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Human CCL3 Protein expressed in Wheat germ - ABIN1348408
Baschuk, Wang, Watt, Halse, House, Bird, Strugnell, Trapani, Smyth, Andrews: NK cell intrinsic regulation of MIP-1? by granzyme M. in Cell death & disease 2014
serum levels of MIP-1alpha could predict survival outcomes in patients with ENKTL.
elevated CCL3 in the leukemic environment suppresses er (show CCL1 Proteins)ythropoiesis 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 (show CD3 Proteins)+ T cells and CD57 (show B3GAT1 Proteins)+ 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 (show VEGFA Proteins) expression and angiogenesis in human osteosarcoma cells by down-regulating miR (show MLXIP Proteins)-374b expression via JNK (show MAPK8 Proteins), ERK (show EPHB2 Proteins), and p38 (show CRK Proteins) 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 (show CCL2 Proteins), 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 (show CCL4 Proteins).
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 (show CCL1 Proteins) CCL3 was elevated in the plasma of AML (show RUNX1 Proteins) mice and patients. CCL3 inhibited erythroid differentiation of hematopoietic stem cells, common myeloid progenitors and especially megakaryocytic-erythroid progenitors.
MCP (show CR1L Proteins) 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 (show BCL11A Proteins) 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 (show BCL11A Proteins).
A marked increase of CCL3 mRNA expression was observed in inflamed paws, with CCL3 protein detected in neutrophils and macrophages by immunohistochemical experiments.
CCL2 (show CCL2 Proteins)/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 (show CCL1 Proteins)-deficient animals.
these data suggest that the chemokine (show CCL1 Proteins) 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 (show CCL1 Proteins) 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.
variation in the CCL18 (show CCL18 Proteins)-CCL3-CCL4 (show CCL4 Proteins) chemokine (show CCL1 Proteins) gene cluster influences HIV Type 1 transmission and AIDS disease progression
CCL3, CCL4 (show CCL4 Proteins) and CCL5 (show CCL5 Proteins) 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 (show CEACAM3 Proteins) lesioned and non-lesioned animals. But, the CeA (show CEACAM3 Proteins) 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