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

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

1. It was shown that MCP2 was able to activate the NF-kappaB (Montrer NFKB1 Anticorps) signaling pathway inducing the epithelial-mesenchymal transition (EMT (Montrer ITK Anticorps)) and promoting the migration and invasion of ESCC cells in vitro.

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

3. 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.

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

5. Dermal fibroblast CCL8 promotes melanoma metastasis.

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

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

8. JAK2 (Montrer JAK2 Anticorps) and STAT3 (Montrer STAT3 Anticorps) activation is not essential for CCL3 (Montrer CCL3 Anticorps), CCL5 (Montrer CCL5 Anticorps) or CCL8 induced chemotaxis.

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

10. Macrophage Colony Stimulating Factor (Montrer CSF2 Anticorps) and Monocyte Chemoattractant Protein are elevated in sera of intrinsic asthmatics compared to normal controls.

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 (Montrer CCL2 Anticorps), CCL5 (Montrer CCL5 Anticorps), CCL7 (Montrer CCL7 Anticorps), CCL8, CCL12 (Montrer Ccl12 Anticorps), CXCL9 (Montrer CXCL9 Anticorps), CXCL10 (Montrer CXCL10 Anticorps) and CX3CL1 (Montrer CX3CL1 Anticorps)), reflected by an enrichment of activated Foxp3 (Montrer FOXP3 Anticorps)(-) and Foxp3 (Montrer FOXP3 Anticorps)(+) T cells

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

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

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

6. Vitamin B6 supplementation downregulates Cd8a (Montrer CD8A Anticorps) 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 (Montrer CR1L Anticorps)/CCL8 was induced via STAT3 (Montrer STAT3 Anticorps) and exhibited anti-tumor metastatic effect

9. promotes atopic dermatitis by recruiting IL-5 (Montrer IL5 Anticorps)+ 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.