HCSGD entry for IGFBP5


1. General information

Official gene symbolIGFBP5
Entrez ID3488
Gene full nameinsulin-like growth factor binding protein 5
Other gene symbolsIBP5
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001558Regulation of cell growthIEAbiological_process
GO:0001649Osteoblast differentiationIEAbiological_process
GO:0001968Fibronectin bindingIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005520Insulin-like growth factor bindingIEAmolecular_function
GO:0005576Extracellular regionIEA NAS TAScellular_component
GO:0006006Glucose metabolic processIEAbiological_process
GO:0007165Signal transductionNASbiological_process
GO:0010906Regulation of glucose metabolic processIEAbiological_process
GO:0014912Negative regulation of smooth muscle cell migrationIDAbiological_process
GO:0016942Insulin-like growth factor binding protein complexICcellular_component
GO:0017148Negative regulation of translationIDAbiological_process
GO:0030336Negative regulation of cell migrationIDAbiological_process
GO:0031069Hair follicle morphogenesisIEAbiological_process
GO:0031994Insulin-like growth factor I bindingIPImolecular_function
GO:0035556Intracellular signal transductionIEAbiological_process
GO:0042593Glucose homeostasisIEAbiological_process
GO:0043568Positive regulation of insulin-like growth factor receptor signaling pathwayIEAbiological_process
GO:0043569Negative regulation of insulin-like growth factor receptor signaling pathwayIDAbiological_process
GO:0044267Cellular protein metabolic processTASbiological_process
GO:0044342Type B pancreatic cell proliferationIEAbiological_process
GO:0045668Negative regulation of osteoblast differentiationIEAbiological_process
GO:0048630Skeletal muscle tissue growthIEAbiological_process
GO:0048662Negative regulation of smooth muscle cell proliferationIDAbiological_process
GO:0051146Striated muscle cell differentiationIEAbiological_process
GO:0051897Positive regulation of protein kinase B signalingIEAbiological_process
GO:0060056Mammary gland involutionIEAbiological_process
GO:0071320Cellular response to cAMPIDAbiological_process
GO:0071407Cellular response to organic cyclic compoundIDAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00009813840.07360793280.02777526880.5110615669

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up0.0957541188
GSE13712_SHEARUp1.8195542454
GSE13712_STATICUp0.0542817447
GSE19018Down-0.0348656355
GSE19899_A1Up0.4896375702
GSE19899_A2Up0.8832788227
PubMed_21979375_A1Up0.0990560476
PubMed_21979375_A2Up1.1427750572
GSE35957Up2.3414590975
GSE36640Up0.6494368332
GSE54402Down-0.4732933318
GSE9593Down-1.4435056428
GSE43922Up0.4705683044
GSE24585Down-1.9470648351
GSE37065Up1.3619224864
GSE28863_A1Up1.4893381701
GSE28863_A2Up1.7121651206
GSE28863_A3Up2.2767426248
GSE28863_A4Down-0.8571356869
GSE48662Up1.3826425519

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-140-5pMIMAT0000431MIRT006556qRT-PCRFunctional MTI (Weak)19948051
hsa-miR-331-3pMIMAT0000760MIRT043414CLASHFunctional MTI (Weak)23622248
hsa-miR-17-5pMIMAT0000070MIRT050836CLASHFunctional MTI (Weak)23622248
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    • mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

hsa-miR-140-5pMIMAT0000431NAhsa-miR-140-5p19948051
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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

26762731Here, 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
26762731We 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
26762731Moreover, 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
24416650IL-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
24164458We 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
22374671Here 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)
22374671We 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
21191810Notably, PGE(2) treatment increased the IGFBP5 protein level
21191810Down-regulation of IGFBP5 inhibited PGE(2)-induced cellular senescence
21191810Taken 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
18676497Most recently, however, a new player in this process has been described, IGF-binding protein-5 (IGFBP5)
18676497IGFBP5 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
18676497We 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
17804819IGFBP-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
17804819Here we show that IGFBP-5 plays important roles in the regulation of cellular senescence
17804819Knockdown 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
17804819In 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
17804819Premature senescence induced by IGFBP-5 up-regulation in young cells was rescued by knockdown of p53, but not by knockdown of p16
17804819These 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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