Database Query Results : , , GSTZ1

GSTZ1, Glutathione S-transferase zeta 1: Click to Expand ⟱
Source:
Type:
GSTZ1 (Glutathione S-transferase zeta 1) is an enzyme involved in phase II detoxification and tyrosine catabolism.

Several studies have reported differences in GSTZ1 expression across cancer types. In some malignancies, GSTZ1 expression is downregulated, which might diminish the cell's ability to detoxify carcinogens and reactive oxygen species (ROS). In other instances, GSTZ1 expression may be upregulated, possibly reflecting an adaptive response to increased oxidative stress or drug exposure.

-Enzyme responsible for conversion of DCA to its inactive metabolite, glyoxylate, is downregulated in liver cancer and upregulated in some breast cancers, leading to abnormal expression of the protein.
(desireable to inhibit GSTZ1 to reduce resistance to DCA)


Scientific Papers found: Click to Expand⟱
1887- DCA,    GSTZ1_expression_and_chloride_concentrations_modulate_sensitivity_of_cancer_cells_to_dichloroacetate">GSTZ1 expression and chloride concentrations modulate sensitivity of cancer cells to dichloroacetate
- in-vitro, Var, NA
GSTZ1∅, eff↓, PDKs↓, Chl∅, eff↓,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

GSTZ1∅, 1,  

Core Metabolism/Glycolysis

PDKs↓, 1,  

Migration

Chl∅, 1,  

Drug Metabolism & Resistance

eff↓, 2,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSTZ1, Glutathione S-transferase zeta 1
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
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1203  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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