Recombinant Human IL-13 R alpha 2 Fc Chimera (CHO), CF

R&D Systems, part of Bio-Techne | Catalog # 7147-IR

R&D Systems, part of Bio-Techne
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7147-IR-100
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Key Product Details

Source

CHO

Accession #

NP_000631.1

Structure / Form

Disulfide-linked homodimer

Conjugate

Unconjugated

Applications

Bioactivity

View all IL-13 R alpha 2 Proteins and Enzymes »

Product Specifications

Source

Chinese Hamster Ovary cell line, CHO-derived human IL-13 R alpha 2 protein
Human IL-13 R alpha 2
(Cys22-Leu342)
Accession # NP_000631		 IEGRMD Human IgG1
(Pro100-Lys330)
N-terminus C-terminus

Purity

>95%, by SDS-PAGE under reducing conditions and visualized by silver stain.

Endotoxin Level

<0.10 EU per 1 μg of the protein by the LAL method.

N-terminal Sequence Analysis

Cys22

Predicted Molecular Mass

64 kDa (monomer)

SDS-PAGE

75-95 kDa, reducing conditions

Activity

Measured by its ability to inhibit IL-13-dependent proliferation of TF-1 human erythroleukemic cells. Kitamura, T. et al. (1989) J. Cell Physiol. 140:323.
The ED50 for this effect is 0.1-0.5 μg/mL in the presence of 8 ng/mL recombinant human IL-13.

Reviewed Applications

Read 1 review rated 4 using 7147-IR in the following applications:

Formulation, Preparation and Storage

7147-IR
Formulation Lyophilized from a 0.2 μm filtered solution in PBS.
Reconstitution
Reconstitute at 100 μg/mL in PBS.

Reconstitution Buffer Available:
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Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.

Background: IL-13 R alpha 2

Interleukin‑13 Receptor alpha 2 (IL‑13 R alpha2), also known as IL‑13 binding protein, and CD213a2, is a widely expressed 55 kDa cytokine receptor that plays an important role in the Th2‑polarized immune responses characteristic of a variety of pathologies, including parasitic infections and allergic asthma (1, 2). Mature human IL‑13 R alpha2 consists of a 317 amino acid (aa) extracellular domain with three fibronectin type‑III domains, a WSxWS motif, a 20 aa transmembrane segment, and a 17 aa cytoplasmic domain (3). Within the ECD, human IL‑13 R alpha2 shares 64% and 62% aa sequence identity with mouse and rat IL‑13 R alpha2, respectively. In both mouse and human, a 40 kDa‑50 kDa soluble form of IL‑13 R alpha2 can be generated by MMP‑8 mediated shedding in vitro (4).  Although this is assumed to occur in vivo in mouse, there is no evidence that shedding occurs in human (5‑7).  In mouse, alternative splicing also leads to sIL‑13 R alpha2, but again, this phenomenon apparently does not occur in human (6‑7).  Thus, the biological effects of human IL‑13 R alpha2 would appear to be mediated exclusively by membrane IL‑13 R alpha2 (7). The biological effects of IL‑13 and IL‑4 are closely related in part due to a shared receptor system. IL‑13 binds to IL‑13 R alpha1 which then forms a signaling complex with IL‑4 R alpha (8, 9). IL‑13 R alpha2 functions as a decoy receptor by binding and internalizing IL‑13 and preventing it from signaling through the IL‑13 R alpha1/IL‑4 R alpha complex (3, 10). IL‑13 R alpha2 can also block IL‑4 induced responses by inhibiting IL‑4 bound IL‑13 R alpha1/IL‑4 R alpha receptor complexes even though it does not itself bind IL‑4 (11, 12). Aside from its decoy function, IL‑13‑activated IL‑13 R alpha2 directly promotes the development of tissue fibrosis by inducing the transcription of TGF‑ beta (13). Presumably, any human soluble IL‑13 R alpha2, if it exists, will retain its ligand binding capability and attenuate responses to IL‑13 but not to IL‑4 (11, 14). The up‑regulation of transmembrane during Th2‑biased immune responses limits the extent of those responses (15‑17).

References

  1. Wynn, T.A. (2003) Annu. Rev. Immunol. 21:425.
  2. Tabata, Y. et al. (2007) Curr. Allergy Asthma Rep. 7:338.
  3. Caput, D. et al. (1996) J. Biol. Chem. 271:16921.
  4. Chen, W. et al. (2008) J. Allergy Clin. Immunol. 122:625.
  5. O’Toole, M. et al. (2008) Clin. Exp. Allergy 38:594.
  6. Chen, W. et al. (2009) J. Immunol. 183:7870.
  7. Kasaian, M.T. et al. (2011) J. Immunol. 187:561.
  8. Andrews, A.-L. et al. (2006) J. Immunol. 176:7456.
  9. Zurawski, S.M. et al. (1995) J. Biol. Chem. 270:13869.
  10. Donaldson, D.D. et al. (1998) J. Immunol. 161:2317.
  11. Andrews, A.-L. et al. (2006) J. Allergy Clin. Immunol. 118:858.
  12. Rahaman, S.O. et al. (2002) Cancer Res. 62:1103.
  13. Fichtner-Feigl, S. et al. (2006) Nat. Med. 12:99.
  14. Zhang, J.G. et al. (1997) J. Biol. Chem. 272:9474.
  15. Chiaramonte, M.G. et al. (2003) J. Exp. Med. 197:687.
  16. Morimoto, M. et al. (2009) J. Immunol. 183:1934.
  17. Zheng, T. et al. (2008) J. Immunol. 180:522.

Long Name

Interleukin 13 Receptor alpha 2

Alternate Names

CD213a2, IL-13Ra2, IL13R alpha 2, IL13RA2

Entrez Gene IDs

3598 (Human); 16165 (Mouse)

Gene Symbol

IL13RA2

UniProt

NP_000631.1 (Human)

Additional IL-13 R alpha 2 Products

Product Documents for Recombinant Human IL-13 R alpha 2 Fc Chimera (CHO), CF

Product Datasheets

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Product Specific Notices for Recombinant Human IL-13 R alpha 2 Fc Chimera (CHO), CF

For research use only

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