ABCA5
- Known as:
- ABCA5
- Catalog number:
- 000887A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCA5
Related genes to: ABCA5
- Gene:
- ABCA5 NIH gene
- Name:
- ATP binding cassette subfamily A member 5
- Previous symbol:
- -
- Synonyms:
- EST90625
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2015-11-13
Related products to: ABCA5
Related articles to: ABCA5
- Graft-versus-host disease (GVHD), a major adverse event following allogeneic hematopoietic stem cell transplantation (allo-HSCT), commonly affects leukemia patients and is associated with reduced survival and impaired quality of life. Early prediction of GVHD remains a major clinical challenge. - Source: PubMed
Publication date: 2026/03/12
Lu WeiHe ZhipengHuang Xianbao - Fertility was impaired in sleep deprivation (SD) male rats. Dutasteride (DUT), a 5-α reductase inhibitor, also had negative effects on fertility, however, its definite mechanisms were still unknown. To this end, SD male model rats, exposed to DUT for a short period of time, were used to observe whether DUT would exacerbate fertility damage and further to explore the possible mechanism of its fertility damage effects. - Source: PubMed
Publication date: 2026/02/26
Zhang ShengxiaoLi WeiZhang Guirong - Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal malignancies characterized by poor prognosis and resistance to therapy. Despite the most widely recognized role of ATP binding cassette (ABC) family transporters in multidrug resistance, emerging evidence suggests that ATP-binding cassette transporter A5 (ABCA5) acts as a tumor suppressor. Nevertheless, the role and molecular mechanism of ABCA5 in PDAC have not yet been fully investigated. - Source: PubMed
Publication date: 2026/02/16
Li ZhenchongMa ZuyiChen YubinYu WeixuanYu JiajieLu JianminZhang QiaolingWu QianlongCai YifengWang ZeyaoShang ChangzhenHou BaohuaZhang ChuanzhaoHuang ShanzhouWang LinheZhou Qi - 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 - Epithelial-mesenchymal transition (EMT) is designated as one of the prime causes of chemoresistance in many cancers. In our previous study we established that cisplatin resistance in ovarian cancer (OC) is associated with EMT using sensitive OV90 cells and its resistant counterparts OV90CisR1 and OV90CisR2. In this study, we revealed through RNAseq analysis that ITGA1 can play essential part in EMT mediated cisplatin resistance in OC. We found large number of EMT related terms predominant in the top gene ontologies (GO). We also found Extracellular matrix (ECM) and actin cytoskeleton genes highly altered in the resistant cells. This was further confirmed by the protein-protein interaction (PPI) analysis where we identified that the core ECM components e.g., collagen, fibronectin, metalloproteases and integrins possessed most interactions. The pathway analysis revealed the Wnt signaling as the leading pathway. Since integrins have significant interaction with Wnt signaling, we focused our study on integrins among which, ITGA1, ITGA6, ITGA11 and ITGAV were primarily altered. We validated our results by western blotting and found that ITGA1 was highly expressed in resistant cells. Additionally, the high ABCA5 (efflux transporter) expression in resistant cells also supports the EMT proposition. The western blotting also revealed high β-catenin expression in resistant cells confirming the high Wnt signaling activity. Further, we induced xenograft tumors in nude mice. The histopathological analysis confirmed the aggressive nature of resistant tumors and showed the presence of necrotic core which could be implicated to EMT. Finally, the immunohistochemical staining confirmed the high protein expression in resistant tumor. - Source: PubMed
Publication date: 2025/01/24
Wani Taha UmairKim Hyun-YiLee Geum-HwaLim Young JeChae Han-JungKim Ji-YeYoon Hyonok