HCSGD entry for IGFBP5
1. General information
Official gene symbol | IGFBP5 |
---|---|
Entrez ID | 3488 |
Gene full name | insulin-like growth factor binding protein 5 |
Other gene symbols | IBP5 |
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:0001558 | Regulation of cell growth | IEA | biological_process |
GO:0001649 | Osteoblast differentiation | IEA | biological_process |
GO:0001968 | Fibronectin binding | IEA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005520 | Insulin-like growth factor binding | IEA | molecular_function |
GO:0005576 | Extracellular region | IEA NAS TAS | cellular_component |
GO:0006006 | Glucose metabolic process | IEA | biological_process |
GO:0007165 | Signal transduction | NAS | biological_process |
GO:0010906 | Regulation of glucose metabolic process | IEA | biological_process |
GO:0014912 | Negative regulation of smooth muscle cell migration | IDA | biological_process |
GO:0016942 | Insulin-like growth factor binding protein complex | IC | cellular_component |
GO:0017148 | Negative regulation of translation | IDA | biological_process |
GO:0030336 | Negative regulation of cell migration | IDA | biological_process |
GO:0031069 | Hair follicle morphogenesis | IEA | biological_process |
GO:0031994 | Insulin-like growth factor I binding | IPI | molecular_function |
GO:0035556 | Intracellular signal transduction | IEA | biological_process |
GO:0042593 | Glucose homeostasis | IEA | biological_process |
GO:0043568 | Positive regulation of insulin-like growth factor receptor signaling pathway | IEA | biological_process |
GO:0043569 | Negative regulation of insulin-like growth factor receptor signaling pathway | IDA | biological_process |
GO:0044267 | Cellular protein metabolic process | TAS | biological_process |
GO:0044342 | Type B pancreatic cell proliferation | IEA | biological_process |
GO:0045668 | Negative regulation of osteoblast differentiation | IEA | biological_process |
GO:0048630 | Skeletal muscle tissue growth | IEA | biological_process |
GO:0048662 | Negative regulation of smooth muscle cell proliferation | IDA | biological_process |
GO:0051146 | Striated muscle cell differentiation | IEA | biological_process |
GO:0051897 | Positive regulation of protein kinase B signaling | IEA | biological_process |
GO:0060056 | Mammary gland involution | IEA | biological_process |
GO:0071320 | Cellular response to cAMP | IDA | biological_process |
GO:0071407 | Cellular response to organic cyclic compound | 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 |
---|---|---|---|
0.0000981384 | 0.0736079328 | 0.0277752688 | 0.5110615669 |
- 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 | 0.0957541188 |
GSE13712_SHEAR | Up | 1.8195542454 |
GSE13712_STATIC | Up | 0.0542817447 |
GSE19018 | Down | -0.0348656355 |
GSE19899_A1 | Up | 0.4896375702 |
GSE19899_A2 | Up | 0.8832788227 |
PubMed_21979375_A1 | Up | 0.0990560476 |
PubMed_21979375_A2 | Up | 1.1427750572 |
GSE35957 | Up | 2.3414590975 |
GSE36640 | Up | 0.6494368332 |
GSE54402 | Down | -0.4732933318 |
GSE9593 | Down | -1.4435056428 |
GSE43922 | Up | 0.4705683044 |
GSE24585 | Down | -1.9470648351 |
GSE37065 | Up | 1.3619224864 |
GSE28863_A1 | Up | 1.4893381701 |
GSE28863_A2 | Up | 1.7121651206 |
GSE28863_A3 | Up | 2.2767426248 |
GSE28863_A4 | Down | -0.8571356869 |
GSE48662 | Up | 1.3826425519 |
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-140-5p | MIMAT0000431 | MIRT006556 | qRT-PCR | Functional MTI (Weak) | 19948051 |
hsa-miR-331-3p | MIMAT0000760 | MIRT043414 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-17-5p | MIMAT0000070 | MIRT050836 | 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-140-5p | MIMAT0000431 | NA | hsa-miR-140-5p | 19948051 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 7 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
26762731 | Here, we use satellite cells and primary myoblasts from mice and humans and an in vitro regeneration model, to show that disrupted expression of microRNA-143-3p and its target gene, Igfbp5, plays an important role in muscle regeneration in vitro |
26762731 | We identified miR-143 as a regulator of the insulin growth factor-binding protein 5 (Igfbp5) in primary myoblasts and show that the expression of miR-143 and its target gene is disrupted in satellite cells from old mice |
26762731 | Moreover, we show that downregulation of miR-143 during aging may act as a compensatory mechanism aiming at improving myogenesis efficiency; however, concomitant upregulation of miR-143 target gene, Igfbp5, is associated with increased cell senescence, thus affecting myogenesis |
24416650 | IL-6/sIL-6Ralpha stimulation forms a senescence-inducing circuit involving the STAT3-insulin-like growth factor-binding protein 5 (IGFBP5) as a key axis triggering and reinforcing component in human fibroblasts |
24164458 | We found that IGFBP5 (insulin-like growth factor binding protein 5), PLAT (plasminogen activator), SNAI2 (snail homolog 2), JAG1 (jagged 1), SPRY4 (Sprouty homolog 4), and CD44 were upregulated, whereas CFB (complement factor B), VCAM1 (vascular cell adhesion molecule 1), AQP1 (aquaporin 1), LOXL1 (lysyl oxidase-like 1), and RBPMS (RNA-binding protein with multiple splicing) were down- regulated in both radiation-damaged and old cells |
22374671 | Here we demonstrate that IL6 and the soluble IL6 receptor (sIL6R) induce premature senescence in normal human fibroblasts by establishing a senescence-inducing circuit involving the signal transducer and activator of transcription 3 (STAT3) and insulin-like growth factor-binding protein 5 (IGFBP5) |
22374671 | We searched for STAT3-downstream molecule(s) responsible for the senescence-inducing activity in the supernatants of stimulated TIG3 and identified IGFBP5 as a major STAT3 mediator, because IGFBP5 was expressed from the early phase through the entire senescence process and was responsible for IL6/STAT3-induced ROS increase and premature senescence |
21191810 | Notably, PGE(2) treatment increased the IGFBP5 protein level |
21191810 | Down-regulation of IGFBP5 inhibited PGE(2)-induced cellular senescence |
21191810 | Taken together, these results suggest that PGE(2) may play an important role in controlling cellular senescence of HDFs through the regulation of IGFBP5 and therefore may contribute to inflammatory disorders associated with aging |
18676497 | Most recently, however, a new player in this process has been described, IGF-binding protein-5 (IGFBP5) |
18676497 | IGFBP5 has also been shown to induce similar effects to TGFB1, but, in addition, it is strongly implicated in the process of senescence which is now believed to be a significant factor in these diseases |
18676497 | We examine the evidence for this role of IGFBP5 and identify some of the therapeutic targets which might be used to ameliorate these diseases of unknown cause |
17804819 | IGFBP-5 is up-regulated during cellular senescence in human dermal fibroblasts and endothelial cells, but the function of IGFBP-5 in cellular senescence is unknown |
17804819 | Here we show that IGFBP-5 plays important roles in the regulation of cellular senescence |
17804819 | Knockdown of IGFBP-5 in old human umbilical endothelial cells (HUVECs) with IGFBP-5 micro-RNA lentivirus caused partial reduction of a variety of senescent phenotypes, such as changes in cell morphology, increases in cell proliferation, and decreases in senescence-associated beta-galactosidase (SA-beta-gal) staining |
17804819 | In addition, treatment with IGFBP-5 protein or up-regulation of IGFBP-5 in young cells accelerates cellular senescence, as confirmed by cell proliferation and SA-beta-gal staining |
17804819 | Premature senescence induced by IGFBP-5 up-regulation in young cells was rescued by knockdown of p53, but not by knockdown of p16 |
17804819 | These results suggest that IGFBP-5 plays a role in the regulation of cellular senescence via a p53-dependent pathway and in aging-associated vascular diseases |
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