ATG9A Antibody (N_term)
- Known as:
- ATG9A Antibody (N_term)
- Catalog number:
- AP1814a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ATG9A Antibody (N_term)
Related genes to: ATG9A Antibody (N_term)
- 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 (N_term)
Related articles to: ATG9A Antibody (N_term)
- 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 - : Autophagy is an evolutionarily conserved intracellular degradation mechanism that is regulated by a set of autophagy-related (ATG) proteins. The only transmembrane protein among ATGs is the lipid scramblase ATG9, which exists in the form of two paralogs, ATG9A and ATG9B, in humans and other vertebrates. : Here, we analyzed human and murine skin transcriptome and proteome datasets for the expression of ATG9 paralogs and performed comparative genomics to determine their conservation during the evolution of amniotes (mammals and sauropsids). : The expression of , but not of , is enriched in differentiated epidermal keratinocytes and in skin appendages of humans and mice. In contrast to the conservation of in all major clades of amniotes, has been lost in at least three phylogenetic lineages. Cetaceans, which have unique skin adaptations to aquatic life, harbor mutations that disrupt the open reading frame of . Many or all species of turtles () and crocodilians () have entirely lost the gene. : has undergone independent pseudogenization or gene loss in different subgroups of amniotes. In mammalian species that have retained the gene, its expression pattern indicates functions of in the skin and skin appendages. - Source: PubMed
Publication date: 2026/06/09
Sukseree SupawadeeEckhart Leopold - Lens fibers undergo organelle degradation during lens terminal differentiation. Defects in organelle degradation of lens fibers lead to congenital cataract. As a member of heat shock factor family, HSF4 governs lens development by regulating the expression of key factors. HSF4 transcriptionally regulates ATG9a to induce organelle degradation via the autophagic pathway during lens terminal differentiation. HSF4 is also required for the organelle membrane translocation of phospholipases PLAATs, which were suggested to promote organelle degradation independent of autophagy in lens fibers. However, the detailed mechanism how HSF4 induces organelle degradation in lens fibers still remains unknown. In this study, we found that lipid peroxidation was extensively suppressed in HSF4 mouse lens fibers. HSF4 likely transcriptionally regulated the expression of lipoxygenase ALOX15 in lens. ALOX15 is uniquely expressed in lens fibers and colocalized with organelles in differentiating lens fibers. Knockout of ALOX15 had little effect on the organelle degradation in lens fibers. Unlike the total inhibition in HSF4 lens fibers, lipid peroxidation was only partially disturbed in ALOX15 lens fibers, possibly due to the compensatory role of ALOX12. Our findings demonstrate that HSF4 promotes lipid peroxidation by transcriptionally regulating ALOX15 expression in lens fibers, thus may contribute to the organelle degradation during lens OFZ formation. These findings expand our understanding of the molecular mechanisms underlying lens terminal differentiation. - Source: PubMed
Publication date: 2026/06/24
Zhang ShaoliWang YinanJiang NingLi XiaoyuHan LuyuanChen SiyuXie TongxinYan HongxinLi JunjieHu YanzhongMu HongmeiZhang JingCui Xiukun - Loss-of-function mutations in the genes encoding PINK1 and PRKN result in early-onset Parkinson disease (EOPD). Together, the encoded enzymes direct a neuroprotective pathway that ensures the elimination of damaged mitochondria via autophagy. We performed a genome-wide high-content imaging miRNA screen for inhibitors of the PINK1-PRKN pathway and identified all three members of the miRNA family 29 (miR-29). RNA sequencing revealed target genes regulated by miR-29 and identified ATG9A as a candidate gene. SiRNA-mediated ATG9A silencing phenocopied the effects of miR-29 and suppressed the initiation of PINK1-PRKN-mediated mitophagy. In addition, expression of ATG9A was able to rescue the effects of miR-29a, suggesting that ATG9A is primarily responsible for the inhibitory effect of miR-29. In an EOPD patient cohort, we further discovered two rare, potentially deleterious, missense variants (p.R631W and p.S828L) and tested them experimentally in cells. Strikingly, neither EOPD variant was able to rescue the phenotype suggesting they both act as loss-of-function mutations and might contribute to the etiology of disease. Together, our study validates miR-29 and its target gene ATG9A as novel regulators of PINK1-PRKN signaling. It further serves as proof-of-concept with the identification of novel, potentially disease-relevant EOPD variants specifically in mitophagy-regulating genes. The nomination of biological pathways is important for the stratification and treatment of patients that suffer from devastating diseases, such as EOPD. - Source: PubMed
Publication date: 2026/04/30
Markham Briana NRamnarine ChloeKim SongeunGrever William ESoto-Beasley Alexandra IHeckman Michael GRen YingxueOsborne Andrew CKehili MohammedBhagwate Aditya VLiu YuanhangWang ChenKim JungsuWszolek Zbigniew KRoss Owen ASpringer WolfdieterFiesel Fabienne C