EPR3972 precipitates pS2 from MCF7 breast cancer cell lysates.
Flow Cytometry
Analyzes pS2 expression on cell surfaces.
PS2GE2 (NBP2-50275) detects pS2 in CyTOF-ready protocols.
Research Findings on pS2 Antibody Specificity
pS2 antibodies exhibit distinct binding behaviors influenced by phosphorylation and spatial context:
Multiphosphorylation-Dependent Recognition
Studies on RNA Pol II CTD antibodies reveal that phosphorylation at nearby residues modulates anti-pS2 binding:
Phosphorylation Site
Effect on Antibody Binding
Antibody
References
pSer2
Primary target site for antibodies (e.g., E1Z3G, 2G1)
EPR18855, 2G1
pThr4 (adjacent)
Blocks binding when at +2 position relative to pSer2
EPR18855, 2G1
pSer5 (adjacent)
Enhances binding when at +3 position
E1Z3G
C-terminal phosphorylation
Increases affinity for EPR18855 and 2G1
EPR18855, 2G1
Key Insight: Antibodies like EPR18855 and 2G1 preferentially bind pSer2 in C-terminal heptads of the CTD, while phosphorylation at Thr4 or Ser5 in proximity can inhibit recognition.
Cancer Biomarker Potential
pS2 expression is linked to hormone receptor-positive breast cancer and serves as a biomarker:
Breast Cancer: Estrogen induces pS2 in MCF7 cells, correlating with tumor progression.
Gastrointestinal Cancers: pS2 is highly expressed in gastric mucosa and stomach carcinomas.
Pancreatic and Ovarian Cancers: Detected via IHC using antibodies like EPR3972 and PS2GE2.
PIS2 Antibody catalyzes the biosynthesis of phosphatidylinositol (PtdIns) and the PtdIns:inositol exchange reaction. This activity may contribute to reducing excessive cellular PtdIns levels. The exchange activity is attributed to the reverse reaction of PtdIns synthase and is dependent on CMP, which binds tightly to the enzyme.
