Cell Signaling Technology

Product Pathways - Neuroscience

GSTP1 (3F2) Mouse mAb #3369

Applications Reactivity Sensitivity MW (kDa) Isotype
W IHC-P IF-IC H Mk Endogenous 23 Mouse IgG1

Applications Key:  W=Western Blotting  IHC-P=Immunohistochemistry (Paraffin)  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

GSTP1 (3F2) Mouse mAb detects endogenous levels of total GSTP1 protein. The antibody does not cross react with GST-tagged proteins.

Source / Purification

Monoclonal antibody is produced by immunizing animals with recombinant GSTP1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from PC3 cells and human cerebellum using GSTP1 (3F2) Mouse mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carcinoma using GSTP1 (3F2) Mouse mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lymphoma using GSTP1 (3F2) Mouse mAb.


IF-IC

IF-IC

Confocal immunofluorescent analysis of PC3 cells using GSTP1 (3F2) Mouse mAb (green). Actin filaments have been labeled with DY-554 phalloidin (red).

Background

Glutathione S-transferases (GSTs) are a family of isoenzymes that detoxify electrophiles through conjugation to thiol-reduced glutathione (GSH). Thus, they are critical in protecting cells from toxins (drugs, pesticides, carcinogens) and oxidative stress (1). Eight isoforms of cytosolic-soluble GSTs (α, κ, μ, π, σ, θ, ζ, and ω) are identified, while only GST-α, -μ, and -π are described in the central nervous system (2). GSTP1 (GSTπ) is overexpressed in early stages of carcinogenesis and can be used as a neoplastic marker in tumor tissues (3). GSTP1 directly inhibits TRAF2 and JNK but not NF-κB (4,5). Corresponding GSTP1 gene polymorphisms affect substrate selectivity and stability, and the oxidative milieu in dopaminergic neurons, which increases the susceptibility to Parkinson’s disease (6).

  1. Hayes, J.D. et al. (2005) Annu Rev Pharmacol Toxicol 45, 51-88.
  2. Mannervik, B. et al. (2005) Methods Enzymol 401, 1-8.
  3. Ali-Osman, F. et al. (1997) Clin Cancer Res 3, 2253-61.
  4. Elsby, R. et al. (2003) J Biol Chem 278, 22243-9.
  5. Wu, Y. et al. (2006) Oncogene 25, 5787-800.
  6. Castro-Caldas, M. et al. (2009) J Mol Neurosci 38, 114-27.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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