ATG9A Antibody (Center)
- Known as:
- ATG9A Antibody (Center)
- Catalog number:
- AP1814b
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ATG9A Antibody (Center)
Related genes to: ATG9A Antibody (Center)
- Gene:
- ATG9A NIH gene
- Name:
- autophagy related 9A
- Previous symbol:
- APG9L1
- Synonyms:
- FLJ22169
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-24
- Date modifiied:
- 2015-09-11
Related products to: ATG9A Antibody (Center)
Related articles to: ATG9A Antibody (Center)
- Understanding how selection shapes disease risk remains challenging. Variants influencing complex traits, including common diseases, can also impact fitness and thus be constrained by purifying selection. Consequently, genetic variance underlying disease susceptibility may be attributed to low-frequency, population-specific variants. We analyzed 509,817 genome-wide variants from 72,635 Han Taiwanese individuals to identify loci showing age-dependent allele frequency shifts that signal ongoing selection. After adjusting for potential age-related population structure, we detected 168 variants deviating from neutrality, with most showing declining frequencies in younger generations, consistent with purifying selection on deleterious alleles influencing disease risk. These variants were enriched for rare alleles (≤0.1%) and disease-associated variants. At BRCA1, we identified 16 rare pathogenic variants in strong linkage disequilibrium undergoing purifying selection that coexist with a positively selected haplotype, revealing temporally fluctuating selection; comparable patterns at BRCA2 and MLH1 suggest recurrent selective trade-offs in DNA repair genes. Phenome-wide association analysis across 30 hematologic and cardiometabolic traits linked a subset of candidates to increased erythrocyte volume and reduced hemoglobin concentration, suggesting subclinical physiological effects. These results demonstrate ongoing natural selection on disease-relevant variation, particularly affecting hematologic traits in the Han Taiwanese population, and highlight opportunities to refine precision-medicine risk models. - Source: PubMed
Publication date: 2026/07/24
Chen Jing-LianKang Mei-LingLin Cheng-JuiLo Yun-HuaChen Yann-JangLee Hsiao-HuiTanapima ValisLin Chao-KuangLee I-HuiSatta YokoKo Wen-Ya - Host microRNAs (miRNAs) are widely proposed as innate antiviral effectors against SARS-CoV-2, yet whether they actually restrict infection in lung epithelial cells remains unresolved. Two of the most-cited candidates, miR-29a-3p and miR-15b-5p, are predicted to bind both the viral genome and key entry/trafficking factors such as Furin and ATG9A, but functional evidence is fragmented and often contradictory. Here, we put both miRNAs to the test in human Calu-3 cells infected with the SARS-CoV-2 Beta and Omicron BA.1 variants, using parallel gain- and loss-of-function strategies coupled to RT-qPCR of viral and cellular transcripts and back-titration of infectious progeny on VeroE6/TMPRSS2 cells. Both miRNAs transiently suppressed viral gene expression at 6 hpi, but this early dampening was followed by a marked transcript rebound at 24 hpi, especially for Omicron, with virtually no impact on total extracellular viral RNA. More strikingly, miR-15b modulation enhanced infectious virus output during Beta infection, and miR-29a overexpression boosted Omicron BA.1 infectivity, while Furin, ATG9A, AKT3, and TFEB showed only modest, condition-dependent shifts. Rather than acting as clean antiviral effectors, miR-29a and miR-15b emerge as context-dependent modulators that can paradoxically favor SARS-CoV-2 replication-a cautionary signal for miRNA-based antiviral strategies. - Source: PubMed
Publication date: 2026/06/29
Criscuolo ElenaMosca NicolaGiuliani BenedettaCastelli MatteoDi Palo ArmandoPezzullo MariacelesteBurioni RobertoRusso AnielloClementi NicolaPotenza Nicoletta - Approximately 200-300 billion cells die daily through apoptosis, a prominent form of programmed cell death, to maintain tissue homoeostasis. If apoptotic cells are not efficiently removed by phagocytes, they progress to secondary necrosis when the plasma membrane (PM) becomes permeabilised and release proinflammatory damage-associated molecular patterns (DAMPs) such as HMGB1 and ATP, which drive inflammation and contribute to autoimmune diseases. Thus, controlling inflammation through maintaining PM integrity is critical, however the molecular mechanisms underpinning this is not well defined. Here, we reveal a calcium-dependent process that delays secondary necrosis by promoting PM repair. Mechanistically, calcium influx through T-type voltage-gated calcium channels mediates the recruitment of the lipid scramblase ATG9A and Golgi components to damaged PM regions, thereby preventing early cellular lysis and DAMP release. Inhibition of calcium influx or loss of ATG9A accelerates PM rupture, increases DAMP secretion, and exacerbates inflammatory cell recruitment in vivo. Taken together, this study establishes a novel role for T-type calcium channels and ATG9A in regulating PM repair during apoptosis and highlights their therapeutic potential for controlling unwanted inflammation. - Source: PubMed
Publication date: 2026/07/08
Audi Omar FOzkocak Dilara CJohnson ChadShi BoSantavanond Jascinta PVella Caitlin LHildebrand Joanne MSharples RobynLe Quan ThinhCheng Sim LesleyBaxter Amy AHulett Mark DPoon Ivan K HPhan Thanh Kha - Non-small-cell lung cancer (NSCLC), the predominant type of lung cancer, is characterized by high invasiveness and significant mortality. Despite its clinical impact, the molecular mechanisms driving its pathogenesis and progression remain poorly understood. This study demonstrates that TMED9 is overexpressed in NSCLC and showed using multiple independent sample sets that its expression level is significantly associated with poor patient prognosis. Gain- and loss-of-function experiments revealed that TMED9 promotes proliferation, invasion, and migration of NSCLC cells in vitro and significantly accelerates tumor growth and metastasis in vivo. Mechanistically, TMED9 interacts with ATG9A and recruits USP5 to facilitate the deubiquitination and stabilization of ATG9A, thereby activating autophagy and driving malignant progression. Notably, genetic depletion of TMED9 enhances the sensitivity of NSCLC cells to osimertinib. Collectively, these findings identify the TMED9-USP5-ATG9A signaling axis as a critical driver of NSCLC malignancy, highlighting TMED9 as a promising therapeutic target. - Source: PubMed
Publication date: 2026/07/02
Liu NaHan GuohuZhang FushengGu QianhuiLiu YuanyuanJia JingZhu XiaorenChen Minbin - Parechoviruses (PeVs) are single-stranded, positive-sense RNA viruses in the family. Although most genotypes are not typically associated with severe disease, PeV-A3 has emerged as an important cause of sepsis and meningoencephalitis in newborns. Despite its clinical relevance, the life cycle and pathogenesis of PeV-A3 remain poorly understood. To identify critical host factors for PeV-A3 replication, we performed a genome-wide CRISPR screen. Our results reveal a set of Golgi-localized proteins important for viral infection, among which the lipid scramblase ATG9A (autophagy-related protein 9A) was determined to be essential across different PeV genotypes. Notably, this requirement appears to be independent of canonical autophagy. We further demonstrate that ATG9A is necessary for viral RNA replication, but not entry or translation, and co-localizes with double-stranded RNA, a marker of viral replication organelles (ROs) during infection. ATG2, a lipid transfer protein known to interact with ATG9A, is also required for optimal viral replication. Therefore, the ATG2-ATG9A complex may function by delivering key lipids into the ROs to support viral replication. - Source: PubMed
Publication date: 2026/06/26
Li YouDurnell-Bettis Lorellin AAlam FahmidaGolding Adriana EBonifacino Juan SVogt Matthew R