trx-1 Antibody
Product Specs
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
TRX-1 shapes the ASJ sensory neuron's biphasic response to NO exposure. Its trans-nitrosylation activity might inhibit calcium flux to the cytoplasm in ASJ neurons when exposed to NO. Conversely, de-nitrosylation activity might promote calcium flux when NO levels diminish. This regulation of NO-induced ASJ sensory neuron activity mediates the avoidance response to NO-producing organisms like P. aeruginosa.
TRX-1 positively regulates lifespan extension under both normal and caloric restriction conditions. It also promotes dauer formation and the oxidative stress response. TRX-1 contributes to the down-regulation of expression of the insulin-like neuropeptide daf-28 in ASJ neurons in a redox-independent fashion, thereby promoting dauer formation. Furthermore, it negatively regulates the nuclear localization of the intestinal skn-1 transcription factor in a p38 MAPK pathway-dependent and redox-independent manner.
- TRX-1 regulates intestinal SKN-1 nuclear localization in a cell non-autonomous manner. PMID: 26920757
- TRX-1 is a thioredoxin homolog. Worms lacking this gene display reduced lifespan and sensitivity toward oxidative stress. PMID: 16324156
- TRX-1 acts as a fluctuating neuronal signaling modulator within ASJ neurons to monitor the adjustment of neuropeptide expression, including insulin-like proteins, during dauer formation in response to adverse environmental conditions. PMID: 21304598
- Dietary restriction activates TRX-1 in ASJ neurons during aging, which in turn triggers TRX-1-dependent mechanisms to extend adult lifespan in the worm. PMID: 21334311
- Suppression of the C. elegans thioredoxin orthologs trx-1 and trx-2, involved in the redox chaperone activity of exo-3, overrides the protective effect of cep-1 RNAi treatment on neuronal integrity, neuronal function, mean and maximum lifespan. PMID: 20346071
- Data describe a Caenorhabditis elegans thioredoxin (TRX-1), encoded by the gene B0228.5, that is expressed in ASJ ciliated sensory neurons. PMID: 16387300
Q&A
FAQs for TRX1 Antibody in Academic Research
Advanced Research Questions
How to resolve conflicting data on TRX1’s impact on NK cells in transplant models?
TRX1 inhibits NK cell cytotoxicity in vitro but shows variable in vivo effects depending on:
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Dosing schedule: Continuous vs. pulse administration alters NK cell recovery timelines .
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Model specificity: Graft-versus-host disease (GVHD) models require concurrent analysis of:
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NK cell activation markers (CD69/CD107a)
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Cytokine profiles (IFN-γ, granzyme B)
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Resolution strategy:
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Conduct time-course multiparametric flow cytometry paired with single-cell RNA sequencing to map NK cell heterogeneity post-TRX1 treatment.
Three-phase framework:
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Tolerization phase: Co-administer TRX1 + antigen (Days 0–14).
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Withdrawal phase: Monitor immune reconstitution (Days 15–60).
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Challenge phase: Re-expose to antigen + adjuvant (Day 68+) .
Key endpoints:
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Treg/Teff cell ratios
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Antigen-specific IgE vs. IgG isotype switching
How to reconcile TRX1’s species-specific efficacy in translational studies?
Cross-species analysis reveals:
| Species | CD4 Binding Affinity (KD) | Tolerance Induction Efficiency |
|---|---|---|
| Baboon | 2.1 nM | 92% |
| Rhesus | 5.8 nM | 67% |
| Solution: |
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Engineer species-specific TRX1 variants via site-directed mutagenesis of CDR-H3.
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Validate using in silico molecular docking against crystallized CD4 structures.
Data Contradiction Analysis
Conflict: TRX1 shows robust tolerance in baboons but limited efficacy in murine GVHD models.
Root cause:
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Differential FcγR expression alters antibody-dependent cellular phagocytosis (ADCP).
Mitigation:
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Generate human CD4-transgenic murine models.
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Use Fc-silent TRX1 variants (e.g., L234A/L235A mutations) to isolate Fab-mediated effects.
