Cell Signaling Technology

Product Pathways - NF-kB Signaling

IRF-6 Antibody #6948

Applications Reactivity Sensitivity MW (kDa) Source
W IP H (Mk) (B) (Dg) Endogenous 58, 60 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  Mk=Monkey  B=Bovine  Dg=Dog
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

IRF-6 Antibody recognizes endogenous levels of total IRF-6 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly121 of human IRF-6 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 IRF-6 Antibody. Absence of IRF-6 in MCF7 cells has been reported previously (5). Doublet has been reported to result from phosphorylation (6).

Background

Interferon regulatory factors (IRFs) comprise a family of transcription factors that function within the Jak/Stat pathway to regulate interferon (IFN) and IFN-inducible gene expression in response to viral infection (1). IRFs play an important role in pathogen defense, autoimmunity, lymphocyte development, cell growth, and susceptibility to transformation. The IRF family includes nine members: IRF-1, IRF-2, ISGF3γ/p48, IRF-3, IRF-4 (Pip/LSIRF/ICSAT), IRF-5, IRF-6, IRF-7, and IRF-8/ICSBP. All IRF proteins share homology in their amino-terminal DNA-binding domains. IRF family members regulate transcription through interactions with proteins that share similar DNA-binding motifs, such as IFN-stimulated response elements (ISRE), IFN consensus sequences (ICS), and IFN regulatory elements (IRF-E) (2).

While IRF family members generally function in innate immune responses, IRF-6 has not been associated in that role. Original studies of IRF-6 found that mutation of the gene for IRF-6 caused Van der Woude Syndrome, an autosomal dominant disorder resulting in mouth abnormalities including cleft lip and palate (3). IRF-6 knockouts show a hyperproliferative epidermis that fails to undergo kerotinocyte differentiation (4). IRF-6 has also been found to interact with the mammary tumor suppressor maspin, and like maspin is expressed in normal mammary epithelial but reduced or absent in breast carcinoma (5). Cellular proliferation may promote IRF-6 phosphorylation leading to its proteasomal dependent degradation (6).

  1. Taniguchi, T. et al. (2001) Annu Rev Immunol 19, 623-55.
  2. Honda, K. and Taniguchi, T. (2006) Nat Rev Immunol 6, 644-58.
  3. Kondo, S. et al. (2002) Nat Genet 32, 285-9.
  4. Richardson, R.J. et al. (2006) Nat Genet 38, 1329-34.
  5. Bailey, C.M. et al. (2005) J Biol Chem 280, 34210-7.
  6. Bailey, C.M. et al. (2008) Mol Cell Biol 28, 2235-43.

Application References

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Companion Products

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

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