gst-42 Antibody

Here’s a structured FAQ collection for researchers working with GST-42 antibodies, synthesized from peer-reviewed studies and technical documentation:

Advanced Research Questions

How to resolve contradictory data in GST-42-mediated cellular protection assays?

• Approach:

  • Variable control: Standardize Aβ42 aggregate forms (monomers vs. fibrils) using TEM/SDS-PAGE .

  • Assay validation: Include cytotoxicity rescue controls (e.g., MTT assays) with GST-I-Aβ28-induced antibodies showing ~70% cell viability restoration .

  • Conflict source: Discrepancies often arise from Aβ42 preparation methods (e.g., protofibrils vs. mature fibrils) .

What mechanistic insights explain GST-42’s dual role in fibril disassembly and cytotoxicity?

• Hypothesis: Epitope accessibility determines function. GST-I-Aβ28 antibodies target Aβ42 oligomers (IC50: 0.8 μM) but not fibrils, suggesting conformational specificity .

• Validation: Use surface plasmon resonance (SPR) to map binding kinetics to Aβ42 structural variants .

How to design a GST-42 study integrating T cell modulation?

• Protocol:

  • Co-stimulation: Pair GST-42 with CTLA-4 blockers (3 μg/mL) to enhance CD4+ T cell TNF production .

  • Readouts: Measure cytokine profiles (e.g., IFN-γ/IL-4 ratios) via intracellular staining or Luminex .

  • Data: Anti-CTLA-4 increased TNF in Na-GST-1-stimulated PBMCs by 2.3-fold vs. isotype controls .

Table 1: Antibody Efficacy Across Aβ42 Aggregates

Table 2: Cytokine Modulation by GST-42 Adjuvants

*: p < 0.05 vs. control

Methodological Notes

• Phage display libraries enable rapid generation of humanized GST-42 variants without animal immunization.

• Th1/Th2 skewing can be quantitatively assessed via IgG subclass ELISAs .

• For in vivo models, prioritize transgenic mice expressing human Aβ42 to avoid cross-reactivity issues .