ATG9B Antibody Autophagy Antibody
- Known as:
- ATG9B Antibody Autophagy Antibody
- Catalog number:
- AUT-5797
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ATG9B Antibody Autophagy
Related genes to: ATG9B Antibody Autophagy Antibody
- Gene:
- ATG9B NIH gene
- Name:
- autophagy related 9B
- Previous symbol:
- NOS3AS
- Synonyms:
- FLJ14885, APG9L2, SONE
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-24
- Date modifiied:
- 2016-10-05
Related products to: ATG9B Antibody Autophagy Antibody
Related articles to: ATG9B Antibody Autophagy Antibody
- Parkinson's disease (PD) is the second most common progressive neurodegenerative disease that severely affects the quality of life and there is an urgent need to explore unique and effective diagnostic markers. The present study aimed to develop and validate a multigene combination model for the diagnosis of PD based on autophagy-related genes (ARGs) and to discover their correlation with immune infiltrating cells. - Source: PubMed
Publication date: 2026/03/31
Dong ZiyeDai FanshuXing NaWu QiaoliGao HezhenKan PengchengHan YuanCheng XiuliWang YaruFeng XuequanZhang Biao - It is well established that many tumor types possess defective autophagic pathways. Several studies have reported that the transmembrane, autophagic lipid scramblase ATG9B is altered in multiple cancers, suggesting that this dysregulation could contribute to oncogenesis. Therefore, the goal of this study was to define the cellular distribution of ATG9B in two different tumor cell types and to provide insights into its cellular function. Surprisingly, we found that ATG9B shows a modest association with autophagic structures and exhibits a unique and prominent localization to mitochondria, in contrast to its related form ATG9A. Upon expression of tagged ATG9B forms, this mitochondrial distribution was accompanied by aberrant changes in mitochondrial morphology as well as a reduction in the mitochondrial membrane potential and the release of mtDNA. Few indicators for ATG9B-dependent mitophagy were noted. Instead, ATG9B overexpression led to pronounced apoptotic cell death as assessed by a variety of indicators. Further, we find that the N-terminal sequence of ATG9B acts as a mitochondrial targeting domain and that expression of this peptide alone can induce apoptotic cell death. These findings provide new insights into a putative cellular localization and function for ATG9B. - Source: PubMed
Publication date: 2026/03/11
Cao HongGuo LixiaChen JingKrueger EugeneRazidlo GinaMcNiven Mark A - Esophageal cancer (EC) remains a highly aggressive malignancy with limited therapeutic options and poor prognosis. To address the shortcomings of conventional therapies, we developed a biomimetic, reactive oxygen species (ROS)-responsive nanoprodrug for synergistic photothermal-chemotherapy of EC. Tannic acid and ellagic acid were chemically linked via boronate ester bonds to form a polyphenol-based nanoparticle (TPE). The epidermal growth factor receptor (EGFR)-targeting peptide GE11 was subsequently introduced onto red blood cell membranes (RBCM) to obtain GE11-RBCM, which was then used to cloak the TPE nanoparticles, yielding GE11-RBCM@TPE. The resulting nanoplatform exhibited excellent photothermal conversion capability under near-infrared irradiation and selectively released the therapeutic payload in response to elevated ROS levels within the tumor microenvironment. In vitro studies showed enhanced cellular uptake in EGFR-overexpressing EC cells and markedly increased cell death following combined photothermal and chemotherapeutic treatment. In vivo, GE11-RBCM@TPE significantly inhibited tumor growth with negligible systemic toxicity and prolonged blood circulation. Transcriptomic analysis further revealed up-regulation of pro-apoptotic (PER1, HK2, BMF, DAPK2) and autophagy-related genes (ATP6V0D2, HDAC10, BNIP3, DEPP1, ATG9B, NAT16), while SQSTM1 and IL6 were down-regulated, indicating simultaneous activation of apoptosis and autophagy. These findings suggest that GE11-RBCM@TPE represents a promising strategy for precise and effective treatment of esophageal cancer. - Source: PubMed
Publication date: 2026/02/27
Chen YangZhu LiXu WeiChen QiTeng FeiBao KaiwenZhang LuWang YuanWu WeiWang Zhiqiang - Macroautophagy (hereafter referred to as autophagy) requires the coordinated action of approximately 20 (autophagy related) genes. Duplication of genes has had a major impact on the evolution of the autophagy pathway among major lineages. One duplication hotspot is in vertebrates. However, the exact duplication timing, post-duplication evolutionary divergence patterns, and its relation to functional differences among paralogs have not been investigated in detail. Here, we demonstrate that most genes were likely duplicated by whole-genome duplication events near the root of vertebrates. We compared the sequence and gene expression divergence between paralogs and categorized the evolutionary fates (i.e., how ancestral function is divided between paralogs). Within the paralog pairs that evolved most asymmetrically, namely , ( and ), and , one paralog likely retained the ancestral function, allowing the other to evolve under less constraint. While no obvious asymmetry was observed between and in non-mammalian vertebrates, experienced marked sequence divergence and expression level reduction in mammals, suggesting a shift in balance. Expression patterns among the ( and ), ( and ), and ( and ) pairs were more consistent with hypofunctionalization/dosage sharing, such that ancestral function depends on both paralogs. We also demonstrate that both and can support autophagy, whereas only , but not , has autophagic function and discuss the relationship between autophagic function and evolutionary divergence. The present detailed analysis of gene duplication in vertebrates provides a critical timeline for interpreting functional differentiation between homologs.: ATG: autophagy related; BLAST: Basic Local Alignment Search Tool; DKO: double knockout; GFP: green fluorescent protein; GLMM: generalized linear mixed model; KO: knockout; LC3: MAP1LC3; MEF: mouse embryonic fibroblast; ns: non-significant; PAML: Phylogenetic Analysis by Maximum Likelihood; RPKM: reads per kilobase per million mapped reads; SVA: surrogate variable analysis; TMM: trimmed mean of M values; TMR: tetramethylrhodamine; WT: wild type. - Source: PubMed
Publication date: 2026/01/24
Zhang SidiKoyama-Honda IkukoHiratsuka DaikiMizushima Noboru - Platinum-based chemotherapy is the first-line therapeutic strategy for ovarian cancer (OC), and resistance to it adversely affects most OC patients. CBX2 plays an essential role in cancer progression and is widely thought to be involved in cisplatin (DDP) resistance. This study aimed to investigate the molecular mechanism of CBX2 in DDP resistance in OC. - Source: PubMed
Publication date: 2026/01/06
Kou XinxinDong LijieZhao ZhengYang XiaoxiaHu Yuanjing