| Field | Specification |
|---|---|
| Mfr No | |
| Clonality | |
| Host | |
| Immunogen | A synthesized peptide derived from human Apg10 (Atg10) was used as the immunogen for the ATG10 antibody. |
| Isotype | |
| Product Type | |
| Purity | |
| Reactivity | |
| Storage | |
| Target | |
| UniProt # |
Overview
ATG10 Antibody / Autophagy-related protein 10 is a anti-ATG10 Rabbit antibody Recombinant Rabbit Monoclonal clone ABBD-1 supplied in Liquid format. Recommended for workflows such as Western blot (WB), Immunoprecipitation (IP) with listed reactivity in Human, Mouse, Rat.
Key elements and design rationale
- Target: ATG10
- Antibody details: Rabbit, Recombinant Rabbit Monoclonal, clone ABBD-1, isotype Rabbit IgG
- Format: Liquid
- Applications (as listed): WB, IP
Biological background
ATG10 is encoded by the ATG10 gene located on human chromosome 5q14.1. The protein is approximately 220 amino acids long and resides in the cytoplasm, where it transiently associates with autophagic membranes. Functionally, ATG10 acts as an E2-like enzyme, transferring the ATG12 conjugate to ATG5 under the direction of E1-like enzyme ATG7. This conjugation system forms the ATG12-ATG5-ATG16L1 complex that defines the site of autophagosome formation.
The ATG10 antibody detects a 25 kilodalton band by western blot and shows diffuse cytoplasmic staining under confocal microscopy. ATG10 expression increases under nutrient deprivation and oxidative stress, linking metabolic signals to autophagy induction. Inhibition or depletion of ATG10 results in defective autophagosome biogenesis, accumulation of damaged organelles, and increased susceptibility to stress-induced apoptosis.
ATG10 also participates in noncanonical autophagy and immune signaling by modulating antigen presentation and cytokine secretion. Variations in ATG10 have been linked to cancers, inflammatory disorders, and aging-related diseases. Its regulation is tightly controlled through transcriptional activation by FOXO and ATF4, and by post-translational modifications that modulate enzyme activity.
Because of its indispensable role in the autophagy conjugation system, ATG10 provides a molecular link between stress sensing and degradative homeostasis.
Research relevance and current trends
- Connecting protein-level changes to phenotype using orthogonal readouts (genetic perturbation, transcriptomics, imaging).
- Considering isoforms and post-translational regulation when interpreting protein-level changes.
- Comparing results across species and model systems with matched controls.
Common research applications
- Western blotting: compare relative abundance and activation-state changes across conditions.
Interpret changes in signal alongside appropriate controls and, when relevant, in parallel with total-protein or pathway readouts.
Notes for experimental interpretation
- Signal can reflect expression level, isoform composition, and post-translational state; interpret results in the context of your model system and stimuli.
- Species differences and sample matrices can influence epitope recognition; prioritize matched controls and orthogonal confirmation when feasible.
Antibody notes: Monoclonal antibodies provide a defined epitope recognition profile that can support consistent comparisons across experiments.
Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.
