sec23a Antibody

2.1. Role in ER-Golgi Transport

SEC23A is essential for vesicle budding from the ER, as part of the COPII complex. Studies using the antibody have shown its localization to ER transitional faces and vesicles , confirming its role in membrane trafficking.

2.2. Autophagy Regulation

Research in melanoma models demonstrates that SEC23A activates autophagy via S100A8 secretion . Western blot analysis revealed a positive correlation between SEC23A expression and LC3-II (a marker of autophagy initiation) levels (Fig. 2d in ). Overexpression enhances basal autophagy, while silencing impairs it, as evidenced by LC3-puncta assays and TEM analysis .

2.3. ER Stress Resistance

In gastric cancer (GC), SEC23A suppresses ER stress by inducing autophagy and reducing BiP expression (a UPR marker) . Antibody-based IHC and Western blotting confirmed SEC23A upregulation in GC tissues, correlating with poor prognosis (Fig. 1A–G in ).

3.1. Cancer Prognosis

• Melanoma: High SEC23A expression associates with favorable outcomes in SKCM and COAD patients .

• Gastric Cancer: Elevated SEC23A levels correlate with advanced tumor stages and reduced survival (Fig. 1B in ).

3.2. Therapeutic Implications

• Chemosensitivity: SEC23A knockdown enhances 5-FU efficacy in GC by inhibiting autophagy and exacerbating ER stress .

• Biomarker Potential: SEC23A expression levels may serve as a diagnostic/prognostic marker for metastatic cancers .