UBL3 antibodies are widely used to investigate the protein’s role in:
UBL3 regulates MHC II and CD86 surface expression in dendritic cells (DCs) and macrophages by modulating MARCH1-mediated ubiquitination .
Ubl3 knockout mice exhibit dysregulated immune homeostasis, including impaired thymic regulatory T-cell development and abnormal antigen presentation .
UBL3 interacts with polyQ-expanded huntingtin (mHTT) fragments in Huntington’s disease (HD) and colocalizes with α-synuclein in Parkinson’s disease models .
In HD patients, UBL3 forms cytoplasmic and nuclear inclusions in striatal neurons, suggesting a role in mHTT aggregation and toxicity .
UBL3 directs membrane-anchored proteins into small extracellular vesicles (sEVs) via prenylation-dependent mechanisms .
Loss of UBL3 reduces sEV protein content by ~60%, impacting vesicle-mediated cellular communication .
IHC Staining: UBL3 antibodies identified cytoplasmic and nuclear UBL3 inclusions in HD patient brains, correlating with polyQ aggregates .
Western Blot: Antibodies confirmed UBL3’s interaction with α-synuclein in MPP+-treated neuronal models .
Co-Immunoprecipitation: Validated UBL3’s binding to mHTT fragments in HEK293 cells .
| Model | Findings |
|---|---|
| Ubl3⁻/⁻ mice | Elevated MHC II/CD86 on antigen-presenting cells; defective T-cell development. |
| Human DCs | UBL3 deletion increases surface MHC II by ~3-fold, altering adaptive immunity. |