Cell Signaling Technology

Product Pathways - Protein Folding

FKBP4 Antibody #11826

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Hm Mk Endogenous 56 Rabbit

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

FKBP4 Antibody recognizes endogenous levels of total FKBP4 protein. This antibody does not cross-react with other FKBP proteins.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Met440 of human FKBP4 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 FKBP4 Antibody.

Background

FKBP4 (also known as FKBP52) is a member of the immunophilin protein family. FKBP4 does not demonstrate appreciable immunosuppressant activity typical of this family, despite its ability to bind the immunosuppressants FK506 and rapamycin (1,2). While FKBP4 plays an important role in immunoregulatory gene expression in B and T lymphocytes, its role in regulating steroid hormone receptor signaling and cytoskeletal dynamics is garnering significant interest. FKBP4 contains two petidyl-prolyl cis-trans isomerase (PPIase) domains, the first of which is implicated in steroid receptor signaling while the second interacts with tubulin and other cytoskeletal components. The maturation of cytoplasmic steroid hormone receptors into a functional conformation requires multiple chaperone and co-chaperone components, including HSP90, p23, and FKBP4 (3,4). FKBP4 interacts with HSP90 to facilitate the folding of androgen, glucocorticoid, and progesterone steroid hormone receptors. Indeed, the functionality of these receptors is impaired in the absence of FKBP4, and research studies have found that null mice demonstrate signs of androgen insensitivity syndrome (5). In addition, FKBP4, which is expressed at high levels in the brain, interacts with hyperphosphorylated Tau and antagonizes Tau's ability to promote microtubule polymerization (6). FKBP4 can also suppress amyloid β toxicity in Drosophila by processing APP (Alzheimer's Amyloid Precursor Protein) to unfold aggregates (7).

  1. Peattie, D.A. et al. (1992) Proc Natl Acad Sci U S A 89, 10974-8.
  2. Wu, B. et al. (2004) Proc Natl Acad Sci U S A 101, 8348-53.
  3. De Leon, J.T. et al. (2011) Proc Natl Acad Sci U S A 108, 11878-83.
  4. Ebong, I.O. et al. (2011) Proc Natl Acad Sci U S A 108, 17939-44.
  5. Sivils, J.C. et al. (2011) Curr Opin Pharmacol 11, 314-9.
  6. Chambraud, B. et al. (2010) Proc Natl Acad Sci U S A 107, 2658-63.
  7. Sanokawa-Akakura, R. et al. (2010) PLoS One 5, e8626.

Application References

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Companion Products

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

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