HCSGD entry for CCL2
1. General information
Official gene symbol | CCL2 |
---|---|
Entrez ID | 6347 |
Gene full name | chemokine (C-C motif) ligand 2 |
Other gene symbols | GDCF-2 HC11 HSMCR30 MCAF MCP-1 MCP1 SCYA2 SMC-CF |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0000165 | MAPK cascade | IMP | biological_process |
GO:0001525 | Angiogenesis | TAS | biological_process |
GO:0001666 | Response to hypoxia | IEA | biological_process |
GO:0001938 | Positive regulation of endothelial cell proliferation | IEA | biological_process |
GO:0002548 | Monocyte chemotaxis | IDA | biological_process |
GO:0004672 | Protein kinase activity | TAS | molecular_function |
GO:0005102 | Receptor binding | TAS | molecular_function |
GO:0005576 | Extracellular region | IDA IEA TAS | cellular_component |
GO:0005615 | Extracellular space | IEA | cellular_component |
GO:0005737 | Cytoplasm | IEA | cellular_component |
GO:0006468 | Protein phosphorylation | TAS | biological_process |
GO:0006874 | Cellular calcium ion homeostasis | IEA | biological_process |
GO:0006935 | Chemotaxis | TAS | biological_process |
GO:0006954 | Inflammatory response | IDA | biological_process |
GO:0006955 | Immune response | IEA | biological_process |
GO:0006959 | Humoral immune response | TAS | biological_process |
GO:0006987 | Activation of signaling protein activity involved in unfolded protein response | TAS | biological_process |
GO:0007010 | Cytoskeleton organization | IDA | biological_process |
GO:0007155 | Cell adhesion | TAS | biological_process |
GO:0007165 | Signal transduction | NAS | biological_process |
GO:0007166 | Cell surface receptor signaling pathway | TAS | biological_process |
GO:0007179 | Transforming growth factor beta receptor signaling pathway | IEA | biological_process |
GO:0007186 | G-protein coupled receptor signaling pathway | TAS | biological_process |
GO:0007187 | G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger | TAS | biological_process |
GO:0007259 | JAK-STAT cascade | TAS | biological_process |
GO:0007568 | Aging | IEA | biological_process |
GO:0008009 | Chemokine activity | IEA | molecular_function |
GO:0008201 | Heparin binding | IEA | molecular_function |
GO:0008360 | Regulation of cell shape | IDA | biological_process |
GO:0009408 | Response to heat | IEA | biological_process |
GO:0009612 | Response to mechanical stimulus | IEA | biological_process |
GO:0009617 | Response to bacterium | IEP | biological_process |
GO:0009887 | Organ morphogenesis | TAS | biological_process |
GO:0010332 | Response to gamma radiation | IEA | biological_process |
GO:0010574 | Regulation of vascular endothelial growth factor production | IEA | biological_process |
GO:0010759 | Positive regulation of macrophage chemotaxis | IEA | biological_process |
GO:0014823 | Response to activity | IEA | biological_process |
GO:0016525 | Negative regulation of angiogenesis | IEA | biological_process |
GO:0019079 | Viral genome replication | TAS | biological_process |
GO:0019221 | Cytokine-mediated signaling pathway | IDA | biological_process |
GO:0019725 | Cellular homeostasis | TAS | biological_process |
GO:0030593 | Neutrophil chemotaxis | IEA | biological_process |
GO:0030968 | Endoplasmic reticulum unfolded protein response | TAS | biological_process |
GO:0031100 | Organ regeneration | IEA | biological_process |
GO:0031663 | Lipopolysaccharide-mediated signaling pathway | IDA | biological_process |
GO:0031727 | CCR2 chemokine receptor binding | ISS TAS | molecular_function |
GO:0032570 | Response to progesterone | IEA | biological_process |
GO:0033552 | Response to vitamin B3 | IEA | biological_process |
GO:0034351 | Negative regulation of glial cell apoptotic process | IDA | biological_process |
GO:0035684 | Helper T cell extravasation | ISS | biological_process |
GO:0042493 | Response to drug | IEA | biological_process |
GO:0043025 | Neuronal cell body | IEA | cellular_component |
GO:0043200 | Response to amino acid | IEA | biological_process |
GO:0043491 | Protein kinase B signaling | IMP | biological_process |
GO:0043524 | Negative regulation of neuron apoptotic process | IDA | biological_process |
GO:0043615 | Astrocyte cell migration | IDA | biological_process |
GO:0044267 | Cellular protein metabolic process | TAS | biological_process |
GO:0044344 | Cellular response to fibroblast growth factor stimulus | IEP | biological_process |
GO:0045471 | Response to ethanol | IEA | biological_process |
GO:0046677 | Response to antibiotic | IEA | biological_process |
GO:0048010 | Vascular endothelial growth factor receptor signaling pathway | IEA | biological_process |
GO:0048246 | Macrophage chemotaxis | IDA | biological_process |
GO:0048247 | Lymphocyte chemotaxis | IEA | biological_process |
GO:0050806 | Positive regulation of synaptic transmission | IEA | biological_process |
GO:0050870 | Positive regulation of T cell activation | ISS | biological_process |
GO:0051384 | Response to glucocorticoid | IEA | biological_process |
GO:0051770 | Positive regulation of nitric-oxide synthase biosynthetic process | ISS | biological_process |
GO:0060137 | Maternal process involved in parturition | IEA | biological_process |
GO:0070098 | Chemokine-mediated signaling pathway | IEA | biological_process |
GO:0071222 | Cellular response to lipopolysaccharide | ISS | biological_process |
GO:0071346 | Cellular response to interferon-gamma | IEP ISS | biological_process |
GO:0071347 | Cellular response to interleukin-1 | IEP ISS | biological_process |
GO:0071356 | Cellular response to tumor necrosis factor | IEP ISS | biological_process |
GO:0071407 | Cellular response to organic cyclic compound | IDA | biological_process |
GO:0090265 | Positive regulation of immune complex clearance by monocytes and macrophages | IEA | biological_process |
GO:2000427 | Positive regulation of apoptotic cell clearance | ISS | biological_process |
GO:2000502 | Negative regulation of natural killer cell chemotaxis | IDA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.0203616542 | 0.0003310247 | 0.3434481126 | 0.0333372624 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Down | -0.1611087019 |
GSE13712_SHEAR | Down | -1.2294631300 |
GSE13712_STATIC | Down | -0.5189451088 |
GSE19018 | Down | -2.0439136510 |
GSE19899_A1 | Down | -2.1290723895 |
GSE19899_A2 | Down | -0.0189835143 |
PubMed_21979375_A1 | Down | -5.2160012554 |
PubMed_21979375_A2 | Down | -5.8515273799 |
GSE35957 | Up | 0.2269050217 |
GSE36640 | Down | -2.6541437824 |
GSE54402 | Down | -1.1412786143 |
GSE9593 | Up | 3.4038940099 |
GSE43922 | Down | -1.2232358136 |
GSE24585 | Up | 0.1985595399 |
GSE37065 | Up | 0.4323800589 |
GSE28863_A1 | Up | 0.7460372013 |
GSE28863_A2 | Up | 1.9581216004 |
GSE28863_A3 | Up | 0.3791537729 |
GSE28863_A4 | Up | 0.0117073189 |
GSE48662 | Down | -0.0711485746 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-124-3p | MIMAT0000422 | MIRT004284 | Luciferase reporter assay | Functional MTI | 19404929 |
hsa-miR-155-5p | MIMAT0000646 | MIRT021047 | Proteomics | Functional MTI (Weak) | 18668040 |
hsa-miR-1 | MIMAT0000416 | MIRT024058 | Microarray | Functional MTI (Weak) | 18668037 |
hsa-miR-26b-5p | MIMAT0000083 | MIRT030277 | Microarray | Functional MTI (Weak) | 19088304 |
hsa-miR-24-3p | MIMAT0000080 | MIRT030558 | Microarray | Functional MTI (Weak) | 19748357 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 28 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27883166 | Adipose tissue expression of mRNAs (arbitrary units) for MCP-1 (3585 vs 2020, p=0 |
26924930 | In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions |
26573462 | Senescence-Associated MCP-1 Secretion Is Dependent on a Decline in BMI1 in Human Mesenchymal Stromal Cells |
26573462 | RESULTS: We found that monocyte chemoattractant protein-1 (MCP-1) was secreted as a dominant component of the SASP during expansion of UCB-MSCs and reinforced senescence via its cognate receptor chemokine (c-c motif) receptor 2 (CCR2) by activating the ROS-p38-MAPK-p53/p21 signaling cascade in both an autocrine and paracrine manner |
26573462 | The activated p53 in turn increased MCP-1 secretion, completing a feed-forward loop that triggered the senescence program in UCB-MSCs |
26573462 | Moreover, BMI1, a polycomb protein, repressed the expression of MCP-1 by binding to its regulatory elements |
26573462 | The reduction in BMI1 levels during UCB-MSC senescence altered the epigenetic status of MCP-1, including the loss of H2AK119Ub, and resulted in derepression of MCP-1 |
26573462 | CONCLUSION: Senescence of UCB-MSCs is orchestrated by MCP-1, which is secreted as a major component of the SASP and is epigenetically regulated by BMI1 |
26284488 | The search for mediators of senescent HPMC activity showed that increased SW480 cell proliferation was stimulated by IL-6, migration by CXCL8 and CCL2, invasion by IL-6, MMP-3 and uPA, and epithelial-mesenchymal transition by TGF-beta1 |
26142204 | Vasodilator responses to acetylcholine (Ach) in the isolated aortic rings were measured, serum concentration of glucose, tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) and the expression of VPO1 in the aorta were determined |
26142204 | Endothelial cells were treated with high glucose or H2O2, the concentrations of MCP-1, TNF-alpha and hypochlorous acid (HOCl) and the expression of VPO1 were determined |
26142204 | RESULTS: Vasodilator responses to Ach were impaired markedly and the serum concentrations of glucose, TNF-alpha and MCP-1 were significantly increased in diabetic rats |
26142204 | High glucose treatment significantly decreased cell viability and elevated the levels of MCP-1, TNF-alpha and HOCl and upregulated the expression of VPO1 |
26105007 | Upon LPS treatment, SV cells also developed senescence-associated secretory phenotype (SASP), as demonstrated by the increased expression of TNFalpha, IL-1beta, IL-6, MCP-1, and VEGFalpha |
25808810 | Senescent dermal fibroblasts enhance stem cell migration through CCL2/CCR2 axis |
25808810 | Furthermore, CCL2 was found to enhance stem cell migration, and the inhibition of CCR2, a receptor for CCL2, reduced stem cell migration |
25808810 | These results suggest that senescent fibroblasts recruit stem cells by secreting various factors and that the CCL2/CCR2 axis is one of the mechanisms underlying this phenomenon |
25319743 | Stromovascular cell composition (flow cytometry), the number of senescent cells (senescence-associated-beta-galactosidase staining) and interleukin (IL)-6, IL-1, TNF-alpha and MCP1 mRNA (reverse transcription-PCR) were measured in each sample |
24681605 | Expression of two senescence-associated cytokines (VEGFA and MCP1) was durably increased by adjuvant chemotherapy |
24616496 | However, men having shorter telomeres with high TA showed blunted poststress recovery in systolic BP, heart rate variability, and monocyte chemoattractant protein-1, together with reduced responsivity in diastolic BP, heart rate, and cortisol, in comparison to men with longer telomeres or men with shorter telomeres and low TA |
24185682 | Given senescent biliary epithelial cells (BECs) in damaged small bile ducts in primary biliary cirrhosis (PBC) show increased expression of chemokines CCL2 and CX3CL1 as SASP, we further examined an involvement of CCL2/CCR2 and CX3CL1/CX3CR1 systems in the pathogenesis of PBC |
24185682 | METHODS: We examined immunohistochemically the expression of CCR2, CX3CR1, CCL2 and CX3CL1 in livers taken from the patients with PBC (n = 45) and control livers (n = 78), such as chronic viral hepatitis (CVH; n = 39) |
24185682 | CONCLUSION: CCL2 and CX3CL1 produced by senescent BECs may promote infiltration of corresponding CCR2 and CX3CR1-expressing cells and further aggravate inflammation in bile duct lesion in PBC |
24046862 | We evaluated the effect on senescence by evaluating the senescence-associated proliferation arrest, the percentage of senescence-associated beta-galactosidase-positive cells, and the expression of senescent molecular markers such as IL-6 and MCP1 |
24043758 | Antibody-mediated neutralization of CCL2, but not CCL3, CCL4 or CCL5, prevented NK cell recruitment to the senescent tumors and reduced their elimination |
23940580 | A higher influx of F4/80(+) macrophages and CD4(+) T lymphocytes is measured and is accompanied by increases in mRNA of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) |
23770676 | Coupling quantitative proteomics with small-molecule screens, we identified multiple SASP components mediating paracrine senescence, including TGF-beta family ligands, VEGF, CCL2 and CCL20 |
23763475 | The present study found that H2 O2 (25-100 mumol/L) decreased iPSC adhesion to matrix proteins and endothelial cells, and downregulated gene expression levels of adhesion-related molecules, such as integrin alpha 7, cadherin 1 and 5, melanoma cell adhesion molecule, vascular cell adhesion molecule 1, and monocyte chemoattractant protein-1 |
23117626 | NF90 elicited these effects mainly by repressing the translation of target SASP mRNAs, since silencing NF90 did not increase the steady-state levels of SASP mRNAs but elevated key SASP factors including MCP-1, GROa, IL-6, and IL-8 |
22904099 | Compared with young EC, senescent cells displayed increased expression of senescence-associated beta-galactosidase, nitric oxide synthase (eNOS), and AKT kinase, and secreted increased amounts of growth factors (VEGF, TGF-beta), cytokines (IL-6, IL-8, MCP-1), adhesion molecules (sICAM-1), and matrix proteins (fibronectin) |
21680897 | Telomere disruption increased monocyte secretion of monocyte chemoattractant protein-1, IL-6, and IL-1beta and oxidative burst, similar to that seen in coronary artery disease patients, and lymphocyte secretion of IL-2 and reduced lymphocyte IL-10 |
21486894 | Such senescent bile ductules frequently express chemotactic protein, CCL2 (MCP-1), which may be responsible for chemoattraction of activated HSC around the bile ductules in portal and septal fibrosis and for portal inflammation |
21486894 | The migration of cultured mouse HSC was significantly facilitated in the presence of cultured senescent mouse biliary epithelial cells (BEC), and this migration was mediated by CCL2 secreted from senescent cultured BEC |
21455109 | Sulodexide partially prevents oxidative stress and totally eliminates other senescence-related changes such as increased release of MCP-1, lengthening of the population doubling time, and impaired healing of the cellular monolayer after its mechanical injury |
20570384 | We also immunohistochemically examined the expression of CCL2 and CX3CX1 in livers taken from patients with PBC (n=37) and control livers (n=75) |
20570384 | The expression of CCL2 and CX3CL1 was significantly higher in BECs in inflamed and damaged small bile ducts in PBC, when compared with non-inflamed bile ducts and control livers (p<0 |
20570384 | The expression of CCL2 and CX3CL1 was co-localized with the expression of senescent markers |
20570384 | The expression of CCL2 and CX3CL1 was increased in senescent BECs in PBC |
20212459 | We examined the effect of autophagy inhibitor (3-methyladenine) on the induction of cellular senescence and senescence-associated secretion (CCL2 and CX3CL1) in cultured murine BECs |
20212459 | Furthermore, the secretion level of CCL2 and CX3CL1 increased significantly by various stress and suppressed by the inhibition of autophagy (P<0 |
19526322 | The mRNA levels of IL6, as well as its secretion, increased as preadipocytes matured and became old cells; a similar trend was also found for MCP-1 |
19526322 | LPS significantly increased the mRNA levels of IL-6, as well as its secretion, with a similar trend also observed for MCP-1 |
19298284 | The neutrophil chemoattractant interleukin (IL)-8 was low while the constitutive production of monocyte chemoattractant protein (MCP)-1 was highly elevated in medium from cultured CRL-7815 fibroblasts |
18313665 | TRAIL-stimulated production of several cytokines, IL-8, RANTES, MCP-1 and bFGF, and activation of caspases 1 and 8 was essential for this effect |
16755088 | Angiogenic growth factors secreted by EPCs, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (b-FGF), hepatocyte growth factor (HGF), and macrophage chemoattractant protein (MCP-1) from the culture medium were also measured by enzyme-linked immunosorbent assay |
16755088 | There was no significant difference of angiogenic growth factors (VEGF, HGF, b-FGF, and MCP-1) secreted by EPCs between the two groups |
15308550 | Exogenous ADMA also stimulated secretion of MCP-1 and interleukin-8 |
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