Ambra1 Rabbit Polyclonal Antibody
- Known as:
- Ambra1 Rabbit Polyclonal Antibody
- Catalog number:
- AUT-4555
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- Ambra1 Rabbit Polyclonal Antibody
Related genes to: Ambra1 Rabbit Polyclonal Antibody
- Gene:
- AMBRA1 NIH gene
- Name:
- autophagy and beclin 1 regulator 1
- Previous symbol:
- -
- Synonyms:
- FLJ20294, KIAA1736, WDR94, DCAF3
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-02-01
- Date modifiied:
- 2016-04-28
Related products to: Ambra1 Rabbit Polyclonal Antibody
Related articles to: Ambra1 Rabbit Polyclonal Antibody
- Mitochondrial DNA (mtDNA) has long been recognized as an intracellular damage-associated molecular pattern, but emerging evidence reveals its role as an intercellular messenger driving post-infarction ventricular remodeling. This review systematically elaborates the transition of mtDNA from an "intracellular DAMP" to an "intercellular messenger" and proposes a conceptual framework termed the "three-threshold model", which integrates existing evidence but requires direct experimental validation. The three thresholds are defined as the release threshold (mitophagy-controlled mtDNA leakage), the transmission threshold (efficiency of intercellular transfer), and the activation threshold (sensitivity of STING signaling). mtDNA is transferred between cells via four modes-naked mtDNA, Ambra1 sEVs, mt-sEVs, and intact mitochondria-mediating inflammation, fibrosis, and vascular dysfunction, respectively. These pathological effects continuously lower all three thresholds through positive feedback loops, driving irreversible remodeling. Time-window-based combination strategies offer a new paradigm for precision intervention. This framework integrates the entire process from mtDNA generation to intercellular transfer and downstream signaling, providing a systematic basis for precision intervention in post-infarction remodeling. Importantly, several components of this model are based on preliminary or indirect evidence and await independent confirmation. - Source: PubMed
Publication date: 2026/05/25
Meng ChaoXia XiaoLiu YiyingLi JunTao ShiyiHuang XuanchunLi Yonghao - The protein activating molecule in Beclin1-regulated autophagy1 (AMBRA1), discovered in 2007, is crucial for autophagy and plays roles in nervous system development, cell survival, and proliferation. Here, we investigated AMBRA1's involvement in various cellular processes using a systems-based "omics" approach, focusing on melanoma. Transcriptomic analysis of AMBRA1 overexpression or knock-down was shown to result in significant dysregulation of several transcripts. We identified several novel roles for AMBRA1 in a range of cellular pathways including cancer signaling pathways such as MAPK, angiogenesis, tissue growth factor signaling, axon guidance, and Wnt signaling. Furthermore, using yeast two-hybrid assays, we identified novel binding partners which provide evidence of new roles for AMBRA1 in different cellular processes. Ultimately, we conclude that AMBRA1 loss upregulates metastatic genes/proteins highlighting AMBRA1 as a tumor suppressor gene in melanoma. - Source: PubMed
Publication date: 2026/06/02
Ibrahim MiladCorazzari MarcoOsman ImanArmstrong JaneCarter Noel - Trichloroethylene (TCE) is extensively utilized within industrial settings. Certain individuals with occupational exposure may develop occupational medicamentosa-like dermatitis due to trichloroethylene (OMDT), with renal injury being a predominant clinical manifestation among OMDT patients. Prior research has demonstrated that TCE-sensitized mice exhibit glomerular podocyte damage and activation of the mTOR signaling pathway, although the precise mechanisms remain unclear. In the present study, we employed Rapamycin, an mTORC1 inhibitor, to intervene in a TCE-sensitized mouse model. This was complemented by TCE-sensitized mice serum-induced mouse podocyte clone-5 (MPC5) cell model to elucidate the mechanism through which mTORC1 contributes to podocyte damage during TCE sensitization. The findings indicate that activation of mTORC1 results in the downregulation of autophagy/beclin-1 regulator-1 (AMBRA1) expression. Following intervention with Rapamycin, there was a significant restoration of AMBRA1 expression in mice, accompanied by increased mitophagy and decreased apoptosis levels. In vitro studies using cell culture models demonstrated that MPC5 cells exposed to serum from TCE-sensitized mice showed markedly reduced expression of PINK1 and Parkin proteins, along with suppressed mitophagy levels. Treatment with Rapamycin or si-AMBRA1 effectively enhanced cellular mitophagy and diminished apoptosis. This study elucidates that TCE sensitization activates the mTORC1 signaling pathway, leading to the downregulation of AMBRA1. The suppression of AMBRA1 impedes the PINK1/Parkin-dependent mitophagy pathway, hindering the timely clearance of damaged mitochondria in podocytes. Consequently, this results in the release of cytochrome C into the cytoplasm, which triggers podocyte apoptosis signaling, compromises the integrity of the glomerular filtration barrier, and ultimately leads to renal dysfunction. - Source: PubMed
Publication date: 2026/06/01
Bai QiruiYou ChenQin ZhuohuiZhu QixingXie Haibo - Environmental pollutants are increasingly recognized as disease modifiers, reshaping host homeostasis and shifting host-pathogen dynamics toward higher infection risk in aquatic ecosystems. Here, we show that the widely used strobilurin fungicide trifloxystrobin (TFS) persistently erodes antiviral competence in fish and increases susceptibility to spring viremia of carp virus (SVCV) by driving dynamin-related protein 1 (Drp1)-mediated excessive mitophagy and sustained mitochondrial dysfunction. Using epithelioma papulosum cyprini (EPC) cells and zebrafish as complementary models, we find that environmentally plausible TFS exposures (2.5-25 μg/L) elevate SVCV permissiveness; notably, this phenotype resolves incompletely after chemical withdrawal. Transcriptomics revealed a dose-concordant shift toward stress/innate immune signaling and mitophagy programs, alongside broad repression of proliferative and DNA-repair pathways. Consistently, TFS induces persistent mitochondrial membrane depolarization, promotes fragmentation and ultrastructural deterioration, and increases mitochondria-lysosome coupling. Mechanistically, TFS elevates Drp1 abundance and Ser616 phosphorylation, promotes Drp1 recruitment to mitochondria, and sustains microtubule-associated protein 1 light chain 3B (LC3B)/lysosomal-associated membrane protein 2 (LAMP2) engagement, accompanied by persistent induction of core autophagy regulators (, , , and ) across extended recovery windows. , prolonged TFS exposure similarly yields durable enhancement of SVCV susceptibility even after long recovery periods, indicating incomplete restoration of host resistance. Together, these findings link a major agricultural fungicide to persistent Drp1-driven mitophagy overactivation and identify long-term antiviral resistance as an ecologically relevant endpoint for pesticide risk assessment and aquatic disease forecasting.IMPORTANCEViral diseases pose a significant challenge to sustainable aquaculture, and effective antiviral interventions remain limited. In this study, we reveal that trifloxystrobin, a widely used fungicide, induces mitochondrial dysfunction and Drp1-mediated excessive mitophagy, leading to long-term suppression of antiviral immune responses in fish. Importantly, this work identifies mitochondrial dynamics as a key determinant of viral susceptibility and demonstrates how environmental pollutants can reshape host-pathogen interactions. By linking mitophagy and Drp1 activation to increased spring viremia of carp virus susceptibility, our findings provide a novel perspective on how pollutants may exacerbate viral infections in aquaculture species. This work underscores the urgent need for ecosystem-based antiviral strategies and offers a mechanistic framework for assessing ecological risks posed by common agricultural chemicals, thereby informing environmental and disease management in aquaculture. - Source: PubMed
Publication date: 2026/06/01
Wang HuanHu YangLiu LeiChen Jiong - Esophageal cancer (EC) remains an extremely lethal cancer with few prognostic biomarkers and specific therapies. Although autophagy is increasingly recognized as a key force behind tumor adaptation and resistance to therapy, its systematic role at the EC progression level for prognostics, as well as for drug target prediction, remains unclear. Here, we attempted to build a systems-wide map linking autophagy- and signaling-related genes and transcriptional dysregulation, patient survival, and druggability in EC. Hub genes were found using an integrative bioinformatics pipeline based on protein-protein interaction networks and further explored using enrichment, expression, survival, and molecular docking analyses. Functional enrichment highlighted autophagy, mitophagy, ferroptosis, and immune signaling as central processes, converging with stress- and metabolism-associated pathways. Expression profile of TCGA-ESCA data demonstrated substantial overexpression of autophagy initiators and elongation factors (ATG3, ATG5, ATG7, ATG12, ATG13), upstream regulators (AMBRA1, UVRAG), and stress/metabolic mediators (TP53, MYD88, GAPDH). Kaplan-Meier analysis indicated three genes, including ATG4A, GABARAPL2, and GAPDH, that exhibited significant expression levels correlating with less survival and emphasizing their prognostic capacities. Screening for drugs also revealed AKT1, TP53, and PIK3R4 as druggable hubs, and many drugs (e.g., Everolimus, Dabrafenib, Trabectedin) showing high-affinity interactions. These findings collectively demonstrate that the progression of EC is supported by a coordinated program that integrates autophagy and metabolic reprogramming with stress and immunological signaling. The study discovers new prognostic markers (ATG4A, GABARAPL2, GAPDH) and druggable targets, which could lead to better risk stratification and smarter drug repurposing. While restricted to in silico analyses, the integrative approach provides a basis for subsequent laboratory confirmation and translational development. - Source: PubMed
Publication date: 2026/05/27
Salehi ShirinMottaghi-Dastjerdi NegarShahbazi BehzadAhmadi NahidGhorbani AbozarSoltany-Rezaee-Rad MohammadYazdani FatemeKhoshdel FarzaneNiazi Mohammad-Javad