Cell Signaling Technology

Product Pathways - Metabolism

MRP2 (R260) Antibody #4446

Applications Reactivity Sensitivity MW (kDa) Source
W IP IF-IC H Endogenous > 200 Rabbit

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

Protocols

Specificity / Sensitivity

MRP2 (R260) Antibody detects endogenous levels of total MRP2 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg260 of human MRP2 protein. Antibodies were purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using MRP2 (R260) Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from COS-7 cells, mock transfected (-) or transfected with human MRP2 construct (+), using MRP2 (R260) Antibody.

IF-IC

IF-IC

Confocal immunofluorescent analysis of HepG2 cells (left) and HeLa cells (right) using MRP2 (R260)) Antibody (green). Actin filaments have been labeled with DY-554 phalloidin (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).


Background

Multi-drug resistance protein 2 (MRP2), also known as cMRP, cMOAT, and ABCC2, is an ATP binding cassette (ABC) transporter and part of the multi-drug resistance (MRP) family (1,2). The MRP proteins are membrane proteins that function as organic anion pumps involved in the cellular removal of cancer drugs (2). MRP2 is associated with resistance to a number of cancer drugs, such as cisplatin, etoposide, doxorubicin, and methotrexate (3-5). MRP2 is predominately expressed on the apical membranes in the liver (6-9) and kidney proximal tubules (10). It is responsible for the ATP-dependent secretion of bilirubin glucuronides and other organic anions from hepatocytes into the bile, a process important for the excretion of endogenous and xenobiotic substances. Loss of MRP2 activity is the cause of Dubin-Johnson syndrome, an autosomal recessive disorder characterized by defects in the secretion of anionic conjugates and the presence of melanin like pigments in hepatocytes (11-13).

  1. Keppler, D. and Konig, J. (1997) FASEB J 11, 509-16.
  2. Borst, P. et al. (2000) J Natl Cancer Inst 92, 1295-302.
  3. Taniguchi, K. et al. (1996) Cancer Res 56, 4124-9.
  4. Hooijberg, J.H. et al. (1999) Cancer Res 59, 2532-5.
  5. Cui, Y. et al. (1999) Mol Pharmacol 55, 929-37.
  6. Büchler, M. et al. (1996) J Biol Chem 271, 15091-8.
  7. Paulusma, C.C. et al. (1996) Science 271, 1126-8.
  8. Mayer, R. et al. (1995) J Cell Biol 131, 137-50.
  9. Ito, K. et al. (1998) J Biol Chem 273, 1684-8.
  10. Schaub, T.P. et al. (1997) J Am Soc Nephrol 8, 1213-21.
  11. Dubin, I.N. and Johnson, F.B. (1954) Medicine (Baltimore) 33, 155-97.
  12. Kartenbeck, J. et al. (1996) Hepatology 23, 1061-6.
  13. Paulusma, C.C. et al. (1997) Hepatology 25, 1539-42.

Application References

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Companion Products

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

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