{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n ABCA10 is a member of the ABCA6‐like subfamily of full‐size ATP‐binding cassette transporters that has been primarily characterized in human macrophages. Cloning studies revealed that the 4.6‐kb coding sequence produces a 1543–amino acid protein featuring a PEST sequence—a potential signal for proteasomal degradation—and multiple transcript variants that may encode truncated forms."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " Expression analyses show that ABCA10 is ubiquitously expressed with the highest levels in heart, brain, and the gastrointestinal tract, and its gene expression is down‐regulated by cholesterol import into macrophages. This cholesterol responsiveness suggests a role for ABCA10 in macrophage lipid homeostasis and intracellular sterol transport."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition to its potential metabolic function, ABCA10 appears to have clinical significance in oncology. It is part of an “ABCA5‐like” transporter cluster that, although showing only weak mRNA expression in a range of tumors"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ", has been incorporated in multi‐gene prognostic signatures. For instance, its inclusion in a four‐gene prognostic model for uterine serous carcinoma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", as well as correlations between its expression and progression‐free survival in ovarian cancers and differential expression in osteosarcoma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ", indicates that ABCA10 may be linked to tumor differentiation and clinical outcomes. A similar observation was noted in ovarian serous cystadenocarcinoma, where ABCA10 was among candidate biomarkers predicting patient survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Interestingly, evolutionary analyses of the ABCA6‐like transporter group have revealed evidence of positive and relaxed selection among these genes. Specifically, the analysis of ABCA10 suggests that it is undergoing relaxed selective pressure—and may be on the path to pseudogenization—in the human lineage."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " This observation implies that while ABCA10 appears to contribute to lipid regulation in specific contexts, its functional importance might be diminishing over evolutionary time in humans.\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, ABCA10 is a cholesterol‐responsive ATP-binding cassette transporter that likely participates in macrophage lipid homeostasis and intracellular sterol trafficking. Concomitantly, its expression has been linked to prognostic outcomes in various cancers. However, evolutionary data point to a potential loss of function in humans, leaving open questions about its long-term physiological and clinical significance.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jürgen J Wenzel, Wolfgang E Kaminski, Armin Piehler, et al. "}, {"type": "b", "children": [{"type": "t", "text": "ABCA10, a novel cholesterol-regulated ABCA6-like ABC transporter."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/s0006-291x(03)01097-0"}], "href": "https://doi.org/10.1016/s0006-291x(03"}, {"type": "t", "text": "01097-0) PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12821155"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12821155"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Doris Hendig, Thomas Langmann, Sarah Kocken, et al. 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