STT3 antibodies detect STT3 isoforms (STT3A and STT3B), which are essential for transferring glycan precursors to nascent proteins during N-glycosylation in the endoplasmic reticulum. Dysregulation of STT3 is linked to cancer progression, immune evasion, and metabolic disorders .
| Property | STT3B Details |
|---|---|
| Molecular Weight | 93.7 kDa (826 amino acids) |
| Subcellular Location | Endoplasmic reticulum (ER) |
| Key Function | Catalyzes initial N-glycosylation step |
| Tissue Expression | Ubiquitous (heart, brain, liver, etc.) |
STT3B, a member of the STT3 family, ensures proper protein folding and surface expression by mediating glycosylation. It recognizes the Asn-X-Ser/Thr motif in nascent polypeptides .
STT3 antibodies are widely used in:
Western Blot (WB): Detects STT3B at ~94 kDa in human, mouse, and rat samples .
Immunohistochemistry (IHC): Localizes STT3B in ER-rich regions of tissues .
Flow Cytometry: Quantifies STT3 expression in cancer stem cells (CSCs) .
Functional Studies: Links STT3 to PD-L1 regulation in immune checkpoint pathways .
PD-L1 Regulation: STT3 isoforms (A/B) drive PD-L1 glycosylation, enabling immune evasion in CSCs. Knockdown of STT3 reduces PD-L1 expression and enhances T-cell-mediated cancer cell killing .
EMT and β-Catenin Signaling: Epithelial-mesenchymal transition (EMT) upregulates STT3 in CSCs via β-catenin/TCF4, promoting tumor aggressiveness .
Therapeutic Synergy: Combining STT3 inhibition with Tim-3 blockade or chemotherapy (e.g., etoposide) enhances anti-tumor efficacy in preclinical models .