HCSGD entry for A2M
1. General information
Official gene symbol | A2M |
---|---|
Entrez ID | 2 |
Gene full name | alpha-2-macroglobulin |
Other gene symbols | A2MD CPAMD5 FWP007 S863-7 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0001869 | Negative regulation of complement activation, lectin pathway | IDA | biological_process |
GO:0002020 | Protease binding | IPI | molecular_function |
GO:0002576 | Platelet degranulation | TAS | biological_process |
GO:0004866 | Endopeptidase inhibitor activity | IEA | molecular_function |
GO:0004867 | Serine-type endopeptidase inhibitor activity | IDA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005576 | Extracellular region | NAS TAS | cellular_component |
GO:0005615 | Extracellular space | IEA | cellular_component |
GO:0005829 | Cytosol | TAS | cellular_component |
GO:0007264 | Small GTPase mediated signal transduction | TAS | biological_process |
GO:0007596 | Blood coagulation | TAS | biological_process |
GO:0007597 | Blood coagulation, intrinsic pathway | TAS | biological_process |
GO:0010951 | Negative regulation of endopeptidase activity | IDA | biological_process |
GO:0019838 | Growth factor binding | IDA | molecular_function |
GO:0019899 | Enzyme binding | IPI | molecular_function |
GO:0019959 | Interleukin-8 binding | IPI | molecular_function |
GO:0019966 | Interleukin-1 binding | IDA | molecular_function |
GO:0030168 | Platelet activation | TAS | biological_process |
GO:0031093 | Platelet alpha granule lumen | TAS | cellular_component |
GO:0043120 | Tumor necrosis factor binding | IDA | molecular_function |
GO:0048863 | Stem cell differentiation | IEA | biological_process |
GO:0051056 | Regulation of small GTPase mediated signal transduction | TAS | biological_process |
GO:0052548 | Regulation of endopeptidase activity | IDA | biological_process |
GO:0070062 | Extracellular vesicular exosome | IDA | cellular_component |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.8713234869 | 0.0534723985 | 0.9999902473 | 0.4358770517 |
- 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 | -0.0712343765 |
GSE13712_SHEAR | Down | -0.1126421028 |
GSE13712_STATIC | Down | -0.1391315569 |
GSE19018 | Up | 0.7964290821 |
GSE19899_A1 | Down | -1.1133019659 |
GSE19899_A2 | Up | 0.2398048796 |
PubMed_21979375_A1 | Down | -0.0083488540 |
PubMed_21979375_A2 | Up | 0.0262450831 |
GSE35957 | Down | -0.1520561246 |
GSE36640 | Down | -0.6111369782 |
GSE54402 | Down | -1.0442674117 |
GSE9593 | Down | -0.2918838823 |
GSE43922 | - | - |
GSE24585 | - | - |
GSE37065 | - | - |
GSE28863_A1 | - | - |
GSE28863_A2 | - | - |
GSE28863_A3 | - | - |
GSE28863_A4 | - | - |
GSE48662 | Up | 0.1728765052 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Name | Drug | Accession number |
---|---|---|
Becaplermin | DB00102 | BTD00053 | BIOD00053 |
Bacitracin | DB00626 | APRD00816 |
Ocriplasmin | DB08888 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-128-3p | MIMAT0000424 | MIRT021948 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-122-5p | MIMAT0000421 | MIRT023224 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-98-5p | MIMAT0000096 | MIRT027430 | Microarray | Functional MTI (Weak) | 19088304 |
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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: 4 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
24807532 | Fucoidan treatment also downregulated the expression of alpha(2)M |
21541797 | Characterization of a novel positive transcription regulatory element that differentially regulates the alpha-2-macroglobulin gene in replicative senescence |
21541797 | Alpha-2-macroglobulin (alpha2M), a protease inhibitor, is implicated in Alzheimer's disease, atherosclerosis, and other age-related diseases |
21541797 | The elevated level of alpha2M mRNA has been described in replicative senescence and it could be used as a biomarker of the aging cells |
21541797 | This report identified a novel transcriptional regulatory element, the alpha2M transcription enhancement element (ATEE), within the alpha2M promoter |
21541797 | This element differentially activates alpha2M expression in senescent versus young fibroblasts |
21541797 | Mutation within ATEE selectively abolished alpha2M promoter activity in senescent (but not young) cells |
21541797 | These results indicated the ATEE, as a positive transcription regulatory element, contributes to the up-regulation of alpha2M during replicative senescence |
15036401 | Among the differentially expressed genes, alpha-2-macroglobulin (alpha(2)M) was selected for further study |
15036401 | Additional assays revealed that the levels of alpha(2)M increased in irreversible growth arrest induced by sublethal H(2)O(2), but not in quiescent state of cultured fibroblasts induced by serum-deprivation, and remained stable in Hela cells |
15036401 | These results suggest that mRNA level of alpha(2)M can be used as a biomarker of aging in cultured fibroblasts |
11250120 | Two-dimensional gel electrophoretic studies on the cellular aging: accumulation of alpha-2-macroglobulin in human fibroblasts with aging |
11250120 | We found that the amount of an alpha-2-macroglobulin (A2M) fragment derived from culture medium increased in the cells with aging |
11250120 | A2M is linked to Alzheimer's disease both genetically and functionally |
11250120 | This is the first report of accumulation of an A2M fragment in senescent fibroblasts |
11250120 | 2D gel analysis revealed that the A2M fragment was down-regulated in the immortalized cells, compared with their normal counterparts, regardless of their passage |
11250120 | Our results suggest: (1) the A2M incorporation into the cells is increased in the process of cellular aging; and (2) A2M may be linked to the age-related phenotypes that were lost during the process of immortalization of human cells |
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