anti-Chemokine (C-C Motif) Ligand 8 (CCL8) Antibodies

Human Chemokine (C-C Motif) Ligand 8 (CCL8) interaction partners

1. Transcriptome analysis identified several novel IPF-related genes. Among them, CCL8 is a candidate molecule for the differential diagnosis and prediction of survival.

2. Findings exemplify how gradients of chemoattractive factors such as CCL8, drive metastasis and suggest that interference with their operation may provide means for breast cancer management.

3. Detecting expression changes in TLR4 (show TLR4 Antibodies) and MCP2 in the peripheral blood is a feasible method for predicting the occurrence of abortion in women of child-bearing age

4. Dermal fibroblast CCL8 promotes melanoma metastasis.

5. Authors show that the previously observed downregulation of hsa (show CD24 Antibodies)-miR (show MLXIP Antibodies)-92a and upregulation of CCL8 during human cytomegalovirus latent infection of myeloid cells are intimately linked via the latency-associated expression of cytomegalovirus UL111A.

6. CCL8 is an antimicrobial protein with bacteriocidal activity against E. coli.

7. JAK2 (show JAK2 Antibodies) and STAT3 (show STAT3 Antibodies) activation is not essential for CCL3 (show CCL3 Antibodies), CCL5 (show CCL5 Antibodies) or CCL8 induced chemotaxis.

8. Results indicate that the induction of MCP-2/CCL8 by mycobacteria is dependent on the activation of TLR2/PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies) signaling pathway.

9. Macrophage Colony Stimulating Factor (show CSF2 Antibodies) and Monocyte Chemoattractant Protein are elevated in sera of intrinsic asthmatics compared to normal controls.

10. Cytokine treatment increases mRNA stability only for chemokines CCL2 (show CCL2 Antibodies) and CCL8 in airway epithelium, and transient silencing and overexpression of human antigen R affects only chemokine (show CCL1 Antibodies) CCL2 (show CCL2 Antibodies) and CCL8 expression in primary and transformed epithelial cells.

Mouse (Murine) Chemokine (C-C Motif) Ligand 8 (CCL8) interaction partners

1. Findings exemplify how gradients of chemoattractive factors such as CCL8, drive metastasis and suggest that interference with their operation may provide means for breast cancer management.

2. tumours are characterized by expression of inflammatory chemokines (CCL2 (show CCL2 Antibodies), CCL5 (show CCL5 Antibodies), CCL7 (show CCL7 Antibodies), CCL8, CCL12 (show Ccl12 Antibodies), CXCL9 (show CXCL9 Antibodies), CXCL10 (show CXCL10 Antibodies) and CX3CL1 (show CX3CL1 Antibodies)), reflected by an enrichment of activated Foxp3 (show FOXP3 Antibodies)(-) and Foxp3 (show FOXP3 Antibodies)(+) T cells

3. these data reveal an important role for BLIMP1 (show PRDM1 Antibodies) in modulating host defenses by suppressing expression of the chemokine (show CCL1 Antibodies) CCL8.

4. Results indicate that the induction of MCP-2/CCL8 by mycobacteria is dependent on the activation of TLR2/PI3K/Akt (show AKT1 Antibodies) signaling pathway.

5. Data indicate mRNA upregulation of CCR2 (show CCR2 Antibodies) and CCR2 (show CCR2 Antibodies) ligands CCL2 (show CCL2 Antibodies), CCL7 (show CCL7 Antibodies), CCL8, and CCL12 (show Ccl12 Antibodies) in aortas from DOCA/salt-treated hypertension.

6. Vitamin B6 supplementation downregulates Cd8a (show CD8A Antibodies) and Ccl8 mRNA expression, so these candidate genes may play a protective role against colonic aberrant crypt foci development.

7. early and preclinical expression of CCL8 in plasma predicts overall survival of graft-vs.-host disease (GVHD) mice. Together with an involvement of allo-recognition in CCL8 expression, it suggests that CCL8 plays an important role in GVHD pathology.

8. MCP (show CR1L Antibodies)/CCL8 was induced via STAT3 (show STAT3 Antibodies) and exhibited anti-tumor metastatic effect

9. promotes atopic dermatitis by recruiting IL-5 (show IL5 Antibodies)+ Th2 cells

10. CCL8 proteins were present in the vast majority of tissues investigated. mRNA for these proteins was also expressed in most of these tissues suggesting local production and the ability to respond in situ to inflammatory stimuli.