Database Query Results : , , Trx2

Trx2, thioredoxin 2: Click to Expand ⟱
Source:
Type:
Trx2 is an essential component of the mitochondrial thioredoxin system, working closely with thioredoxin reductase 2 (TrxR2) to reduce oxidized proteins and protect cells from oxidative stress.
- Mitochondrial thioredoxin (TRX-2).
• By preserving mitochondrial integrity and regulating reactive oxygen species (ROS) levels, Trx2 contributes to cell survival, apoptosis regulation, and metabolic adaptation—all of which are critical in cancer biology.

• Elevated levels of Trx2 may protect tumor cells against oxidative damage, potentially contributing to chemoresistance.
- Overexpression of Trx2 might be associated with more aggressive phenotypes and poorer clinical outcomes, although further studies are needed for definitive prognostic conclusions.
Scientific Papers found: Click to Expand⟱
1981- CUR,    Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity
- in-vitro, Lung, NA
eff↑, Mitocurcumin, showed 25-50 fold higher efficacy in killing lung cancer cells as compared to curcumin
ROS↑, Mitocurcumin increased the mitochondrial reactive oxygen species (ROS
mt-GSH↓, decreased the mitochondrial glutathione levels
Bax:Bcl2↑, increased BAX to BCL-2 ratio
Cyt‑c↑, cytochrome C release into the cytosol
MMP↓, loss of mitochondrial membrane potential
Casp3↑, increased caspase-3 activity
Trx2↓, mitocurcumin revealed that it binds to the active site of the mitochondrial thioredoxin reductase (TrxR2) with high affinity
TrxR↓, In corroboration with the above finding, mitocurcumin decreased TrxR activity in cell free as well as the cellular system.
mt-DNAdam↑, mitochondrial DNA damage

1973- GamB,    Gambogic acid deactivates cytosolic and mitochondrial thioredoxins by covalent binding to the functional domain
- in-vitro, Liver, SMMC-7721 cell
Apoptosis↑, selectively induces apoptosis in cancer cells, at least partially, by targeting the stress response to reactive oxygen species (ROS).
ROS↑,
Trx↓, deactivates TRX-1/2 proteins by covalent binding to the active cysteine residues in the functional domain via Michael addition reactions.
Trx1↓,
Trx2↓,
Mich↑, can react with small nucleophilic molecules, such as GSH and a cysteine-containing peptide, via a Michael addition reaction.


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

mt-GSH↓, 1,   Mich↑, 1,   ROS↑, 2,   Trx↓, 1,   Trx1↓, 1,   Trx2↓, 2,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Bax:Bcl2↑, 1,   Casp3↑, 1,   Cyt‑c↑, 1,  

DNA Damage & Repair ⓘ

mt-DNAdam↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Trx2, thioredoxin 2
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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