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Validated All-in-One™ qPCR Primer for CCL3(NM_002983.2) Search again
Product ID:
HQP016622
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
G0S19-1, LD78, LD78ALPHA, MIP-1-alpha, MIP1A, SCI, SCYA3
Gene Description:
C-C motif chemokine ligand 3
Target Gene Accession:
NM_002983.2(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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Summary
Macrophage inflammatory protein-1 is a so-called monokine that is involved in the acute inflammatory state in the recruitment and activation of polymorphonuclear leukocytes (Wolpe et al., 1988 [PubMed 3279154]). Sherry et al. (1988) [PubMed 3058856] demonstrated 2 protein components of MIP1, called by them alpha and beta.[supplied by OMIM].
Gene References into function
- Inhibition of macrophage inflammatory protein-1 alpha production by Epstein-Barr virus.
- enhances the migration of bone marrow stromal cells
- role in the development of osteolytic lesions in multiple myeloma
- Expression of MIP-1 alpha is induced by stimulation of monocytic cells through Fc gamma receptors and involves activation of CCAAT/enhancer-binding protein beta sites.
- Burned patients seem to be more susceptible to infectious complications when the production of MIP-1 alpha is impaired.
- role of IL-12 and IFN-gamma on inducing inflammatory chemokine (MIP-1alpha) secretion and down-regulating CCR5 expression in human T cells
- After stimulation via high-affinity FcepsilonRI, the transcriptional levels of I-309 (CCL1), MIP-1alpha (CCL3) and MIP-1beta (CCL4) were found among the 10 most increased human and mouse transcripts from approximately 12 000 genes
- Lymphotactin, (MIP)-1alpha, and MIP-1beta chemokines were all rapidly induced by engagement of CD28 and were calcineurin sensitive.
- MIP-1alpha and MIP-1beta show diverging signaling capacities [review]
- The polymorphisms of the MCP-1 and MIP-1A genes do not play a substantial role in genetic predisposition for sarcoidosis or in clinical manifestations of sarcoidosis in this Japanese population.
- may not only mark a subset of patients with a greater risk of having more severe disease but also may play a relevant pathophysiological role in human schistosomiasis mansoni
- Besides its role in development of osteolytic bone destruction, MIP-1 alpha also directly affects cell signaling pathways mediating growth, survival, and migration in MM cells and might play a pivotal role in the pathogenesis of MM.
- AML-1A and AML-1B regulate the expression of this protein in multiple myeloma cells.
- IL-1beta-induced MIP-1alpha and -1beta expression in NT2-N cells
- Cathepsin D specifically cleaves this protein that is expressed in human breast cancer.
- Potential interaction between CCR1 and its ligand, this protein is enduced by endogenously produced interleukin-1 in human hepatomas.
- Transcriptional activation of the MIP-1alpha promoter by RUNX1 and MOZ.
- Therefore, soluble factors such as prostaglandin E(2) released from lung fibroblasts are responsible for the co-culture-induced inhibition of macrophage-derived MIP-1alpha production.
- MIP-1-alpha is substantially regulated upon monocyte contact with various cell wall components from Gran-positive and Gram-negative bacteria.
- Collagen II-reactive T cells in rheumatoid arthritis joints can increase the production of chemokines such as IL-8, MCP-1, and MIP-1 alpha through interaction with synoviocytes.
- lymphocytes of HIV patients display a disrupted capacity to secrete the beta-chemokines MIP-1 alpha and MIP-1 beta, which may constitute a mechanism of immune dysfunction in progressive HIV infection
- produced by neonatal natural killer cells and contributes to suppession of HIV replication
- Role in the development of bronchiolitis associated with influenza and RSV infections in infants and children.
- severe periodontal tissue destruction in Papillon-Lefevre syndrome may be related to excess accumulation of LD78beta and LD78alpha and dysregulation of the microbial-induced inflammatory response in the periodontium
- Involvement of the 3 10 helical-turn motif in chemokine function identifies a novel, functionally essential motif within chemokines.
- Higher amounts of MIP-1alpha, MIP-1beta, and RANTES were detected in plasma of HIV-1-positive individuals, particularly those with concomitant pulmonary tuberculosis, although the increase was not found to be statistically significant.
- HIV p17 was able to reduce MIP-1alpha secretion in IL-15 stimulated monocytes
- High levels of CCL3 are present in synovial fluid of children with juvenile idiopathic arthritis.
- MIP-1 alpha promoter function, gene expression, and protein secretion were each down-regulated following inhibition of FGFR3 signaling.
- findings show that CCL3, CCL4 and CCL5 bind on the Leishmania promastigotes
- MIP-1alpha and other chemokines may constitute a link between the innate immune system and familial Mediterranean fever
- CCL3 concentration was much lower in CSF than in serum of the tickborne encephalitis patients, which argues against its significant role as chemoattractant in this condition.
- found a negative correlation between the tear levels of MIP-1alpha and clinical severity in Cystic fibrosis (CF) patients and a positive correlation between the tear levels of MIP-1alpha and the presence of dry eye findings in CF patients
- brain Alzheimer's disease-derived microvessels express high levels of MIP-1alpha mRNA and release high levels of MIP-1alpha protein
- Significantly higher expression of CCL3 is associated with tumor metastasis and local host defense in oral squamous cell carcinoma
- CCL2 and CCL3 induce both immediate and delayed skin reactions in atopics and nonatopics, and evoke a similar profile of local T cell/macrophage and granulocyte recruitment
- The strong upregulation of CCL3 and CCL4 implicates these chemokines in the etiology and pathogenesis of TLE.
- TNF-alpha unveils a previously unknown capacity of neutrophils to migrate to CCL3 through the intervention of Mac-1.
- Plasma soluble CD40 ligand and stimulated MIP-1alpha production were both reduced (p < or = 0.05) by systemic beta-adrenergic stimulation.
- The results indicate that the MIP-1alpha-906 (TA)(6)/(TA)(6) genotype, either by itself or interacting with the APOE varepsilon4 gene seems to be a genetic risk factor for AD.
- Data show that MIP-1 alpha and MIP-1 beta bind to the HIV co-receptor CCR5 and blok HIV entry into CD4(+) lymphocytes.
- analysis of binding of CC-chemokine receptor 1 (CCR1) to CC-chemokine 3 and 5 (CCL3 and CCL5)
- In support of a direct association with cardiac ischemia, CCL3 levels are elevated in patients with unstable angina pectoris.
- Data show that basal level of Mip-1a is higher in Parkinson's disease patients than in healthy control subjects.
- there was a significant correlation between MIP-1alpha serum level and the overall survival of patients with lymphoid malignancy; patients with higher MIP-1alpha level showed an increased percentage of death & relapse than patients with normal MIP-1alpha
- CysLTs induce MIP-1alpha and MIP-1beta production mediated by ERK via binding to the CysLT(1) receptor in human monocytes/macrophages.