TRAIL-R2: The Trail Less Traveled

Cells undergo apoptotic programmed cell death in response to various stimuli, and this key mechanism is necessary for cellular morphogenesis, tissue homeostasis, and host defense. Particular cytokines such as tumor necrosis factor (TNF) and the Fas ligand signal through their cooperative death domain-containing receptors tumor necrosis factor receptor 1 (TNFR1) and Fas. Like its cousin TRAIL-R1, TRAIL-R2 is widely expressed in both normal tissues as well as in many types of tumor cells. TRAIL-R2 mediates apoptosis and NF-kB activation in a variety of cells and tissues just the rest of its family receptor proteins TNFR1, Fas, and death receptor 3 (DR3). The TRAIL-R2 antibody was employed by Kim’s group in their characterizations of apoptotic signaling in TRAIL-resistant cancer cell lines – they found that expression of both TRAIL-R1 and the caspase activation inhibitor FLIP were potential TRAIL-sensitivity indicators¹. Liver researchers employed the TRAIL-R2 antibody in their studies on both necrotic and apoptotic cellular responses to novel adenovirus gene therapy treatment approaches². Their studies found that including a soluble Fc in the therapy vectors reduces natural killer cell activation and TNF-alpha production, allowing for a more prolonged and effective treatment. A group of investigators at Wayne State performed immunoprecipitations with the TRAIL-R2 antibody in human breast cancer cells to identify the role of the transcription factor Sp1 in chemosensitization to MS275 and adriamycin³.

Immunohistochemistry-Paraffin: TRAIL-R2 Antibody

In soft tissue sarcoma xenografts, TRAIL also plays a role in apoptosis and antiangiogenesis triggered by low dose chemotherapy doxorubicin regimens, as evidenced by Wang’s work⁴. Furthermore, immunohistochemistry and immunofluorescence experiments with the TRAIL-R2 antibody enabled ophthalmology researchers to demonstrate dual signaling pathways downstream of interferon-gamma in conjunctival apoptosis seen in dry eye syndrome⁵.