6Ckine/CCL21B, Mouse

6Ckine/CCL21B Protein, Mouse is a homeostatic lymphoid chemokine that contributes to the entry of T cells and dendritic cells into the lymphoid T-zone. It acts through chemokine receptors CCR7 and CXCR3 to promote fibrogenic and inflammatory cytokine production. Exodus-2/CCL21 Protein, Mouse is a recombinant mouse 6Ckine/CCL21B (S24-G133) expressed by E. coli[1].

Product Specifications

Product Name Alternative

6Ckine/CCL21B Protein, Mouse, Mouse, E. coli

UNSPSC

12352202

Type

Recombinant Proteins

Assay Protocol

https://www.medchemexpress.com/cytokines/exodus-2-ccl21-protein-mouse.html

Purity

98.0

Smiles

SDGGGQDCCLKYSQKKIPYSIVRGYRKQEPSLGCPIPAILFLPRKHSKPELCANPEEGWVQNLMRRLDQPPAPGKQSPGCRKNRGTSKSGKKGKGSKGCKRTEQTQPSRG

Molecular Formula

65956 (Gene_ID) P86792 (S24-G133) (Accession)

Molecular Weight

Approximately 17 kDa, based on SDS-PAGE under reducing conditions.

References & Citations

[1]Förster R, et al. CCR7 and its ligands: balancing immunity and tolerance. Nat Rev Immunol. 2008 May;8 (5) :362-71.|[2]Tanabe, S. et al. Identification of a new mouse beta-chemokine, thy-mus-derived chemotactic agent 4, with activity on T lymphocytes and mesangial cells. J Immunol 1997. 159:5671.|[3]Alt C, et al. Functional expression of the lymphoid chemokines CCL19 (ELC) and CCL 21 (SLC) at the blood-brain barrier suggests their involvement in G-protein-dependent lymphocyte recruitment into the central nervous system during experimental autoimmune encephalomyelitis. Eur J Immunol. 2002 Aug;32 (8) :2133-44.|[4]Balsam Rizeq, et al. The Role of CCL21/CCR7 Chemokine Axis in Breast Cancer Progression. Cancers (Basel) . 2020 Apr 23;12 (4) :1036.|[5]Knut Biber, et al. Neuronal CCL21 up-regulates microglia P2X4 expression and initiates neuropathic pain development. EMBO J. 2011 May 4;30 (9) :1864-73.|[6]Michael Hirth, et al. CXCL10 and CCL21 Promote Migration of Pancreatic Cancer Cells Toward Sensory Neurons and Neural Remodeling in Tumors in Mice, Associated With Pain in Patients. Gastroenterology. 2020 Aug;159 (2) :665-681.e13.