ABCA3 Pre-design Chimera RNAi
- Known as:
- ABCA3 Pre-design Chimera RNAi
- Catalog number:
- H00000021-R02
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ABCA3 Pre-design Chimera RNAi
Related genes to: ABCA3 Pre-design Chimera RNAi
- Gene:
- ABCA3 NIH gene
- Name:
- ATP binding cassette subfamily A member 3
- Previous symbol:
- ABC3
- Synonyms:
- ABC-C, EST111653, LBM180
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-08
- Date modifiied:
- 2015-11-13
Related products to: ABCA3 Pre-design Chimera RNAi
Related articles to: ABCA3 Pre-design Chimera RNAi
- - Source: PubMed
Queener PageRoss Emma LDeterding Robin - Obstructive total anomalous pulmonary venous connection (TAPVC) and ABCA3-related interstitial lung disease (ILD) rarely coexist. We report a neonate with TAPVC complicated by compound heterozygous ABCA3 variants (c.4180dup/p.V1394fs maternal, c.3446A>G/p.D1149G paternal). Overlapping neonatal respiratory symptoms mask the underlying surfactant disorder, easily causing misdiagnosis and delayed targeted management. This case highlights that the genetic screening for ABCA3 deficiency is mandatory for infants with persistent severe hypoxemia and ventilator dependence after complete TAPVC surgical repair. To our knowledge, this is the first documented co-occurrence of TAPVC and congenital ABCA3-related ILD. - Source: PubMed
Publication date: 2026/09/03
Hao XiaoyanYang ShuangWang QiangZhang YeHe Yihua - Neonatal lung biopsy guides management of unusually severe, diffuse lung disease with an uncertain diagnosis. Childhood interstitial lung disease (chILD) constitutes a diverse group of uncommon respiratory diseases which are associated with major morbidity and mortality. The incidence, outcome and mortality of chILD and other severe respiratory diseases in resource-limited settings (RLS) are unclear. - Source: PubMed
Goussard PierreSchubert Pawelvan Wyk LizelleBooysen LynnGie AndréUrban MichaelJanson JacquesAndronikou SavvasEber Ernst - H9N2 avian influenza virus (AIV) poses significant threats to poultry and public health, with the potential to contribute to the emergence of more virulent influenza strains. Hypoxia-inducible factor 1-alpha (HIF-1α) plays a crucial role in viral pathogenesis, immune regulation, and inflammation, making it a promising target for therapeutic intervention. Here, we explored the involvement of HIF-1α in H9N2 AIV pathogenesis and associated inflammatory responses. Our data revealed that HIF-1α exacerbates inflammation induced by H9N2 AIV infection through its regulation of mitochondrial fitness. Additionally, we investigated Sotetsuflavone (Seo), a naturally derived flavonoid, for its potential to modulate inflammatory responses following H9N2 infection. Molecular docking coupled with surface plasmon resonance assays indicated that Seo exhibits robust binding affinity to HIF-1α, implying a direct inhibitory mechanism. Subsequent studies demonstrated that Seo greatly reduced the production of inflammatory cytokines, including IL-1β, IL-6, and TNF-α, through suppressing the HIF-1α signaling pathway in HD11 cells infected with H9N2 AIV. Correspondingly, experiments established that Seo administration significantly ameliorated pulmonary inflammation in H9N2-infected mice, while also enhancing alveolar epithelial repair, as evidenced by increased expression of type II alveolar epithelial cell markers Abca3 and Sftpb. Collectively, these findings identify Seo as a potent inhibitor of HIF-1α, highlighting its therapeutic potential in mitigating inflammation and lung damage associated with influenza virus infection.IMPORTANCEH9N2 avian influenza virus triggers inflammatory lung injury via hypoxia-inducible factor-1 alpha (HIF-1α)-mediated dysregulation of mitochondrial function. The natural flavonoid Sotetsuflavone (Seo) directly binds and inhibits HIF-1α, as confirmed by molecular docking and surface plasmon resonance assays. In H9N2-infected HD11 cells, Seo suppresses HIF-1α signaling, reducing IL-1β, IL-6, and TNF-α production. , Seo treatment attenuates pulmonary inflammation and enhances alveolar epithelial repair in mice, upregulating type II pneumocyte markers (Abca3 and Sftpb). These findings identify Seo as a promising HIF-1α-targeted therapeutic for influenza-associated immunopathology. - Source: PubMed
Publication date: 2026/08/25
Zhu SuyingLi BeibeiWang YaqiTian YuhanZhang JiayueWang Hongshan - Spread through air spaces (STAS) is an adverse invasive pattern in lung adenocarcinoma (LUAD), but reliable biomarkers for preoperative or intraoperative prediction remain limited. We investigated whether the intratumoral microbiome and metabolome are associated with STAS. - Source: PubMed
Publication date: 2026/08/05
Qin ChuJiang HuachiFan XiaodongYu HaodaZhang Liang