Cell Signaling Technology

Product Pathways - Nuclear Receptor Signaling

Aromatase Antibody #8799

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R (Mk) Endogenous 51 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
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

Aromatase Antibody recognizes endogenous levels of total aromatase protein. This antibody also cross-reacts with a 32 kDa protein of unknown origin in some cells.

Source / Purification

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

Western Blotting

Western Blotting

Western blot analysis of extracts from human and mouse placenta using Aromatase Antibody.

IP

IP

Immunoprecipitation of aromatase from mouse placenta extracts, using Normal Rabbit IgG #2729 (lane 2) or Aromatase Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Aromatase Antibody and secondary antibody Mouse Anti-rabbit IgG (Conformation Specific) (L27A9) mAb #3678.

Background

Aromatase is a member of the cytochrome P450 superfamily of enzymes, which are monooxygenases that catalyze reactions involved in drug metabolism and cholesterol and steroid synthesis (1,2). Aromatase is responsible for the conversion of testosterone into 17-β estradiol (2). Aromatase is mainly expressed in the brain (3), ovaries (4), and placenta (5). Aromatase plays an important role in development of the central nervous system during ontogenesis (6,7), gonadal development, and sex differentiation (8,9). Research studies have suggested that inhibition of aromatase may be an effective therapeutic strategy for postmenopausal breast cancers that are estrogen receptor positive (10,11). Researchers have also linked mutations in aromatase to aromatase excess syndrome (AEXS) and aromatase deficiency (AROD) (12-15).

  1. Harada, N. (1988) Biochem Biophys Res Commun 156, 725-32.
  2. Chen, S.A. et al. DNA 7, 27-38.
  3. Hinshelwood, M.M. et al. (2000) Endocrinology 141, 2050-3.
  4. Pezzi, V. et al. (2003) J Steroid Biochem Mol Biol 87, 181-9.
  5. Peruffo, A. et al. (2011) Gen Comp Endocrinol 172, 211-7.
  6. Montelli, S. et al. (2012) Brain Res , .
  7. Kuntz, S. et al. (2003) Cytogenet Genome Res 101, 283-8.
  8. Ramsey, M. et al. (2007) Differentiation 75, 978-91.
  9. Hu, Q. et al. (2012) J Med Chem 55, 7080-9.
  10. Gilani, R.A. et al. (2012) Breast Cancer Res Treat , .
  11. Montelli, S. et al. (2012) Brain Res , .
  12. Ito, Y. et al. (1993) Proc Natl Acad Sci U S A 90, 11673-7.
  13. Morishima, A. et al. (1995) J Clin Endocrinol Metab 80, 3689-98.
  14. Carani, C. et al. (1997) N Engl J Med 337, 91-5.
  15. Fukami, M. et al. (2012) Int J Endocrinol 2012, 584807.

Application References

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Companion Products


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

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