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ATAD3A region deletions cause cerebellar dysfunction associated with altered mitochondrial DNA and cholesterol metabolism.
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identification of a recurrent de novo ATAD3A c.1582C>T (p.Arg528Trp) variant by whole-exome sequencing in five unrelated individuals with a core phenotype of global developmental delay, hypotonia, optic atrophy, axonal neuropathy, and hypertrophic cardiomyopathy
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Mutations in ATAD3A can thus be dominantly inherited and underlie variable neurological phenotypes, including hereditary spastic paraplegia with intrafamiliar variability. This finding extends the group of mitochondrial inner membrane AAA proteins associated with spasticity.
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stabilization of WASF3 function occurs through its interaction with ATAD3A and GRP78, which may provide a bridge between the ER and mitochondria, allowing communication between the two organelles
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These results demonstrate that ATAD3-mediated mitochondrial membrane formation participates in the optimal transfer of cholesterol from the endoplasmic reticulum into mitochondria.
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High ATAD3A expression correlates with radioresistance in glioblastoma.
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exploring ATAD3 mRNA expression, we confirmed the existence of an alternative splicing in rodent and of several mRNA isoforms in human
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ATAD3B is a negative regulator of ATAD3A and may function as an adaptor of mitochondrial homeostasis and metabolism in human pluripotent embryonic stem cells and cancer cells.
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Engineered a high copy strain expressing human ATAD3A-Myc-HIS at a relative high level (2.5mg/l of yeast culture)without significantly affecting yeast growth.Urea-denaturated ATAD3A-Myc-HIS bound to agarose-nickel beads and could be renatured and eluted.
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ATAD3 may be implicated in an unknown but essential and growth-linked mitochondrial function existing since pluri-cellular organization and involved in tumorigenesis.
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Results show that HPV infection correlates with increased ATAD3A expression and drug resistance in uterine cervical cancer.
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ATAD3 may therefore be implicated in an unknown but essential and growth-linked mitochondrial function existing since pluri-cellular -organization and involved in tumorigenesis.
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silencing of ATAD3A expression reduced PSA secretion and cisplatin resistance, suggesting that ATAD3A was associated with PSA secretion and drug resistance in PCa.
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gene expression in lung adenocarcinoma correlates with drug resistance and poor prognosis
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The N-terminal part of ATAD3A is outside the inner mitochondrial membrane and that the C-terminal part is inside the matrix.
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Data show that ATAD3A is a calcium-dependent S100B target protein in oligodendrocyte progenitor cells and suggest that S100B could assist the newly synthesized ATAD3A protein in proper folding and subcellular localization.
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Data show that the mitochondrial AAA(+) ATPase protein ATAD3A is involved in dynamic interactions between components of the outer and inner mitochondrial membranes which control a number of critical mitochondrial functions.
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Results suggest that mitochondrial DNA displacement loops serve to recruit ATAD3 protein for the purpose of forming or segregating mitochondrial nucleoids.
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We also have shown that the loss of ATAD 3A/3B may be involved in the transformation pathway and the chemosensitivity of oligodendrogliomas.
