Symbol
| CCL2
| contributors: mct/ - updated : 27-01-2017
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HGNC name
| chemokine (C-C motif) ligand 2
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HGNC id
| 10618
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Other morbid association(s)
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Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
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constitutional
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| --over
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in chronic hepatite C virus infection and in amyotrophic lateral sclerosis progressing most rapidly | constitutional
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| --over
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associated with chronic inflammation may contribute to the development of heart failure | tumoral
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| --over
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clinical association of CCL2 overexpression in human cancers with poor prognosis | tumoral
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| --over
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CCL2 expression and macrophage infiltration are correlated with poor prognosis and metastatic disease in human breast cancer | constitutional
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| --over
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CCL2 and CCL3 are upregulated in the injured peripheral nerve through epigenetic histone modification in infiltrating immune cells such as macrophages | |
Susceptibility
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to severe chronic hepatite C virus infection (HCV) to pulmonary tuberculosis to idiopathic dilated cardiomyopathy (IDC) |
Variant & Polymorphism
other
| associated with the susceptibility to RA |
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2518 CCL2 G allele, may predispose HCV patients to more severe hepatic inflammation and fibrosis, and predisposing to severe pulmonary tuberculosis |
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G allele at -2518 may be a novel genetic marker of susceptibility to nonfamilial IDC |
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Candidate gene
Marker
| CCL2 and CCL3 are associated with progression of oral squamous cell carcinoma (OSCC) and may be potential biomarkers | Therapy target
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System | Type | Disorder | Pubmed |
neuromuscular | neuropathy | | |
attenuation of CCL2 upregulation by inhibition of ERK phosphorylation appears to be a most promising approach to treat a broader spectrum of inherited peripheral neuropathies | diabete | | | |
use of therapeutic strategies aimed at antagonizing CCL2 or IL6 signaling in diabetic kidney injury | miscelleaneous | pain | | |
antagonists of CCL2/CCR2 are promising agents from treating neuropathic pain. | miscelleaneous | pain | | |
targeting CCL2-CCR2 signaling may be a potentially important new treatment strategy for trigeminal neuralgia |
| | |
| Mcp1 -/- mice synthesized extremely low levels of interleukin-4, interleukin-5, and interleukin-10 | |
in Gjb1-deficient mice (Cx32def), Ccl2 is upregulated in a MEK–ERK-dependent manner (CCL2 reduction is a promising strategy to treat CMT1 neuropathies, particularly in disease forms where axon damage is predominant as in Cx32def mice and the corresponding human disorder, CMT1X) |
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macrophages from Ccr2-null mice were not capable of promoting trans-endothelial migration of tumour cells |