HCSGD entry for CCS
1. General information
Official gene symbol | CCS |
---|---|
Entrez ID | 9973 |
Gene full name | copper chaperone for superoxide dismutase |
Other gene symbols | |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

This gene isn't in Literature mining network.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0004784 | Superoxide dismutase activity | IBA IEA | molecular_function |
GO:0005375 | Copper ion transmembrane transporter activity | TAS | molecular_function |
GO:0005507 | Copper ion binding | TAS | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005634 | Nucleus | IDA | cellular_component |
GO:0005737 | Cytoplasm | IDA | cellular_component |
GO:0005743 | Mitochondrial inner membrane | IBA | cellular_component |
GO:0005829 | Cytosol | IBA | cellular_component |
GO:0006801 | Superoxide metabolic process | IEA TAS | biological_process |
GO:0008270 | Zinc ion binding | IBA | molecular_function |
GO:0015680 | Intracellular copper ion transport | IBA | biological_process |
GO:0016532 | Superoxide dismutase copper chaperone activity | IBA | molecular_function |
GO:0019430 | Removal of superoxide radicals | IBA | biological_process |
GO:0030001 | Metal ion transport | IEA | biological_process |
GO:0034220 | Ion transmembrane transport | TAS | biological_process |
GO:0035434 | Copper ion transmembrane transport | TAS | biological_process |
GO:0046872 | Metal ion binding | IEA | molecular_function |
GO:0051353 | Positive regulation of oxidoreductase activity | IEA | biological_process |
GO:0055085 | Transmembrane transport | TAS | biological_process |
GO:0055114 | Oxidation-reduction process | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.6753697504 | 0.1960952129 | 0.9999902473 | 0.8576268982 |
- 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 | Up | 0.0439715305 |
GSE13712_SHEAR | Down | -0.7556260249 |
GSE13712_STATIC | Down | -0.2916148021 |
GSE19018 | Up | 0.2176000420 |
GSE19899_A1 | Down | -0.3074012960 |
GSE19899_A2 | Down | -0.2138798440 |
PubMed_21979375_A1 | Down | -0.0301625234 |
PubMed_21979375_A2 | Down | -0.7243493883 |
GSE35957 | Down | -0.4236714625 |
GSE36640 | Up | 0.2352523471 |
GSE54402 | Down | -0.1804197451 |
GSE9593 | Up | 0.0217153058 |
GSE43922 | Up | 0.0466462347 |
GSE24585 | Up | 0.4504039151 |
GSE37065 | Up | 0.0204937842 |
GSE28863_A1 | Up | 0.1418703830 |
GSE28863_A2 | Down | -0.1430222755 |
GSE28863_A3 | Up | 0.0433713026 |
GSE28863_A4 | Up | 0.0546107333 |
GSE48662 | Up | 0.2715437920 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-484 | MIMAT0002174 | MIRT042263 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 2 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27268410 | Since CCs play an integral role in oocyte maturation and direct access to human oocytes is limited, we used whole transcriptome analysis of these somatic cells to gain insights into the molecular mechanisms playing a role in follicular senescence |
27268410 | RNA sequencing and bioinformatic tools were used to identify differentially expressed genes between CCs from seven aged and eight young patients (<35 (years old) y |
24666838 | It is used to show how cancer stem cells can drive tumour progression, while non-stem cancer cells (CCs) interfere with this by impeding cancer stem-cell dynamics |
24666838 | Model simulations reveal that reactivation of the replicative senescence programme in CCs initially increases total tumour burden, as attrition from cell death is partially averted, but evolves to provide tumour control in the long-term through increasing constraints on stem-cell compartment kinetics |
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