Zornitza Stark reviewed gene: CHCHD4: Rating: RED; Mode of pathogenicity: None; Publications: ; Phenotypes: Mitochondrial disease, MONDO:0044970, CHCHD4-related; Mode of inheritance: BIALLELIC, autosomal or pseudoautosomal
Mendeliome v1.4844 CHCHD4 Isabelle Adant gene: CHCHD4 was added
gene: CHCHD4 was added to Mendeliome. Sources: Literature
Mode of inheritance for gene: CHCHD4 was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: CHCHD4 were set to 41981912; 26004228
Phenotypes for gene: CHCHD4 were set to IUGR; lactic acidosis; liver disease; hypoglycaemia; dystonia; hypertonia; regression
Review for gene: CHCHD4 was set to RED
Added comment: 41981912
1 individual compound heterozygous for missense variant and large deletion
encompassing the whole CHCHD4 gene (and adjacent gene) of biparental inheritance,
presenting with IUGR, liver dysfunction, lactic acidosis and short-fasting
hypoglycaemia, developmental delay and regression, hypertonia and
dystonia. Early demise at 11months.
Minimal supporting biochemical evidence (protein expression studies) in patient-derived fibroblasts.

26004228 : Chchd4−/− mouse model
Biallelic Chchd4 in mouse embryos causes a developmental arrest coupled
with embryonic lethality at the onset of gastrulation. The developmental
retardation of Chchd4−/− embryos was accompanied by a major defect in the
expression of respiratory chain complex I subunit CI-20.
Sources: Literature