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Validated All-in-One™ qPCR Primer for CCL20(NM_001130046.1) Search again
Product ID:
HQP055004
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CKb4, Exodus, LARC, MIP-3-alpha, MIP-3a, MIP3A, SCYA20, ST38
Gene Description:
C-C motif chemokine ligand 20
Target Gene Accession:
NM_001130046.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- B-cell chemotaxis responsiveness to MIP-3alpha is profoundly suppressed by surrogate antigen.
- MIP-3 alpha-induced calcium flux and chemotaxis can be enhanced significantly on peripheral blood and tonsillar B cells after activation by cross-linking surface antigen receptors.
- Increased serum levels of macrophage inflammatory protein-3alpha in chronic viral hepatitis
- MIP-3alpha, in periodontal diseased tissue appears to have an important role in the selective recruitment of T cells in the context of periodontal inflammation.
- x-ray crystal structure of human MIP-3alpha refined to a resolution of 1.7 A compared with the crystal structures of human beta-defensin-1 and -2
- LARC plays a crucial role in the tumor immunity of human malignant glioma
- These results show that the concentration of MIP-3alpha in the endometrium is modulated by these inflammatory mediators.
- co-ordinate activation and binding of ESE-1, Sp1, and NF-kappaB to the MIP-3alpha promoter is required for maximal gene expression by cytokine-stimulated Caco-2 human intestinal epithelial cells.
- demonstrated that P. aeruginosa can provide a direct signal to stimulate CCL20 and GM-CSF production by human mast cells
- Results describe the relationship between cancer-related factors and serum levels of macrophage inflammatory protein-3alpha in hepatocellular carcinoma.
- Cells were also exposed to small size-fractions of ambient particulate matter. Each of these stimuli induced MIP-3alpha/CCL20 gene and protein expression.
- MIP-3alpha and BD-2 have the ability to stimulate odontoblast differentiation in addition to their more traditional role in inflammation
- Calcium triggers beta-defensin (hBD-2 and hBD-3) and chemokine macrophage inflammatory protein-3 alpha (MIP-3alpha/CCL20) expression in monolayers of activated human keratinocytes
- in non-transformed human colonocytes, MEK activation following flagellin/TLR5 engagement is a key modulator for NFkappaB-independent, IL-8 and MIP3alpha expression.
- rowth of a proportion of human hapatocellular carcinoma cells may be mediated by CCL20-CCR6 axis.
- MIP-3alpha was present in follicular fluid and correlated with oocyte maturation, and was regulated by IL-1alpha and TNF-alpha. MIP-3alpha may play an important role in the human preovulatory process.
- the alveolar epithelium is an important source of CCL20 in the lung and may play a critical role in controlling the movement of dendritic cells through the lung both under normal and inflammatory conditions
- plays a role in the advancement of pulpal inflammation via the recruitment of Chemokine (C-C motif) Receptor 6-expressing lymphocytes
- IL-1alpha, TNF-alpha, CCL20, CCL27, and CXCL8 alarm signals are induced in human cells after allergen and irritant exposure
- MIP-3 alpha expression may be involved in the recruitment of CD45R0-positive T cell subsets into the intestinal lamina propria
- MIP-3alpha/CCL20 has a role in amplification of the immune response during renal allograft rejection by attraction of CCR6+ inflammatory cells, which may include DC, to the site of inflammation
- In conclusion, IEC and CRC express CCL20 and its receptor CCR6. CCL20 expression is increased in intestinal inflammation, while CCR6 is upregulated during cell differentiation.
- Vaginal epithelial cells respond to factors present in semen by secreting CCL20, leading to the enhancement of langerhans cells recruitment during HIV transmission.
- Of all chemokines found to be expressed in normal liver and hepatocellular carcinoma (HCC) tissues, CCL20 was the only chemokine showing significant upregulation in HCC tissues.
- The structure of the human macrophage inflammatory protein-3alpha has been determined at 1.81 angstroms resolution by X-ray crystallography
- CXCR4 expression in colorectal liver metastases suggests it is a predictive factor. CCL20 and receptor CCR6 expression in hepatocellular carcinomas indicates a role of a CCL20/CCR6 ligand-receptor pair in liver carcinogenesis and progression.
- Our results add new insight to the important role of the CCL20/CCR6, RANKL system in the bone tissue of rheumatoid arthritis.
- Stimulation of intestinal epithelial cells with IL-21 resulted in enhanced phosphorylation of ERK1/2 and p38 and increased synthesis of macrophage inflammatory protein-3 alpha (MIP-3alpha), a T-cell chemoattractant
- UTP up-regulated approximately 2- to 3-fold the antimicrobial chemokine CCL20 expression and release in primary airway epithelial cells
- MIP-3alpha can regulate mitogenic signaling in colonic epithelial cells.
- Interaction between CCL20 and CCR6 may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation in Helicobacter infection.
- the role of TGF beta 1 in high glucose-induced MIP-3 alpha expression
- H. pylori activates NF-kappaB through an intracellular signaling pathway that involves IkappaB kinase and NF-kappaB-inducing kinase, leading to CCL20 gene transcription
- CCL19, CCL20 and CCL22 factors could play an additive role in the pathogenesis of the inflammatory process leading to bronchiolar fibro-obliteration in lung transplant patients
- The C-terminal alpha-helical region of MIP-3alpha plays a significant part in its broad anti-infective activity
- CCL20(macrophage inflammatory protein 3) concentrations were significantly higher in Synovial fluie (SF) compared with peripheal blood samples; SF mononuclear cells constitutively expressed CCL20 messenger RNA
- exodus-1is a physiologic constituent of amniotic fluide; its concentration increases as term approaches;elevated levels are found in intraamniotic infection/inflammation
- the Th2 cytokine IL-21 is abnormally expressed in Hodgkin lymphoma cells, which regulates STAT3 signaling and attracts Treg cells via regulation of MIP-3alpha
- CCL20 is overexpressed in myeloma microenvironment related to osteolytic bone lesions.
- Data demonstrate that lysophosphatidic acid stimulates thymic stromal lymphopoietin and CCL20 expression in bronchial epithelial cells via CARMA3-mediated NF-kappaB activation.
- study provides evidence that MIP-3alpha is overexpressed in nasopharyngeal carcinoma (NPC) cells and that its serum level is significantly elevated in NPC patients and tightly associated with the disease status and treatment outcome of NPC
- CCL20 mRNA and protein levels were significantly elevated in H. pylori-positive patients and substantially decreased after successful eradication