Cell Signaling Technology
XP Monoclonal Antibody

Product Pathways - Nuclear Receptor Signaling

RARγ1 (D3A4) XP® Rabbit mAb #8965

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IHC-P IF-IC H M (R) (Hm) (B) (Dg) Endogenous 58 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  M=Mouse  R=Rat  Hm=Hamster  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

RARγ1 (D3A4) XP® Rabbit mAb recognizes endogenous levels of total RARγ1 protein. Based upon sequence alignment, this antibody is not predicted to cross-react with RARγ2. This antibody does not cross-react with either RARα or RARβ.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human RARγ1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using RARγ1 (D3A4) XP® Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, either mock transfected (-) or transfected with a Myc/DDK-tagged cDNA expression construct encoding full-length human RARγ1 (hRARγ1-Myc/DDK, +), using RARγ1 (D3A4) XP® Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded cell pellets, HaCaT (positive, left) and Hep3B (negative, right), using RARγ1 (D3A4) XP® Rabbit mAb.


IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carcinoma using RARγ1 (D3A4) XP® Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human skin using RARγ1 (D3A4) XP® Rabbit mAb.

IF-IC

IF-IC

Confocal immunofluorescent analysis of HaCaT cells (positive, left) and Hep3B cells (negative, right) using RARγ1 (D3A4) XP® Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red).


Background

Nuclear retinoic acid (RA) receptors (RARs) consist of three subtypes encoded by separate genes: α (NR1B1), β (NR1B2), and γ (NR1B3). For each subtype, there are at least two isoforms, which are generated by differential promoter usage and alternative splicing and differ only in their N-terminal regions. Retinoids, which are metabolites of vitamin A, serve as ligands for RARs (1). RARs function as ligand-dependent transcriptional regulators and are found to be heterodimerized with retinoid X receptors (RXRs). These transcriptionally active dimers regulate the expression of genes involved in cellular differentiation, proliferation, and apoptosis (2,3). Consequently, RARs play critical roles in a variety of biological processes, including development, reproduction, immunity, and organogenesis (4-6). RAR mutations, fusion proteins, altered expression levels, or aberrant post-translational modifications result in multiple diseases due to altered RAR function and disruption of homeostasis.In contrast to the ubiquitously expressed RARα subtype, RARγ displays a complex tissue-specific expression pattern (7). The hematopoietic system expresses significant levels of RARγ, and a recent study identified a role for RARγ in hematopoietic stem cell maintenance (8). RARγ is the predominant subtype in human and mouse epidermis, representing 90% of the RARs in this tissue (9-11). Given the high level of RARγ expression in the skin, it has been suggested that this nuclear receptor participates in a transcriptional program that governs maintenance and differentiation of normal epidermis and skin appendages. The transcriptional activity of RARγ is under stringent control, in part, through retinoic acid-induced phosphorylation and proteasomal degradation (12).

  1. Rochette-Egly, C. and Germain, P. (2009) Nucl Recept Signal 7, e005.
  2. Delacroix, L. et al. (2010) Mol Cell Biol 30, 231-44.
  3. Eifert, C. et al. (2006) Mol Reprod Dev 73, 796-824.
  4. Mark, M. et al. (2006) Annu Rev Pharmacol Toxicol 46, 451-80.
  5. Niederreither, K. and Dollé, P. (2008) Nat Rev Genet 9, 541-53.
  6. Mark, M. et al. (2009) Nucl Recept Signal 7, e002.
  7. Dollé, P. (2009) Nucl Recept Signal 7, e006.
  8. Purton, L.E. et al. (2006) J Exp Med 203, 1283-93.
  9. Fisher, G.J. et al. (1994) J Biol Chem 269, 20629-35.
  10. Zelent, A. et al. (1989) Nature 339, 714-7.
  11. Elder, J.T. et al. (1991) J Invest Dermatol 96, 425-33.
  12. Giannì, M. et al. (2002) EMBO J 21, 3760-9.

Application References

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Companion Products

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

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