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anti-Human CCL3 Antikörper:
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Mouse (Murine) Monoclonal CCL3 Primary Antibody für FACS - ABIN4896814
Eberlein, Nguyen, Victorino, Golden-Mason, Rosen, Homann: Comprehensive assessment of chemokine expression profiles by flow cytometry. in The Journal of clinical investigation 2010
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Human Monoclonal CCL3 Primary Antibody für FACS - ABIN4897110
Payne, Blackinton, Frisbee, Pickeral, Sawant, Vandergrift, Freel, Ferrari, Keene, Tomaras: Transcriptional and posttranscriptional regulation of cytokine gene expression in HIV-1 antigen-specific CD8+ T cells that mediate virus inhibition. in Journal of virology 2014
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Human Monoclonal CCL3 Primary Antibody für FACS - ABIN4897111
Hutnick, Carnathan, Demers, Makedonas, Ertl, Betts: Adenovirus-specific human T cells are pervasive, polyfunctional, and cross-reactive. in Vaccine 2010
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Human Polyclonal CCL3 Primary Antibody für IHC (p), WB - ABIN652466
Wang, Lin, Izumi, Jiang, Lai, Xu, Fang, Lu, Li, Xia, Chang: Increased infiltrated macrophages in benign prostatic hyperplasia (BPH): role of stromal androgen receptor in macrophage-induced prostate stromal cell proliferation. in The Journal of biological chemistry 2012
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Mouse (Murine) Polyclonal CCL3 Primary Antibody für IP, WB - ABIN223561
Neff, Zgraggen, Neff, Jamnicki-Abegg, Suter, Schimmer, Booy, Joch, Pasch, Ward, Beck-Schimmer: Inflammatory response of tracheobronchial epithelial cells to endotoxin. in American journal of physiology. Lung cellular and molecular physiology 2005
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Human Monoclonal CCL3 Primary Antibody für CyTOF, FACS - ABIN4900053
Masih-Khan, Trudel, Heise, Li, Paterson, Nadeem, Wei, Roodman, Claudio, Bergsagel, Stewart: MIP-1alpha (CCL3) is a downstream target of FGFR3 and RAS-MAPK signaling in multiple myeloma. in Blood 2006
Mouse (Murine) Monoclonal CCL3 Primary Antibody für FACS - ABIN4896811
Kieckbusch, Gaynor, Moffett, Colucci: MHC-dependent inhibition of uterine NK cells impedes fetal growth and decidual vascular remodelling. in Nature communications 2015
Human Polyclonal CCL3 Primary Antibody für ELISA, WB - ABIN2475702
Cocchi, DeVico, Garzino-Demo, Arya, Gallo, Lusso: Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8+ T cells. in Science (New York, N.Y.) 1996
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Mouse (Murine) Polyclonal CCL3 Primary Antibody für ELISA, WB - ABIN2475703
Keepers, Gross, Obrig: Monocyte chemoattractant protein 1, macrophage inflammatory protein 1 alpha, and RANTES recruit macrophages to the kidney in a mouse model of hemolytic-uremic syndrome. in Infection and immunity 2007
Tumor levels of CCL2 (mean +/- standard deviation = 530.1 +/- 613.9 pg/mg), CCL3 (102.7 +/- 106.0 pg/mg), and CCL4 (64.98 +/- 48.09 pg/mg) were higher than those found in healthy tissue
During early remission from methamphetamine (MA), model mice exhibited increased anxiety-like behavior and reduced expression of chemokine (C-C motif) ligand 3 (ccl3) in the hippocampus relative to saline-treated mice. Human adults actively dependent on MA and those in early remission had elevated symptoms of anxiety as well as reductions in plasma levels of CCL3, relative to adults with no history of MA abuse.
As depression became more severe the serum levels of MIP-1alpha increased.
results suggested that genetic variants at the CCL3 and CCL4 loci may be marker SNPs for risk of HCV treatment outcome.
Telomere length and mRNA expressions of IL6 and MIP1alpha were significantly longer or higher in bone marrow mesenchymal stem cells of multiple myeloma than those of controls.
The CCL3 and CCL4 chemokines might not be involved in differential susceptibility to the digestive and cardiac clinical forms of chronic Chagas disease, and it seems they do not influence the development of LVSD.
The serum levels of IL-8, MIP-1 alpha, MIP-1 beta, MMP-8, Resistin, FLRG, and BCAM were significantly higher in breast cancer patients, but LAP and TSH-beta levels were lower.
the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.
serum levels of MIP-1alpha could predict survival outcomes in patients with ENKTL.
elevated CCL3 in the leukemic environment suppresses erythropoiesis via CCR1-p38 activation
analysis of sudden infant death syndrome brains shows downregulation of MyD88 in tissue from SIDS brains, as well as the downregulation of the genes encoding CCL3 and UNC13 in the liver
we demonstrate an association of CCL3 expression by CLL cells with increased numbers of CD3+ T cells and CD57+ cells in the lymph node microenvironment, which may promote CLL cell survival and proliferation.
The N termini of CC chemokines are shown to be involved in receptor binding and oligomerization. We also report an alternative CCL3 oligomer structure that reveals how conformational changes in CCL3 N termini profoundly alter its surface properties and dimer-dimer interactions to affect GAG binding and oligomerization. Such complexity in oligomerization and GAG binding enables intricate, physiologically relevant regulatio
CCL3 promotes VEGF-A expression and angiogenesis in human osteosarcoma cells by down-regulating miR-374b expression via JNK, ERK, and p38 signaling pathways.
The residues on the N-loop and beta-sheets of MIP-1a are close to both CCR1 and CCR5, and those in the C-terminal helix region are close to CCR5.
CCL2, 3, 14 have roles in stimulating macrophage bone marrow homing, proliferation, and polarization in multiple myeloma
An increased MIP-1alpha level in nasopharyngeal aspirates from patients with acute respiratory symptoms during the first wheezing episode caused by viral infections might predict recurrent wheezing.
Tregs from subjects with established type 1 diabetes were impaired in their ability to produce CCL3 and CCL4.
Pleural and serum MIP1a were lower in patients with lung cancer compared to lung metastasis, pneumonia, tuberculosis, and transudate pleural effusion.
AEG-1 mediates CCL3/CCR5-induced EMT development via both Erk1/2 and Akt signaling pathway in CM patients, which indicates CCL3/CCR5-AEG-1-EMT pathway could be suggested as a useful target to affect the progression of CM.
miR-125b could play an important role in inflammatory injury of chondrogenic cells and miR-125b affected inflammatory injury of ATDC5 cells via regulating expression of MIP-1alpha and regulating NF-kappaB and JNK signaling pathways.
Leukemogenic effects of the Ptpn11E76K/+mutation in the stem-cell microenvironment is abolished in Ptpn11E76K/+Prx1-Cre+CCL3-/- mice, indicating that CCL3 is important for leukemic transformation.
Parenchymal polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), have a positive correlation with IL1a, IL8, CXCL5, and Mip-1a, suggesting they may attract PMN-MDSC into the tumor
CCL3 plays a significant role in the clearance of infection and resolution of otitis media inflammation and contributes to mucosal host defense of the nasopharyngeal niche, a reservoir for middle ear and upper respiratory infections.
Cytokine array analysis demonstrated that the chemokine CCL3 was elevated in the plasma of AML mice and patients. CCL3 inhibited erythroid differentiation of hematopoietic stem cells, common myeloid progenitors and especially megakaryocytic-erythroid progenitors.
MCP chemokines are activated in peripheral tissues of breast cancer-bearing mice, by a mechanism that involves breast cancer cell-derived Ccl3.
These observations suggest that intra-BM basophil expansion can favor leukemia-tropic hematopoiesis in myeloid leukemia by providing CCL3, a potent inhibitor of normal hematopoiesis and that basophil-derived CCL3 may be a novel target molecule for the treatment of myeloid leukemia.
A marked increase of CCL3 mRNA expression was observed in inflamed paws, with CCL3 protein detected in neutrophils and macrophages by immunohistochemical experiments.
CCL2/CCL3 double-mutant animals are viable, fertile, and do not present with gross abnormalities. Cuprizone increased CCL3 expression in wild-type but not mutant mice. Cuprizone-induced demyelination, oligodendrocyte loss, and astrogliosis were significantly ameliorated in the cortex but not corpus callosum of chemokine-deficient animals.
these data suggest that the chemokine CCL3 is an hippocampal neuromodulator able to regulate synaptic plasticity mechanisms involved in learning and memory functions.
Ccl3 mRNAs increased within 5 h after injury in mouse cortical slices.
Previous exposure to noninjurious ventilation induces a state of tolerance to ventilator-induced lung injury. Down regulation of the chemokine gene Ccl3 could be the mechanism responsible for this effect.
the tissue fibrinolytic system contributes to the induction of macrophage recruitment and CCL3 at the bone injury site, thereby, leading to the enhancement of the repair process.
APOE varepsilon4 genotype specifically modulates astrocyte secretion of potent microglial chemotactic agents, including CCL3
The chemokines monocyte chemotactic protein 1 (MCP1), MIP1alpha, MIP1beta, interferon gamma-induced protein 10 (IP-10), and eotaxin were induced in Saa1 TG mice.
In experimental autoimmune encephalomyelitis there was a significant increase in activation of astrocytes with increased MIP-1alpha expression.
Aged mice had similar levels of IL-1beta, TNF, IFN-gamma, IL-17, and granulocyte colony-stimulating factor following S. pneumoniae infection, compared with young mice, but increased levels of the chemokines CXCL9, CXCL12, CCL3, CCL4, CCL5, CCL11, and CCL17.
Negative modulation of PGE2 signaling reduced infection-induced anti-inflammatory cytokine polarization and enhanced inflammatory chemokines, CCL3 and CCL5.
Granzyme M regulates the release of natural killer cell MIP-1alpha to initiate innate immune responses.
variation in the CCL18-CCL3-CCL4 chemokine gene cluster influences HIV Type 1 transmission and AIDS disease progression
CCL3, CCL4 and CCL5 gene expression was evaluated in response to simian-human immunodeficiency virus (SHIV) infection in a rhesus macaque model.
Stress decreased MIP-1alpha gene expression in both CeA lesioned and non-lesioned animals. But, the CeA lesions increased the tissue expression of MIP-1alpha mRNA prior to and after stress exposure.
This locus represents a small inducible cytokine. The encoded protein, also known as macrophage inflammatory protein 1 alpha, plays a role in inflammatory responses through binding to the receptors CCR1, CCR4 and CCR5. Polymorphisms at this locus may be associated with both resistance and susceptibility to infection by human immunodeficiency virus type 1.
C-C motif chemokine 3
, macrophage inflammatory protein 1 alpha
, G0/G1 switch regulatory protein 19-1
, PAT 464.1
, macrophage inflammatory protein 1-alpha
, small inducible cytokine A3 (homologous to mouse Mip-1a)
, tonsillar lymphocyte LD78 alpha protein
, Macrophage inflammatory protein 1 alpha (Small inducible cytokine A3)
, small inducible cytokine A3
, small-inducible cytokine A3
, MIP-1 alpha
, MIP1 (a)
, heparin-binding chemotaxis protein
, macrophage inflammatory protein-1alpha
, chemokine (C-C motif) ligand 3-like 1
, CC chemokine ligand 3
, chemokine (C-C motif) ligand 3-like 3
, CCL3-like 1