ABCA10
- Known as:
- ABCA10
- Catalog number:
- 000892A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCA10
Related genes to: ABCA10
- Gene:
- ABCA10 NIH gene
- Name:
- ATP binding cassette subfamily A member 10
- Previous symbol:
- -
- Synonyms:
- EST698739
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2016-10-05
Related products to: ABCA10
Related articles to: ABCA10
- Myxofibrosarcoma (MFS) is a common yet understudied type of soft tissue sarcoma. It is characterized by diverse cellular morphology, unusual growth patterns, and a propensity for local tumor recurrences. A 76-year-old patient underwent multiple surgical removals of MFS recurrences of the thoracic cavity and surrounding tissues with the subsequent development of metastases. Single-cell RNA sequencing was used to analyze the earlier (R7) and later (R8) MFS recurrences, with R8 removed less than a year before the detection of metastases in the lungs. The earlier MFS recurrence displays tumor clusters with multiple immunomodulatory markers (, , , ) and genes involved in lipid metabolism and cell stress (, , , , ), combined with an anti-inflammatory TME. The later MFS recurrence shifts to a functionally less diverse phenotype, enriched in fibroblast-typical markers (, , ), and a pro-inflammatory TME. The proliferative (, , ) and mRNA splicing and processing (, , , , ) tumor clusters are observed in both MFS recurrences, and their signatures match the previous data on primary MFS tumor populations. ScRNA-seq analysis of two subsequent MFS recurrences from one patient show a change from functionally diverse to more uniform ECM remodeling enriched tumor populations, an accompanying shift to the pro-inflammatory TME, and the presence of two common tumor clusters enriched in proliferative and mRNA-processing gene signatures. - Source: PubMed
Publication date: 2026/07/13
Kopantseva Elena EToropov Artem LFetisov Timur IIkonnikov Alexander VSentyabreva Alexandra VMenyailo Maxim ETararykova Anastasia AShtompel Polina AZinovieva Victoria YKirsanov Kirill IDenisov Evgeny VYakubovskaya Marianna G - We describe three unrelated individuals with congenital generalized hypertrichosis with gingival hyperplasia (CGHGH), each carrying a distinct structural rearrangement (duplication, deletion, inversion) at 17q24.2-q24.3 identified by CMA and WGS. Despite differences in the type of rearrangement, all three patients seem to exhibit alterations affecting the genomic architecture of a cluster of genes, particularly involving the ABCA family (notably ABCA5, ABCA6, ABCA9, ABCA10), MAP2K6, and potassium channels (KCNJ16, KCNJ2). These findings suggest that disruption of the local chromatin organization, including topologically associating domains (TADs), may contribute to the pathogenesis of CGHGH. Although previous studies implicated deletions affecting ABCA5 as the likely cause of CGHGH, our findings emphasize a broader spectrum of structural variation capable of producing similar phenotypes. Interestingly, one patient involved a cryptic 1.2 Mb inversion that disrupted the region between ABCA9 and KCNJ2, detectable only by whole genome sequencing, reinforcing the need for advanced molecular diagnostics in patients with syndromic hypertrichosis. In all three individuals, gingival overgrowth co-occurred with typical facial features, coarse hair, and normal cognitive development, adding evidence to the phenotype-genotype correlation. Overall, this study strengthens the hypothesis that disruption of regulatory elements and chromatin architecture at 17q24.2-q24.3, rather than single nucleotide variants alone, can be a primary driver of CGHGH. These findings underscore the need to incorporate genome-wide structural variant analysis in the diagnostic workflow of rare developmental disorders, especially those with heterogeneous or subtle clinical presentations. - Source: PubMed
Publication date: 2026/01/23
Tenorio-Castano JairFeito Martade Lucas RaúlSendagorta ElenaGómez-Fernández CristinaParra AlejandroVallespin ElenaGallego-Zazo NataliaCazalla MarioJiménez-Estrada Juan AMiranda-Alcaraz LuciaMora-Gómez MónicaRodríguez-Canó Manuel JesúsVázquez-Amell ValeriaRamos SergioValle TomásMansilla ElenaSantiago Fe GarcíaGalán-Gómez EnriqueCalpena EduardoRuíz-Pérez Víctor LNevado JuliánLapunzina Pablo - Next-generation sequencing technology enables uniform and impartial assessment of cancer diagnoses and prognosis. However, such studies are mostly type-specific, and capturing shared genomic abnormalities responsible for neoplastic transformation and progression is a challenging task. Pan-cancer analysis offers insights into the shared and unique molecular mechanisms driving cancer. We conducted an integrated gene-expression analysis using 10,629 samples from 30 distinct cancer types characterized by The Cancer Genome Atlas (TCGA). A gene co-expression network was constructed and genes overlapping between the selected modules and Differentially Expressed Genes (DEGs) were designated as genes of interest. Following a comprehensive literature review, ATP binding cassette subfamily A member 10 (ABCA10) and ATP binding cassette subfamily B member 5 (ABCB5) were selected as key candidates for downstream analysis due to the absence of systematic pan-cancer analysis of these genes. This study presents a unique contribution as the first comprehensive pan-cancer analysis of ABCA10 and ABCB5, highlighting their roles in tumor biology and clinical outcomes. We employed a variety of bioinformatics tools to explore the role of these genes across different tumors. Our research demonstrated that ABCA10 shows reduced expression, while ABCB5 displays variable expression patterns across tumors, indicating their opposing roles and flexible functions in pan-cancer. In many cancer patients, these expression patterns are correlated with worse survival outcomes. Furthermore, immunotherapy responses and immune infiltration across a variety of tumor types are associated with the expression levels of both ABCA10 and ABCB5. These results imply that ABCA10 and ABCB5 could serve as valuable predictive markers and potential therapeutic targets across various cancers. - Source: PubMed
Publication date: 2025/05/30
Masood Madahiah Bint EShafique IqraRafique Muhammad InamIman AyeshaAbbasi AribaRafiq MehakHabib Uzma - Cisplatin (DDP) resistance is one of the causes of treatment failure for ovarian cancer (OV). Mitochondrial cholesterol level was reported to be associated with OV chemoresistance. We found that ABCA10, a potential cholesterol transport protein, was highly expressed in ovarian tissues and downregulated in OV tissues. Our study aimed to explore TCF21/ABCA10 axis resistance to DDP therapy in ovarian cancer based on regulating mitochondrial cholesterol efflux. Thirty epithelial ovarian cancer tumors and thirty ovarian tissues from non-cancer patients were collected. Western blot and RT-qPCR were used to measure ABCA10 and TCF21 expression levels in these tissues, as well as in a human ovarian epithelial cell line (IOSE-80), OV cells (A2780 and SKOV3), and DDP-resistant OV cell lines (A2780/DDP and SKOV3/DDP). IOSE-80 cells were also infected with ABCA10 knockdown lentivirus to identify the most effective ABCA10 knockdown plasmid. Lentiviral infection was used to create ABCA10 knockdown, ABCA10 overexpression, and TCF21 overexpression anti-DDP OV cell lines. Cell proliferation was detected by CCK-8 and EDU staining, flow cytometry for apoptosis, MTT for metabolic activity, calcium-induced Cytochrome C release, and mitochondrial matrix swelling for mitochondrial function and Oil Red O staining for lipid accumulation. Cholesterol metabolism was evaluated by measuring mitochondrial cholesterol and cholesterol efflux. Protein concentration was determined using the BCA method. A dual-luciferase reporter assay confirmed TCF21's interaction with ABCA10. ChIP also verified this interaction. The mRNA level (P < 0.01) and protein level (P < 0.001) of ABCA10 were downregulated in cancer tissues of OV patients relative to normal ovarian tissues. Relative to human ovarian epithelial cells, ABCA10 expression was significantly downregulated in OV cells (P < 0.01) and even more significantly downregulated in DDP-resistant OV cells (P < 0.001). Compared to the group treated solely with DDP, the overexpression of ABCA10 significantly inhibited the proliferation of DDP-resistant OV cells (P < 0.01), markedly reduced the staining intensity of EDU in these cells (P < 0.05), and substantially accelerated apoptosis in DDP-resistant OV cells (P < 0.01).Overexpression of ABCA10 further accelerated Cytochrome C expression and mitochondrial matrix swelling in DDP-resistant OV cells compared to the DDP-alone group (P < 0.01). The addition of cholesterol reversed the decrease in lipid accumulation, the decrease in mitochondrial cholesterol levels (P < 0.05), and the increase in cholesterol efflux (P < 0.01) in DDP-resistant OV cells caused by overexpression of ABCA10. The transcription factor TCF21 was bound to the promoter of ABCA10. Overexpression of TCF21 significantly increased ABCA10 expression in DDP-resistant OV cells (P < 0.01) and increased cytochrome C expression in A2780/DDP (P < 0.05) and SKOV3/DDP (P < 0.01) cells, with accelerated mitochondrial matrix swelling in A2780/DDP (P < 0.01) and SKOV3/DDP (P < 0.001) cells, while knockdown of ABCA10 reversed these effects. Our study found that TCF21 boosts ABCA10 expression, which in turn reduces DDP resistance in OV cells by enhancing mitochondrial cholesterol efflux. This mechanism increases the sensitivity of DDP-resistant OV cells to DDP. Our findings will provide new therapeutic targets for the treatment of ovarian cancer. - Source: PubMed
Publication date: 2024/10/22
Li LiCheng HuiPeng YangTang Dihong - The human brain is highly enriched in lipids and increasing evidence indicates that dysregulation of lipids in the brain is associated with neurodegeneration. ATP-binding cassette subfamily A (ABCA) transporters control the movement of lipids across cellular membranes and are implicated in a number of neurodegenerative diseases. However, very little is known about the role of ABCA transporters in frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP), which is a common form of younger-onset dementia. We therefore undertook a comprehensive analysis of the expression of ABCA transporters (ABCA1-13) in five key brain regions (amygdala, inferior temporal cortex, superior frontal cortex, cerebellum and parietal cortex) in FTLD-TDP and controls. We found that the expression of ABCA2, ABCA3, ABCA4, ABCA7, ABCA9, ABCA10 and ABCA13 was significantly altered in FTLD-TDP in a region-specific manner. In addition, the expression of ABCA transporters correlated specifically to different neural markers and TARDBP. These results suggest substantial dysregulation of ABCA transporters and lipid metabolism in FTLD-TDP and these changes are associated with neuroinflammation. - Source: PubMed
Publication date: 2022/11/01
Katzeff Jared SLok Hiu ChuenBhatia SurabhiFu YuHongHalliday Glenda MKim Woojin Scott