Cell Signaling Technology

Product Pathways - Metabolism

PGRMC1 Antibody #12444

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk Endogenous 25 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  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

PGRMC1 Antibody recognizes endogenous levels of total PGRMC1 protein. This antibody does not cross-react with PGRMC2.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human PGRMC1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using PGRMC1 Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing Myc-tagged full-length human PGRMC1 (hPGRMC1-Myc; +), using PGRMC1 Antibody.

Background

PGRMC1 (Progesterone Receptor Membrane Component 1) is a member of a multi-protein progesterone-binding complex (1,2). PGRMC1 has also been named Hpr6.6 (Human membrane progesterone receptor) (3). PGRMC1 does not bind directly to progesterone and has no homology with steroid receptors (4,5). The only known biochemical function of PGRMC1 is binding to heme (6,7), and PGRMC1 shares key structural motifs with cytochrome b5 (5), a heme binding protein that activates cytochrome P450 proteins. PGRMC1 binds and activates P450 proteins (4,8,9), which metabolize drugs, hormones, and lipids. In muticellular organisms, PGRMC1 has binding partners in addition to P450 proteins, complex expression patterns, and prosurvival activities (2,10). A number of research studies have shown that PGRMC1 is induced in tumors, including hormone-responsive tumors. Disrupting PGRMC1 in tumors inactivates pro-survival signaling and sensitizes cells to DNA damage (7,11). Genetic evidence suggests that PGRMC1 inhibition could improve the outcome of genotoxic chemotherapy and hormonal anti-cancer therapies.

  1. Meyer, C. et al. (1996) Eur J Biochem 239, 726-31.
  2. Peluso, J.J. et al. (2008) Endocrinology 149, 534-43.
  3. Gerdes, D. et al. (1998) Biol Chem 379, 907-11.
  4. Min, L. et al. (2005) FEBS J 272, 5832-43.
  5. Mifsud, W. and Bateman, A. (2002) Genome Biol 3, RESEARCH0068.
  6. Ghosh, K. et al. (2005) Biochemistry 44, 16729-36.
  7. Crudden, G. et al. (2006) J Pharmacol Exp Ther 316, 448-55.
  8. Min, L. et al. (2004) Mol Cell Endocrinol 215, 143-8.
  9. Hughes, A.L. et al. (2007) Cell Metab 5, 143-9.
  10. Cahill, M.A. J Steroid Biochem Mol Biol 105, 16-36.
  11. Peluso, J.J. et al. (2008) J Clin Endocrinol Metab 93, 1592-9.

Application References

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Companion Products

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

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