Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AAA domain-containing 3A (ATAD3A) is a member of the AAA-ATPase family. Three forms of ATAD3 have been identified: ATAD3A, ATAD3B and ATAD3C. In this study, we examined the type and expression of ATAD3 in lung adenocarcinoma (LADC). Expression of ATAD3A was detected by reverse transcription-polymerase chain reaction, immunoblotting, immunohistochemistry and confocal immunofluorescent microscopy. Our results show that ATAD3A is the major form expressed in LADC. Silencing of ATAD3A expression increased mitochondrial fragmentation and cisplatin sensitivity. Serum deprivation increased ATAD3A expression and drug resistance. These results suggest that ATAD3A could be an anti-apoptotic marker in LADC.
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PMID:ATPase family AAA domain-containing 3A is a novel anti-apoptotic factor in lung adenocarcinoma cells. 2033 22

ATAD3 (ATPase family AAA domain-containing protein 3) is a mitochondrial membrane bound ATPase whose function has not yet been discovered but its role is essential for the embryonic development. The ATAD3 gene exists since the pluri-cellular organisms with specialized tissues and remains unique until vertebrates. In primates and humans, two other genes have appeared (called ATAD3B and ATAD3C versus ATAD3A the ancestral gene). ATAD3 knock down in different non-transformed cell lines is associated with drastic changes in the mitochondrial network, inhibition of proliferation and modification of the functional interactions between mitochondria and endoplasmic reticulum. However, the analysis of the functions of ATAD3A and ATAD3B in different human cancer cell lines shows on the contrary that they can have anti-proliferative effects and induce chemoresistant properties. 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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PMID:[ATAD3, a vital membrane-bound mitochondrial ATPase involved in tumor progression]. 2219 48

ATAD3 (ATPase family AAA Domain-containing protein 3) is a mitochondrial membrane bound ATPase whose function has not yet been discovered but its role is essential for embryonic development. The ATAD3 gene has existed since the pluri-cellular organisms with specialized tissues and has remained unique until vertebrates. In primates and human, two other genes have appeared (called ATAD3B and ATAD3C versus ATAD3A the ancestral gene). ATAD3 knock-down in different non-transformed cell lines is associated with drastic changes in the mitochondrial network, inhibition of proliferation and modification of the functional interactions between mitochondria and endoplasmic reticulum. However, the analysis of the cellular properties of ATAD3A and ATAD3B in different human cancer cell lines shows on the contrary that they can present anti-proliferative and chemoresistant properties. 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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PMID:ATAD3, a vital membrane bound mitochondrial ATPase involved in tumor progression. 2231 59

ATPase family AAA-domain containing protein 3A (ATAD3A) is a nuclear-encoded mitochondrial membrane protein implicated in mitochondrial dynamics, nucleoid organization, protein translation, cell growth, and cholesterol metabolism. We identified a recurrent de novo ATAD3A c.1582C>T (p.Arg528Trp) variant by whole-exome sequencing (WES) in five unrelated individuals with a core phenotype of global developmental delay, hypotonia, optic atrophy, axonal neuropathy, and hypertrophic cardiomyopathy. We also describe two families with biallelic variants in ATAD3A, including a homozygous variant in two siblings, and biallelic ATAD3A deletions mediated by nonallelic homologous recombination (NAHR) between ATAD3A and gene family members ATAD3B and ATAD3C. Tissue-specific overexpression of borR534W, the Drosophila mutation homologous to the human c.1582C>T (p.Arg528Trp) variant, resulted in a dramatic decrease in mitochondrial content, aberrant mitochondrial morphology, and increased autophagy. Homozygous null bor larvae showed a significant decrease of mitochondria, while overexpression of borWT resulted in larger, elongated mitochondria. Finally, fibroblasts of an affected individual exhibited increased mitophagy. We conclude that the p.Arg528Trp variant functions through a dominant-negative mechanism that results in small mitochondria that trigger mitophagy, resulting in a reduction in mitochondrial content. ATAD3A variation represents an additional link between mitochondrial dynamics and recognizable neurological syndromes, as seen with MFN2, OPA1, DNM1L, and STAT2 mutations.
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PMID:Recurrent De Novo and Biallelic Variation of ATAD3A, Encoding a Mitochondrial Membrane Protein, Results in Distinct Neurological Syndromes. 2764 Mar 7

ATPase family AAA domain-containing protein 3 (ATAD3) is a mitochondrial membrane-bound ATPase that is involved in a number of cellular processes and is linked with the progression of various types of malignancies. In primates, the ATAD3 gene cluster contains ATAD3A, ATAD3B and ATAD3C. The association between ATAD3 gene cluster expression and hepatocellular carcinoma (HCC) remains unknown. Therefore, the present study examined the prognostic significance of ATAD3 gene cluster expression in patients with HCC. Box plots of expression differences between HCC and normal liver tissues for the ATAD3 family genes were obtained from the online tool Gene Expression Profiling Interactive Analysis. Data from 360 patients with HCC in The Cancer Genome Atlas database were analyzed. Kaplan-Meier analysis and a Cox regression model were used to calculate median survival time (MST) and overall survival (OS). ATAD3A and ATAD3B expression levels were higher in HCC compared with normal liver tissues (P<0.05). However, ATAD3C expression was significantly decreased in HCC tissues compared with normal liver tissues (P<0.05). ATAD3A [P=0.017, hazard ratio (HR)=1.54, 95% confidence interval (CI)=1.08-2.20; adjusted P=0.032; adjusted HR=1.52; 95% CI=1.04-2.22] and ATAD3B (P=0.026, HR=1.49, 95% CI=1.05-2.13; adjusted P=0.031, adjusted HR=1.52, 95% CI=1.04-2.21) expression levels were significantly associated with OS. A joint-effects analysis revealed that patients with high ATAD3A and ATAD3B expression had reduced OS rates compared with patients with low ATAD3A and ATAD3B expression (P=0.007, HR=1.77, 95% CI=1.16-2.69; adjusted P=0.013, adjusted HR=1.76, 95% CI=1.13-2.75). In conclusion, ATAD3A and ATAD3B may serve as potential prognostic biomarkers for patients with HCC.
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PMID:Prognostic value of ATAD3 gene cluster expression in hepatocellular carcinoma. 3142 90