HCSGD entry for CLU
1. General information
Official gene symbol | CLU |
---|---|
Entrez ID | 1191 |
Gene full name | clusterin |
Other gene symbols | APO-J APOJ CLI CLU1 CLU2 KUB1 NA1/NA2 SGP-2 SGP2 SP-40 TRPM-2 TRPM2 |
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:0001836 | Release of cytochrome c from mitochondria | IC | biological_process |
GO:0002576 | Platelet degranulation | TAS | biological_process |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005576 | Extracellular region | TAS | cellular_component |
GO:0005615 | Extracellular space | IDA | cellular_component |
GO:0005634 | Nucleus | IEA | cellular_component |
GO:0005739 | Mitochondrion | IDA | cellular_component |
GO:0005783 | Endoplasmic reticulum | IEA | cellular_component |
GO:0005829 | Cytosol | IEA | cellular_component |
GO:0006629 | Lipid metabolic process | NAS | biological_process |
GO:0006956 | Complement activation | TAS | biological_process |
GO:0006958 | Complement activation, classical pathway | IEA | biological_process |
GO:0007596 | Blood coagulation | TAS | biological_process |
GO:0008219 | Cell death | IEA | biological_process |
GO:0009615 | Response to virus | IEP | biological_process |
GO:0016887 | ATPase activity | IDA | molecular_function |
GO:0030168 | Platelet activation | TAS | biological_process |
GO:0031012 | Extracellular matrix | IDA | cellular_component |
GO:0031093 | Platelet alpha granule lumen | TAS | cellular_component |
GO:0031625 | Ubiquitin protein ligase binding | IDA | molecular_function |
GO:0031966 | Mitochondrial membrane | IEA | cellular_component |
GO:0032436 | Positive regulation of proteasomal ubiquitin-dependent protein catabolic process | IMP | biological_process |
GO:0032463 | Negative regulation of protein homooligomerization | IMP | biological_process |
GO:0034366 | Spherical high-density lipoprotein particle | IDA | cellular_component |
GO:0042583 | Chromaffin granule | IEA | cellular_component |
GO:0043065 | Positive regulation of apoptotic process | IMP | biological_process |
GO:0043691 | Reverse cholesterol transport | TAS | biological_process |
GO:0045087 | Innate immune response | IEA | biological_process |
GO:0048471 | Perinuclear region of cytoplasm | IDA | cellular_component |
GO:0050821 | Protein stabilization | IDA | biological_process |
GO:0051092 | Positive regulation of NF-kappaB transcription factor activity | IMP | biological_process |
GO:0051787 | Misfolded protein binding | IDA IPI | molecular_function |
GO:0051788 | Response to misfolded protein | IDA | biological_process |
GO:0061077 | Chaperone-mediated protein folding | IDA | biological_process |
GO:0097193 | Intrinsic apoptotic signaling pathway | IDA | biological_process |
GO:1902230 | Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage | IMP | biological_process |
GO:2000060 | Positive regulation of protein ubiquitination involved in ubiquitin-dependent protein catabolic process | IMP | biological_process |
GO:2001244 | Positive regulation of intrinsic apoptotic signaling pathway | IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.2707066031 | 0.0004957031 | 0.9680564325 | 0.0411066038 |
- 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 | 1.7735378435 |
GSE13712_SHEAR | Down | -1.4970800457 |
GSE13712_STATIC | Down | -1.7999239206 |
GSE19018 | Down | -1.1248229379 |
GSE19899_A1 | Down | -0.9017296375 |
GSE19899_A2 | Down | -2.3594716564 |
PubMed_21979375_A1 | Down | -2.2514731370 |
PubMed_21979375_A2 | Down | -1.9492706390 |
GSE35957 | Down | -0.7964657760 |
GSE36640 | Up | 1.0539120327 |
GSE54402 | Down | -0.7501805942 |
GSE9593 | Up | 0.3635162523 |
GSE43922 | Down | -1.0712588292 |
GSE24585 | Down | -0.7811399802 |
GSE37065 | Up | 0.2252269731 |
GSE28863_A1 | Up | 0.8568749167 |
GSE28863_A2 | Up | 0.2955979271 |
GSE28863_A3 | Up | 0.2496727230 |
GSE28863_A4 | Down | -0.4280544426 |
GSE48662 | - | - |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-425-5p | MIMAT0003393 | MIRT039321 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-18a-3p | MIMAT0002891 | MIRT040971 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
---|---|---|---|---|---|---|---|
hsa-miR-125b-5p | MIMAT0000423 | NA | hsa-miR-125b | 18056640 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 17 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
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24937130 | ATM regulates insulin-like growth factor 1-secretory clusterin (IGF-1-sCLU) expression that protects cells against senescence |
24937130 | Here, we show that expression of secretory clusterin (sCLU), a known pro-survival extracellular chaperone, is transcriptionally up-regulated during both RS and SIPS, but not in oncogene-induced senescence, consistent with a DNA damage-inducible mechanism |
23468063 | Following pretreatment with subcytotoxic concentrations of copper sulfate, U87-MG tumor cells showed typical aging characteristics, including reduced cell proliferation, cell enlargement, increased level of senescence-associated beta-galactosidase (SA beta-gal) activity, and overexpression of several senescence-associated genes, p16, p21, transforming growth factor beta-1 (TGF-beta1), insulin growth factor binding protein 3 (IGFBP3) and apolipoprotein J (ApoJ) |
23155386 | Expression of apolipoprotein J (Apo J), connective tissue growth factor (CTGF), fibronectin, and laminin were examined by real-time PCR, western blot, or ELISA experiments |
23155386 | Exposure to 8% of CSE markedly increased the number of SA-ss-Gal positive cells to up to 82%, and the mRNA expression of Apo J, CTGF, and fibronectin by approximately 3-4 fold |
23155386 | Treatment with 8% of CSE also increased the protein expression of Apo J and CTGF and the secretion of fibronectin and laminin |
22465014 | Over-expression of human clusterin increases stress resistance and extends lifespan in Drosophila melanogaster |
22465014 | Clusterin is a disulfide-linked heterodimeric glycoprotein that has been implicated in a variety of biological processes |
22465014 | Its expression has been shown to be elevated during cellular senescence and normal aging, but it is uncertain whether clusterin protects against aging or whether its expression is a consequence of aging |
22465014 | To investigate the functions of clusterin during organismal aging, we established transgenic Drosophila alleles to induce the expression of the secretory form of human clusterin (hClu(S)) using the Gal4/UAS system |
22465014 | In addition, clusterin was found to prevent the inactivation of glutamine synthetase (GS) by metal-catalyzed oxidation (MCO) in vitro, and this protection was only supported by thiol-reducing equivalents, such as, DTT or GSH, and not by ascorbate (a non-thiol MCO system) |
22465014 | Furthermore, this protection against GS inactivation by clusterin was abolished by reacting clusterin with N-ethylmaleimide, a sulfhydryl group-modifying agent |
22465014 | Taken together, these results suggest that a disulfide-linked form of clusterin functions as an antioxidant protein via its cysteine sulfhydryl groups to reduce ROS levels and delay the organismal aging in fruit flies |
22016805 | Apolipoprotein J/clusterin in human erythrocytes is involved in the molecular process of defected material disposal during vesiculation |
20554622 | Levels of apolipoprotein J (Apo J), SM22, and osteonectin (SPARC) mRNA were determined by real-time PCR analysis |
20554622 | RESULTS: TGF-beta2 increased SA-beta-Gal activity, lipid peroxidation, and the mRNA expressions of Apo J, SM22, and SPARC |
19171648 | Expression of senescence-associated genes (apolipoprotein J [Apo J], connective tissue growth factor [CTGF], fibronectin, and SM22) was examined by real-time PCR and induction of signal transduction proteins (p21, p16, and pRb) by Western blot analysis |
19171648 | RESULTS: H(2)O(2) markedly increased the number of SA-beta-Gal-positive cells to up to 89% and the expression of Apo J, CTGF, fibronectin, and SM22 by approximately three to fourfold |
18464919 | In vitro data showed that exposure of human diploid fibroblasts to hexavalent chromium (Cr(VI)) resulted in premature senescence and significant upregulation of the ApoJ/CLU protein |
18464919 | In this study we analyzed blood and urine samples from shipyard industry welders being exposed to different levels of Cr(VI) over a period of five months in order to assay in vivo the relation of ApoJ/CLU serum levels with Cr(VI) |
18464919 | Our findings confirmed the previously reported in vitro data since reduction of Cr levels, after a worksite intervention, associated with lower levels of ApoJ/CLU serum levels |
18464919 | We concluded that the human ApoJ/CLU gene is responsive to the acute in vivo oxidative stress induced by heavy metals such as hexavalent chromium |
16955214 | Clusterin/Apolipoprotein J (CLU) is a cellular senescence biomarker implicated in several physiological processes |
16955214 | In this work we have investigated CLU expression and function in human haematopoietic cells |
16955214 | We found that early passage human T cell clones (TCC) express minimal endogenous amounts of CLU, which are significantly elevated in late passage cells |
16955214 | Moreover, exposure of TCC to increased levels of the essential micronutrient zinc in culture resulted in intense induction of CLU |
16955214 | Because haematopoietic cells cease proliferation following induction of terminal differentiation, we also studied the expression profile of CLU in the leukemic progenitor cell lines K562 and HL-60 |
16955214 | We found that, like TCC, both cell lines express minimal endogenous levels of CLU in their actively proliferating state |
16955214 | However, when induced to differentiate into their distinct cell types, CLU was found to be up-regulated specifically in those cells expressing the main differentiation markers |
16955214 | Enforced stable over-expression of CLU in K562 cells inhibited the expression of the CD14 differentiation marker and blocked differentiation to either monocytes/megacaryoblasts or to erythrocytes |
16955214 | Overall, our results suggest that CLU is actively involved in both replicative senescence and terminal differentiation in different types of human haematopoietic cells |
16827160 | Subsequent analysis of the expression levels of two pro-survival proteins, bcl-2 and clusterin/apolipoprotein J (CLU), in cells exposed to hypoxic conditions, revealed that although bcl-2 was up-regulated independently of the cell type, CLU was induced only in the CoCl2-treated immortalized HDFs |
15236767 | In the current work we provide evidence that workers chronically exposed to CrVI have considerably reduced serum levels of the biomarker of senescence and cell survival, Apolipoprotein J/Clusterin (ApoJ/CLU) |
15236767 | Moreover, we have found that both the degree and the time of exposure to CrVI associate negatively with ApoJ/CLU serum levels |
15236767 | More specifically, treated cells were growth arrested, acquired an irregular shape, were positive to beta-galactosidase staining, accumulated oxidized proteins and over-expressed the cyclin-dependent kinase inhibitor p21 and ApoJ/CLU |
12200037 | Clusterin/Apolipoprotein J (ApoJ) is a heterodimeric highly conserved secreted glycoprotein being expressed in a wide variety of tissues and found in all human fluids |
12200037 | Despite being cloned since 1989, no genuine function has been attributed to ApoJ so far |
12200037 | ApoJ gene is differentially regulated by cytokines, growth factors and stress-inducing agents, while another defining prominent and intriguing ApoJ feature is its upregulation in many severe physiological disturbances states and in several neurodegenerative conditions mostly related to advanced aging |
12200037 | Moreover, ApoJ accumulates during the viable growth arrested cellular state of senescence, that is thought to contribute to aging and to tumorigenesis suppression; paradoxically ApoJ is also upregulated in several cases of in vivo cancer progression and tumor formation |
11741605 | In a previous study aiming to identify genes that are differentially regulated during cellular senescence we have cloned clusterin/apolipoprotein J (Apo J), a 80 kDa secreted glycoprotein |
11741605 | In the current report we pursue our studies and show that senescence of human diploid fibroblasts is accompanied by up-regulation of both Apo J mRNA and protein levels, but with no altered biogenesis, binding partner profile or intracellular distribution of the two Apo J forms detected |
11741605 | To analyze the causal relationship between senescence and Apo J protein accumulation, we stably overexpressed the Apo J gene in primary as well as in SV40 T antigen-immortalized human fibroblasts and we showed no alteration of the proliferative capacity of the transduced cells |
11741605 | Despite previous reports on tumor-derived cell lines, overexpression of Apo J in human fibroblasts did not provide protection against apoptosis or growth arrest induced by hydrogen peroxide |
11741605 | Overall, our results suggest that Apo J overexpression does not induce senescence but it is rather a secondary consequence of the senescence phenotype |
11668329 | Apolipoprotein J inhibits the migration, adhesion, and proliferation of vascular smooth muscle cells |
11668329 | PURPOSE: Apolipoprotein J (ApoJ) is expressed during tissue injury and remodeling and has been implicated in vascular smooth muscle cell (VSMC) differentiation |
11668329 | Recently, the gene for ApoJ was identified as upregulated in distal anastomotic intimal hyperplasia after prosthetic arterial grafting |
11668329 | In this study we investigate the effect of ApoJ on VSMC migration, adhesion, proliferation, and gene expression |
11668329 | The influence of extracellular matrix interactions on ApoJ and chemotaxis was studied in a similar way, except membranes were collagen coated |
11668329 | Furthermore, cells were exposed to ApoJ 15 minutes before or after seeding on the coated membrane (n = 10) |
11668329 | The influence of ApoJ on cell adhesion to collagen was assessed with cell exposure to ApoJ 15 minutes before or after seeding on a collagen-coated membrane (n = 10) |
11668329 | The effect of ApoJ in 0 |
11668329 | RESULTS: ApoJ alone was not chemotactic for VSMCs |
11668329 | ApoJ did not induce VSMC proliferation |
11668329 | ApoJ alone decreased VSMC thymidine incorporation by 41 |
11668329 | Interleukin-8 and endothelin-1 were demonstrated by means of the microarray to be differentially expressed more than twofold in VSMCs that were exposed to ApoJ |
11668329 | CONCLUSION: ApoJ is a potent inhibitor of VSMC migration, adhesion, and proliferation |
11668329 | Therefore, ApoJ may play a role, in part, in modulating the VSMC response to injury |
11302695 | Treating young HDFs with 150 microM H(2)O(2) once or 75 microM H(2)O(2) twice in 2 weeks causes long-term growth arrest, an enlarged morphology, activation of senescence-associated beta-galactosidase, and elevated expression of collagenase and clusterin mRNAs |
11060295 | In this work, we show that transforming growth factor-beta1 (TGF-beta1) regulates the induction of several of these biomarkers in SIPS: cellular morphology, senescence-associated beta-galactosidase activity, increase in the steady-state level of fibronectin, apolipoprotein J, osteonectin, and SM22 mRNA |
11060295 | In the presence of each of these antibodies, the steady-state level of fibronectin, osteonectin, apolipoprotein J, and SM22 mRNA is no more increased at 72 h after stress |
9570922 | Construction of cDNA libraries from two conditional cell lines and application of differential screening and subtractive hybridization techniques have resulted in the cloning of eight senescence-induced genes (SGP-2/Apo J, alpha 1-procollagen, osteonectin, fibronectin, SM22, cytochrome C oxidase, GTP-alpha, and a novel gene) and a senescence-repressed gene (FRS-2) |
9570922 | Three of these genes encode for extracellular matrix proteins, others are involved in the calcium-dependent signal transduction pathways, while the SGP-2/Apo J gene may have a cellular protective function |
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