| Name | distal membrane arm assembly component 2 like |
| Description | This gene encodes a subunit of mitochondrial ATP synthase. Mitochondrial ATP synthase catalyzes ATP synthesis, utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. ATP synthase is composed of two linked multi-subunit complexes: the soluble catalytic core, F1, and the membrane-spanning component, Fo, comprising the proton channel. This gene encodes the subunit s, also known as factor B, of the proton channel. This subunit is necessary for the energy transduction activity of the ATP synthase complexes. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008] |
| Summary |
{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Although none of the studies explicitly examined DMAC2L, a synthesis of the findings across these diverse investigations suggests that factors related to mitochondrial energy production and protein complex assembly play central roles in cellular homeostasis and disease. In particular, several reports have underscored how finely tuned assembly and function of the mitochondrial ATP‐synthase machinery—and its regulatory subunits—directly influence ATP generation, cellular oxidative status, and downstream metabolic reprogramming. For example, detailed structural and functional analyses of coupling factor B and ATP‐synthase subunits reveal that alterations in these molecular complexes affect mitochondrial morphology, energy transfer efficiency, and the capacity to respond to metabolic stress signals, which in turn modulate cell proliferation, apoptosis, and tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In parallel, studies in models of malignant transformation and ethanol‐exposed neurons indicate that changes in mitochondrial oxidation and ATP synthase gene expression are closely linked to shifts in metabolic flux and stress vulnerability."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In clinical settings—as evidenced by analyses in renal cell carcinoma and biotherapeutic production systems—dysregulation of ATP synthase components correlates with altered energy homeostasis and cellular adaptation, underscoring the broader impact of mitochondrial proteostasis on disease outcomes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " \n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n By analogy, DMAC2L may serve a similar role as a regulatory or scaffolding factor that contributes to the proper assembly, stability, or function of the mitochondrial ATP‐synthase complex. In this context, DMAC2L would be expected to participate in the modulation of oxidative phosphorylation, ensuring adequate ATP production under both physiological and stressed conditions. Such a role would be consistent with effects on cellular energy balance, adaptation to metabolic challenges, and even the progression of disease processes—ranging from cancer to neurodegeneration—that depend on precise mitochondrial performance. Overall, these integrated observations point to a potential function for DMAC2L in maintaining mitochondrial bioenergetic integrity and, thereby, influencing key cell fate decisions.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Grigory I Belogrudov "}, {"type": "b", "children": [{"type": "t", "text": "Recent advances in structure-functional studies of mitochondrial factor B."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Bioenerg Biomembr (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s10863-009-9210-1"}], "href": "https://doi.org/10.1007/s10863-009-9210-1"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19377834"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19377834"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Fengyun Wen, Bin Li, Chunyan Huang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "MiR-34a is Involved in the Decrease of ATP Contents Induced by Resistin Through Target on ATP5S in HepG2 Cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Genet (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s10528-015-9693-x"}], "href": "https://doi.org/10.1007/s10528-015-9693-x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26385595"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26385595"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Giuseppe Lonetto, Gabriela Koifman, Alon Silberman, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mutant p53-dependent mitochondrial metabolic alterations in a mesenchymal stem cell-based model of progressive malignancy."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Differ (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41418-018-0227-z"}], "href": "https://doi.org/10.1038/s41418-018-0227-z"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30413783"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30413783"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Ana Spataru, Diana Le Duc, Leon Zagrean, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Ethanol exposed maturing rat cerebellar granule cells show impaired energy metabolism and increased cell death after oxygen-glucose deprivation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neural Regen Res (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.4103/1673-5374.245474"}], "href": "https://doi.org/10.4103/1673-5374.245474"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30539817"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30539817"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Maria Brüggemann, Arabella Gromes, Mirjam Poss, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Systematic Analysis of the Expression of the Mitochondrial ATP Synthase (Complex V) Subunits in Clear Cell Renal Cell Carcinoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Transl Oncol (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.tranon.2017.06.002"}], "href": "https://doi.org/10.1016/j.tranon.2017.06.002"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28672194"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28672194"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Pao-Chun Lin, Ren Liu, Krista Alvin, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Improving Antibody Production in Stably Transfected CHO Cells by CRISPR-Cas9-Mediated Inactivation of Genes Identified in a Large-Scale Screen with Chinese Hamster-Specific siRNAs."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biotechnol J (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/biot.202000267"}], "href": "https://doi.org/10.1002/biot.202000267"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33079482"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33079482"}]}]}]}
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| NCBI Gene ID | 27109 |
| API | |
| Download Associations | |
| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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DMAC2L has 2,371 functional associations with biological entities spanning 6 categories (chemical, functional term, phrase or reference, disease, phenotype or trait, cell line, cell type or tissue, gene, protein or microRNA, sequence feature) extracted from 43 datasets.
Click the + buttons to view associations for DMAC2L from the datasets below.
If available, associations are ranked by standardized value
| Dataset | Summary | |
|---|---|---|
| Allen Brain Atlas Aging Dementia and Traumatic Brain Injury Tissue Sample Gene Expression Profiles | tissue samples with high or low expression of DMAC2L gene relative to other tissue samples from the Allen Brain Atlas Aging Dementia and Traumatic Brain Injury Tissue Sample Gene Expression Profiles dataset. | |
| Carcinogenome Chemical Perturbation Carcinogenicity Signatures | small molecule perturbations changing expression of DMAC2L gene from the Carcinogenome Chemical Perturbation Carcinogenicity Signatures dataset. | |
| CCLE Cell Line Proteomics | Cell lines associated with DMAC2L protein from the CCLE Cell Line Proteomics dataset. | |
| CellMarker Gene-Cell Type Associations | cell types associated with DMAC2L gene from the CellMarker Gene-Cell Type Associations dataset. | |
| ChEA Transcription Factor Targets 2022 | transcription factors binding the promoter of DMAC2L gene in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets 2022 dataset. | |
| CM4AI KOLF21J CRISPRi Gene Perturbation Atlas | gene perturbations changing expression of DMAC2L gene from the CM4AI KOLF21J CRISPRi Gene Perturbation Atlas dataset. | |
| COMPARTMENTS Curated Protein Localization Evidence Scores 2025 | cellular components containing DMAC2L protein from the COMPARTMENTS Curated Protein Localization Evidence Scores 2025 dataset. | |
| COMPARTMENTS Text-mining Protein Localization Evidence Scores 2025 | cellular components co-occuring with DMAC2L protein in abstracts of biomedical publications from the COMPARTMENTS Text-mining Protein Localization Evidence Scores 2025 dataset. | |
| DeepCoverMOA Drug Mechanisms of Action | small molecule perturbations with high or low expression of DMAC2L protein relative to other small molecule perturbations from the DeepCoverMOA Drug Mechanisms of Action dataset. | |
| DepMap CRISPR Gene Dependency | cell lines with fitness changed by DMAC2L gene knockdown relative to other cell lines from the DepMap CRISPR Gene Dependency dataset. | |
| DISEASES Text-mining Gene-Disease Association Evidence Scores 2025 | diseases co-occuring with DMAC2L gene in abstracts of biomedical publications from the DISEASES Text-mining Gene-Disease Assocation Evidence Scores 2025 dataset. | |
| DisGeNET Gene-Disease Associations | diseases associated with DMAC2L gene in GWAS and other genetic association datasets from the DisGeNET Gene-Disease Associations dataset. | |
| GO Biological Process Annotations 2023 | biological processes involving DMAC2L gene from the curated GO Biological Process Annotations 2023 dataset. | |
| GO Biological Process Annotations 2025 | biological processes involving DMAC2L gene from the curated GO Biological Process Annotations2025 dataset. | |
| GO Cellular Component Annotations 2023 | cellular components containing DMAC2L protein from the curated GO Cellular Component Annotations 2023 dataset. | |
| GO Cellular Component Annotations 2025 | cellular components containing DMAC2L protein from the curated GO Cellular Component Annotations 2025 dataset. | |
| GO Molecular Function Annotations 2023 | molecular functions performed by DMAC2L gene from the curated GO Molecular Function Annotations 2023 dataset. | |
| GO Molecular Function Annotations 2025 | molecular functions performed by DMAC2L gene from the curated GO Molecular Function Annotations 2025 dataset. | |
| GTEx eQTL 2025 | SNPs regulating expression of DMAC2L gene from the GTEx eQTL 2025 dataset. | |
| GTEx Tissue Gene Expression Profiles 2023 | tissues with high or low expression of DMAC2L gene relative to other tissues from the GTEx Tissue Gene Expression Profiles 2023 dataset. | |
| GTEx Tissue-Specific Aging Signatures | tissue samples with high or low expression of DMAC2L gene relative to other tissue samples from the GTEx Tissue-Specific Aging Signatures dataset. | |
| GWAS Catalog SNP-Phenotype Associations 2025 | phenotypes associated with DMAC2L gene in GWAS datasets from the GWAS Catalog SNP-Phenotype Associations 2025 dataset. | |
| IMPC Knockout Mouse Phenotypes | phenotypes of mice caused by DMAC2L gene knockout from the IMPC Knockout Mouse Phenotypes dataset. | |
| JASPAR Predicted Human Transcription Factor Targets 2025 | transcription factors regulating expression of DMAC2L gene predicted using known transcription factor binding site motifs from the JASPAR Predicted Human Transcription Factor Targets dataset. | |
| JASPAR Predicted Mouse Transcription Factor Targets 2025 | transcription factors regulating expression of DMAC2L gene predicted using known transcription factor binding site motifs from the JASPAR Predicted Mouse Transcription Factor Targets 2025 dataset. | |
| LINCS L1000 CMAP Chemical Perturbation Consensus Signatures | small molecule perturbations changing expression of DMAC2L gene from the LINCS L1000 CMAP Chemical Perturbations Consensus Signatures dataset. | |
| LINCS L1000 CMAP CRISPR Knockout Consensus Signatures | gene perturbations changing expression of DMAC2L gene from the LINCS L1000 CMAP CRISPR Knockout Consensus Signatures dataset. | |
| MGI Mouse Phenotype Associations 2023 | phenotypes of transgenic mice caused by DMAC2L gene mutations from the MGI Mouse Phenotype Associations 2023 dataset. | |
| MoTrPAC Rat Endurance Exercise Training | tissue samples with high or low expression of DMAC2L gene relative to other tissue samples from the MoTrPAC Rat Endurance Exercise Training dataset. | |
| NIBR DRUG-seq U2OS MoA Box Gene Expression Profiles | drug perturbations changing expression of DMAC2L gene from the NIBR DRUG-seq U2OS MoA Box dataset. | |
| PFOCR Pathway Figure Associations 2023 | pathways involving DMAC2L protein from the PFOCR Pathway Figure Associations 2023 dataset. | |
| Reactome Pathways 2024 | pathways involving DMAC2L protein from the Reactome Pathways 2024 dataset. | |
| Replogle et al., Cell, 2022 K562 Essential Perturb-seq Gene Perturbation Signatures | gene perturbations changing expression of DMAC2L gene from the Replogle et al., Cell, 2022 K562 Essential Perturb-seq Gene Perturbation Signatures dataset. | |
| Replogle et al., Cell, 2022 K562 Genome-wide Perturb-seq Gene Perturbation Signatures | gene perturbations changing expression of DMAC2L gene from the Replogle et al., Cell, 2022 K562 Genome-wide Perturb-seq Gene Perturbation Signatures dataset. | |
| Replogle et al., Cell, 2022 RPE1 Essential Perturb-seq Gene Perturbation Signatures | gene perturbations changing expression of DMAC2L gene from the Replogle et al., Cell, 2022 RPE1 Essential Perturb-seq Gene Perturbation Signatures dataset. | |
| Rummagene Transcription Factor Associations 2026 | transcription factors regulating expression of DMAC2L gene from the Rummagene Transcription Factor Associations 2026 dataset. | |
| RummaGEO Drug Perturbation Signatures | drug perturbations changing expression of DMAC2L gene from the RummaGEO Drug Perturbation Signatures dataset. | |
| RummaGEO Gene Perturbation Signatures | gene perturbations changing expression of DMAC2L gene from the RummaGEO Gene Perturbation Signatures dataset. | |
| Sci-Plex Drug Perturbation Signatures | drug perturbations changing expression of DMAC2L gene from the Sci-Plex Drug Perturbation Signatures dataset. | |
| TISSUES Curated Tissue Protein Expression Evidence Scores 2025 | tissues with high expression of DMAC2L protein from the TISSUES Curated Tissue Protein Expression Evidence Scores 2025 dataset. | |
| TISSUES Experimental Tissue Protein Expression Evidence Scores 2025 | tissues with high expression of DMAC2L protein in proteomics datasets from the TISSUES Experimental Tissue Protein Expression Evidence Scores 2025 dataset. | |
| TISSUES Text-mining Tissue Protein Expression Evidence Scores 2025 | tissues co-occuring with DMAC2L protein in abstracts of biomedical publications from the TISSUES Text-mining Tissue Protein Expression Evidence Scores 2025 dataset. | |
| WikiPathways Pathways 2024 | pathways involving DMAC2L protein from the WikiPathways Pathways 2024 dataset. | |
