|CSC-DC003878||Panoply™ Human CXCR5 Knockdown Stable Cell Line||Inquiry|
|CSC-RG0223||Human CXCR5-FLAG Stable Cell Line-CHO||Inquiry|
|CSC-RG0224||Human CXCR5-FLAG Stable Cell Line-HEK293T||Inquiry|
|CSC-RG0506||Human CXCR5/Gi Stable Cell Line-CHO||Inquiry|
|CSC-RG0643||Human CXCR5/Galpha15 Stable Cell Line-Chem-10||Inquiry|
|CSC-RG1467||Human CXCR5/beta-Arrestin Stable Cell Line-C2C12||Inquiry|
|CSC-RG1468||Human CXCR5/beta-Arrestin Stable Cell Line-CHO||Inquiry|
|CSC-RG1662||Human CXCR5 Stable Cell Line-CHO-K1/Gα15||Inquiry|
|CSC-SC003878||Panoply™ Human CXCR5 Over-expressing Stable Cell Line||Inquiry|
|CDCB156633||Cynomolgus CXCR5 ORF clone||Inquiry|
|CDCB163018||Chicken CXCR5 ORF Clone (NM_001030912)||Inquiry|
|CDCB181140||Rabbit CXCR5 ORF clone (XM_002722702.2)||Inquiry|
|CDCL183858||Mouse CXCR5 ORF clone(NM_007551.2)||Inquiry|
|CDCR313170||Human CXCR5 ORF Clone(NM_032966.2)||Inquiry|
|CDCR380108||Rat Cxcr5 ORF Clone(NM_053303.1)||Inquiry|
|CDFG021921||Mouse Cxcr5 cDNA Clone(BC064059)||Inquiry|
|CDFR013061||Rat Cxcr5 cDNA Clone(NM_053303.1)||Inquiry|
|MiUTR1M-02220||CXCR5 miRNA 3'UTR clone||Inquiry|
|MiUTR1R-00576||CXCR5 miRNA 3'UTR clone||Inquiry|
|MiUTR3H-04249||CXCR5 miRNA 3'UTR clone||Inquiry|
|MiUTR3H-04250||CXCR5 miRNA 3'UTR clone||Inquiry|
Recent Research Progress
CXCR5 (alternative name-burkitt's lymphoma receptor 1 (BLR1)) is a G-protein-coupled seven-transmembrane domain chemokine receptor. Binding of CXCR5 to its ligand CXCL13 leads to activation of multiple intracellular signaling pathways which regulate cell proliferation, survival and migration. Under normal conditions, CXCR5 is expressed by mature B cells and follicular helper T cells and controls their migration to the secondary lymphoid organs from the CXCL13 gradient produced by follicular stromal cells. CXCR5 knockout in mice results in the loss of lymphocytes to the B cell region of the secondary lymphoid organs, resulting in normal homing of B lymphocytes to the B cell region. There is also a lack of coordinated interaction between T helper cells and B cells in CXCR5 deficient mice.
CXCR5 and breast cancer
Recently, studies have found a negative correlation between the expression levels of p53 tumor suppressor and CXCR5 chemokine receptor in MCF-7 human breast cancer cell lines. Lentiviral transduction of MCF-7 cells with p53 shRNA resulted in an increase in CXCR5 at the mRNA and protein levels. The functional activity of CXCR5 in p53 knockdown MCF-7 cells was also increased, as indicated by activation of target gene expression and in response to chemotaxis of the B-lymphocyte chemoattractant CXCL13. Using deletion analysis and site-directed mutagenesis of the CXCR5 gene promoter and enhancer elements, it has been shown that p53 appears to act indirectly on the CXCR5 promoter by inhibiting the activity of the nuclear factor kB (NF-kB) transcription factor. Using chromatin immunoprecipitation and reporter gene analysis, it was further demonstrated that p65/RelA binds to the CXCR5 promoter in a p53-dependent manner and directly transactivates it when overexpressed. Elevated CXCR5 expression may result in abnormal cell survival and migration in breast tumors lacking functional p53 by the mechanisms described.
CXCR5 and trigeminal nerve damage-induced neuropathic pain
Neuropathic pain caused by trigeminal nerve injury is a severely debilitating chronic oral pain syndrome. The spinal chemokine CXCL13 and its receptor CXCR5 have recently been shown to play a key role in the pathogenesis of spinal nerve ligation-induced neuropathic pain. CXCL13 and CXCR5 cause facial and facial pain through extracellular regulated protein kinases (ERK)-mediated proinflammatory cytokine production. Targeting the CXCL13/CXCR5/ERK/tumor necrosis factor-α (TNF-α) and IL-1β pathways in the trigeminal ganglion provides an effective treatment for oral neuropathic pain.
CXCR5 and colon cancer
Colon cancer is one of the most common malignancies in the world and the second most common cause of cancer-related death. Invasion and metastasis are the leading causes of cancer death. CXCL13 and CXCR5 are reported to be overexpressed in colon cancer tissues and are associated with a lower overall survival rate in colon cancer patients. In addition, CXCL13 increases the expression and secretion of MMP-13 and stimulates activation of the PI3K/protein kinase B (AKT) pathway. After CXCR5 was knocked down by small interfering RNA (siRNA), the biological function of CXCL13-regulated colon cancer cells was significantly inhibited. In conclusion, the results suggest that the CXCL13-CXCR5 axis may promote colon cancer cell growth, migration and invasion through the PI3K/AKT pathway.
In addition, studies have shown that CXCL13-CXCR5 mediates prostate cancer cell proliferation via ERK1/2 signaling via JNK signaling. In conclusion, the CXCL13-CXCR5 axis has been shown to be involved in regulating lymphocyte migration and promoting inflammation. In addition, the CXCR5-CXCL13 axis is proposed to be involved in tumor development. Therefore, further study on the occurrence and development mechanism of CXCR5-CXCL13 in tumors has important clinical significance for the diagnosis and treatment of cancer.
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