CCL11


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CCL11

A gene on chromosome 17q21.1-q21.2 that encodes eotaxin-1, a CC-type cytokine, which is characterised by two adjacent cysteines and, as with all cytokines, is involved in immunoregulatory and inflammatory processes. Eotaxin-1/CCL11 binds CCR3, is chemotactic for eosinophils—but not mononuclear cells or neutrophils—and is involved in eosinophilic type inflammatory responses (e.g., atopic dermatitis, allergic rhinitis, asthma and parasitic infections).
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Genetic variations in CCL11 and FLNB were shown to be potentially associated with the clinical benefit from ENMD-2076, while gene variations in EGFR and CYP4B1 polymorphism could be associated with lack of clinical benefit.
For example, CCL11, a normal eosinophil associated chemokine, increases in plasma with age and when administered to young mice reduces neurogenesis.
Although we did not detect any SNP associated with either oxidative DNA damage or IUGR, in univariate analysis we found four genes (MBL2, CCL7, CCL11, and CCL18) modifying the incidence of LBW.
4] also induced expression of CCL11, CCL5, CCL3, and CXCL2, and BB exposure resulted in upregulation of CCL4.
4] Human genes: RPLPO, ribosomal protein, large, P0; PPIA, peptidylprolyl isomerase A (cyclophilin A); TNFRSF1A, tumor necrosis factor receptor superfamily, member 1A; CCL11, CCL17, CCL19, CCL22, CCL3, CCL4, chemokine (C-C motif) ligand 11, 17, 19, 22, 3, and 4; CL5 chemokine (C-C motif) ligand 5; CCR1, CCR7, CCR8, chemokine (C-C motif) receptor 1, 7, and 8; CD86, CD86 molecule; CXCL12, chemokine (C-X-C motif) ligand 12 (stromal cell-derived factor 1); CXCL2, chemokine (C-X-C motif) ligand 2; CXCR4, chemokine (C-X-C motif) receptor 4; L128, interleukin 12B (natural killer cell-stimulating factor 2, cytotoxic lymphocyte maturation factor 2, p40); IL15, IL4, IL8, interleukin 15, 4, and 8; HPRT1, hypoxanthine phosphoribosyltransferase 1; PGK1, phosphoglycerate kinase 1.
Especially, by removing chemokine called CCL11 which prevents regeneration of brain tissues, MSCs induce regeneration of stem cells called Nestin-positive cells in animal brains, which eventually regenerated brain cells.
Rando's laboratory used shared circulation in mice to discover the chemical CCL11 in the blood of old mice responsible for inhibiting stem cells in the brain.
Decreased protein concentration without gene down-regulation was observed for CCL, CCL11, IL-1[alpha], and vascular endothelial growth factor (VEGF).
No change in protein and mRNA expression was concordantly found for CCL5, CCL11, CXCL10, and VEGF.