Premium Phosphosite-Specific 7TM Antibodies
Your Resource for GPCR Research
Select Your Country of Delivery below

CXC Chemokine Receptor 3 Antibodies

Close filters
No results were found for the filter!
NEW
Agonist-induced Serine358/Threonine360/Serine361 phosphorylation of the CXC Chemokine Receptor 3
pS358/pT360/pS361-CXCR3 (phospho-CXC Chemokine...
Serine358/Threonine360/Serine361 (S358/T360/S361) are a major phosphorylation sites of the CXCR3 receptor. The pS358/pT360/pS361-CXCR3 detects phosphorylation in response to high- and low-efficacy agonists. S358/T360/S361 phosphorylation...
$ 375.00 *
Details
NEW
Validation of the CXCR3 Receptor in transfected HEK293 cells.
CXCR3 (non-phospho), CXCR3 Chemokine Receptor...
The non-phospho-CXCR3 receptor antibody is directed against the distal end of the carboxyl-terminal tail of human CXCR3. It can be used to detect total CXCR3 receptors in Western blots independent of phosphorylation.
$ 375.00 *
Details

 

C-X-C chemokine receptor 3 (CXCR3), encoded by CXCR3, is a class A G protein-coupled receptor activated by the interferon-inducible chemokines CXCL9, CXCL10, and CXCL11. The canonical human splice variant, CXCR3-A, couples predominantly to Gi/o and directs cell migration along chemokine gradients. CXCR3 is expressed mainly on activated T cells, including T helper 1 and effector CD8⁺ T cells, as well as on subsets of natural killer cells. It helps recruit these cells to sites of infection and inflammation and can support effector T-cell infiltration into tumors. Human CXCR3 also produces alternative splice variants, including CXCR3-B, whose signaling properties differ from those of CXCR3-A. The three endogenous ligands differ in their ability to recruit β-arrestins and induce receptor internalization, with CXCL11 generally producing stronger internalization in experimental systems. The small-molecule antagonist AMG 487 reached phase 2a testing for psoriasis, where it did not significantly improve disease severity compared with placebo. No CXCR3-selective drug is currently approved for therapeutic use. CXCR3 receptor desensitization, β-arrestin recruitment and internalization are regulated by phosphorylation of carboxyl-terminal serine358, threonine360, serine361 (pS358/pT360/ps361-CXCR3). This nomenclature refers to the human CXCR3 but is conserved in mice and rats. For more information on CXCR3 pharmacology please refer to the IUPHAR database. For further reading refer to:

Bachelerie F, Ben-Baruch A, Burkhardt AM, Combadiere C, Farber JM, Graham GJ, Horuk R, Sparre-Ulrich AH, Locati M, Luster AD, Mantovani A, Matsushima K, Murphy PM, Nibbs R, Nomiyama H, Power CA, Proudfoot AE, Rosenkilde MM, Rot A, Sozzani S, Thelen M, Yoshie O, Zlotnik A. International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors. Pharmacol Rev. 2013 Nov 11;66(1):1-79. doi: 10.1124/pr.113.007724. Print 2014. Review. Erratum in: Pharmacol Rev. 2014 Apr;66(2):467. PubMed PMID: 24218476; PubMed Central PMCID: PMC3880466.

  C-X-C chemokine receptor 3 (CXCR3), encoded by CXCR3 , is a class A G protein-coupled receptor activated by the interferon-inducible chemokines CXCL9, CXCL10, and CXCL11. The canonical... read more »
Close window
CXC Chemokine Receptor 3 Antibodies

 

C-X-C chemokine receptor 3 (CXCR3), encoded by CXCR3, is a class A G protein-coupled receptor activated by the interferon-inducible chemokines CXCL9, CXCL10, and CXCL11. The canonical human splice variant, CXCR3-A, couples predominantly to Gi/o and directs cell migration along chemokine gradients. CXCR3 is expressed mainly on activated T cells, including T helper 1 and effector CD8⁺ T cells, as well as on subsets of natural killer cells. It helps recruit these cells to sites of infection and inflammation and can support effector T-cell infiltration into tumors. Human CXCR3 also produces alternative splice variants, including CXCR3-B, whose signaling properties differ from those of CXCR3-A. The three endogenous ligands differ in their ability to recruit β-arrestins and induce receptor internalization, with CXCL11 generally producing stronger internalization in experimental systems. The small-molecule antagonist AMG 487 reached phase 2a testing for psoriasis, where it did not significantly improve disease severity compared with placebo. No CXCR3-selective drug is currently approved for therapeutic use. CXCR3 receptor desensitization, β-arrestin recruitment and internalization are regulated by phosphorylation of carboxyl-terminal serine358, threonine360, serine361 (pS358/pT360/ps361-CXCR3). This nomenclature refers to the human CXCR3 but is conserved in mice and rats. For more information on CXCR3 pharmacology please refer to the IUPHAR database. For further reading refer to:

Bachelerie F, Ben-Baruch A, Burkhardt AM, Combadiere C, Farber JM, Graham GJ, Horuk R, Sparre-Ulrich AH, Locati M, Luster AD, Mantovani A, Matsushima K, Murphy PM, Nibbs R, Nomiyama H, Power CA, Proudfoot AE, Rosenkilde MM, Rot A, Sozzani S, Thelen M, Yoshie O, Zlotnik A. International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors. Pharmacol Rev. 2013 Nov 11;66(1):1-79. doi: 10.1124/pr.113.007724. Print 2014. Review. Erratum in: Pharmacol Rev. 2014 Apr;66(2):467. PubMed PMID: 24218476; PubMed Central PMCID: PMC3880466.

Recently viewed