Cell Signaling Technology

Product Pathways - Nuclear Receptor Signaling

RARα Antibody #2554

Applications Reactivity Sensitivity MW (kDa) Source
W M R Endogenous 55 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

RARα Antibody detects endogenous levels of total RARα protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the sequence of human RARα. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from NIH/3T3 and C6 cells, using RARα Antibody.

Background

Retinoids (vitamin A and its active retinoic acid derivatives) are non-steroid hormones that regulate cell proliferation, differentiation and apoptosis. Retinoic acid receptors (RARalpha, -beta and -gamma) and retinoid X receptors (RXRalpha, -beta and -gamma) are nuclear receptors that function as RAR-RXR heterodimers or RXR homodimers (1-2). In response to retinoid binding, these dimers control gene expression by binding to specific retinoic acid response elements, by recruiting cofactors and the transcriptional machinery, and by indirectly regulating chromatin structure. Finally, ligand binding and phosphorylation of RARalpha by JNK at Thr181, Ser445 and Ser461 controls the stability of RAR-RXR through the ubiquitin-proteasome pathway (3-4). At least four distinct genetic lesions affect RARalpha and result in acute promyelocytic leukemia (APL). The t(15;17) translocation that results in the PML-RARalpha fusion protein is responsible for more than 99% of APL cases, and the fusion protein inhibits PML-dependent apoptotic pathways in a dominant negative fashion. In addition PML-RARalpha inhibits transcription of retinoic acid target genes by recruiting co-repressors, attenuating myeloid differentiation (5-6).

  1. Mangelsdorf, D. J. et al. (1995) Cell 83, 835-839.
  2. Mangelsdorf, D.J. and Evans, R.M. (1995) Cell 83, 841-850.
  3. Bastien, J. and Rochette-Egly, C. (2004) Gene 328, 1-16.
  4. Srinivas, H. et al. (2005) Mol. Cell. Biol. 25, 1054-1069.
  5. de The, H. et al. (1990) Nature 347, 558-561.
  6. Slack, J.L. and Rusiniak, M.E. (2000) Ann. Hematol. 79, 227-238.

Application References

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Companion Products

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

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