HCSGD entry for ICAM1

1. General information

Official gene symbolICAM1
Entrez ID3383
Gene full nameintercellular adhesion molecule 1
Other gene symbolsBB2 CD54 P3.58
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:0001541Ovarian follicle developmentIEAbiological_process
GO:0001618Virus receptor activityIEAmolecular_function
GO:0001772Immunological synapseIEAcellular_component
GO:0001910Regulation of leukocyte mediated cytotoxicityTASbiological_process
GO:0001975Response to amphetamineIEAbiological_process
GO:0002291T cell activation via T cell receptor contact with antigen bound to MHC molecule on antigen presenting cellIMPbiological_process
GO:0002457T cell antigen processing and presentationIEAbiological_process
GO:0002693Positive regulation of cellular extravasationIMPbiological_process
GO:0004872Receptor activityTASmolecular_function
GO:0004888Transmembrane signaling receptor activityTASmolecular_function
GO:0005178Integrin bindingIPImolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005615Extracellular spaceIDAcellular_component
GO:0005886Plasma membraneTAScellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0007155Cell adhesionIDAbiological_process
GO:0007157Heterophilic cell-cell adhesionTASbiological_process
GO:0007159Leukocyte cell-cell adhesionIMPbiological_process
GO:0007569Cell agingIEAbiological_process
GO:0008360Regulation of cell shapeIEAbiological_process
GO:0009897External side of plasma membraneIEAcellular_component
GO:0010212Response to ionizing radiationIEAbiological_process
GO:0010477Response to sulfur dioxideIEAbiological_process
GO:0014070Response to organic cyclic compoundIEAbiological_process
GO:0016020MembraneIEAcellular_component
GO:0016337Cell-cell adhesionIEAbiological_process
GO:0019221Cytokine-mediated signaling pathwayTASbiological_process
GO:0022614Membrane to membrane dockingIEPbiological_process
GO:0030155Regulation of cell adhesionIEAbiological_process
GO:0030838Positive regulation of actin filament polymerizationIEAbiological_process
GO:0031669Cellular response to nutrient levelsIEAbiological_process
GO:0032321Positive regulation of Rho GTPase activityIEAbiological_process
GO:0033627Cell adhesion mediated by integrinIEAbiological_process
GO:0034698Response to gonadotropinIEAbiological_process
GO:0042493Response to drugIEAbiological_process
GO:0043200Response to amino acidIEAbiological_process
GO:0045429Positive regulation of nitric oxide biosynthetic processIEAbiological_process
GO:0045471Response to ethanolIEAbiological_process
GO:0045907Positive regulation of vasoconstrictionIEAbiological_process
GO:0046688Response to copper ionIEAbiological_process
GO:0046813Receptor-mediated virion attachment to host cellIDAbiological_process
GO:0050731Positive regulation of peptidyl-tyrosine phosphorylationIEAbiological_process
GO:0050776Regulation of immune responseTASbiological_process
GO:0050900Leukocyte migrationIEPbiological_process
GO:0051092Positive regulation of NF-kappaB transcription factor activityIEAbiological_process
GO:0051856Adhesion to symbiontIDAbiological_process
GO:0051926Negative regulation of calcium ion transportIEAbiological_process
GO:0060333Interferon-gamma-mediated signaling pathwayTASbiological_process
GO:0071222Cellular response to lipopolysaccharideIEAbiological_process
GO:0071312Cellular response to alkaloidIEAbiological_process
GO:0071333Cellular response to glucose stimulusIEAbiological_process
GO:0071347Cellular response to interleukin-1IEAbiological_process
GO:0071356Cellular response to tumor necrosis factorIEAbiological_process
GO:0071456Cellular response to hypoxiaIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00005262720.87620615480.01923888891.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.7660851133
GSE13712_SHEARUp0.3480426461
GSE13712_STATICUp0.8315660249
GSE19018Down-0.8004644593
GSE19899_A1Up2.7109180311
GSE19899_A2Up5.5851205783
PubMed_21979375_A1Up5.0245540344
PubMed_21979375_A2Up3.9931376177
GSE35957Up0.5808931309
GSE36640Up0.4215189280
GSE54402Up0.9654021033
GSE9593Up0.8249209543
GSE43922Up3.5694315961
GSE24585Up0.0861198416
GSE37065Up1.1608827725
GSE28863_A1Up0.3128237089
GSE28863_A2Up0.9838947287
GSE28863_A3Up0.1756037707
GSE28863_A4Down-0.2060416878
GSE48662Up0.1877933590

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

NatalizumabDB00108 BTD00083 | BIOD00083
Hyaluronic acidDB08818 -

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-17-3pMIMAT0000071MIRT004020Immunocytochemistry//Northern blot//qRT-PCR//Western blotFunctional MTI19949084
hsa-miR-221-3pMIMAT0000278MIRT004430Luciferase reporter assay//Western blotFunctional MTI20110463
hsa-miR-221-3pMIMAT0000278MIRT004430Luciferase reporter assayNon-Functional MTI19949084
hsa-miR-222-3pMIMAT0000279MIRT004595Luciferase reporter assayNon-Functional MTI19949084
hsa-miR-31-5pMIMAT0000089MIRT005707Luciferase reporter assayNon-Functional MTI19949084
hsa-miR-17-5pMIMAT0000070MIRT005708Luciferase reporter assayNon-Functional MTI19949084
hsa-miR-155-5pMIMAT0000646MIRT005709Luciferase reporter assayNon-Functional MTI19949084
hsa-miR-155-5pMIMAT0000646MIRT005709qRT-PCRFunctional MTI (Weak)21310411
hsa-miR-1256MIMAT0005907MIRT005710Luciferase reporter assayNon-Functional MTI19949084
hsa-miR-21-5pMIMAT0000076MIRT005952Luciferase reporter assay//Microarray//qRT-PCRFunctional MTI21131358
hsa-miR-335-5pMIMAT0000765MIRT018131MicroarrayFunctional MTI (Weak)18185580
hsa-miR-98-5pMIMAT0000096MIRT027615MicroarrayFunctional MTI (Weak)19088304
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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-221-3pMIMAT00002781hsa-miR-221{Western blot}{downregulation by anti-miRNA oligonucleotide}20110463
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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

25220188Six genes independently correlated with either age (IL-6, TNFRSF-11B, IGFBP-3, SAA4, and COPG), prognosis (IL-6, SAA4), or the grade of the glioma (IL-6, IL-8, ICAM-1, IGFBP-3, and COPG)
25077560Interestingly, unlike amphiregulin and TNFRI, full-length intercellular adhesion molecule 1 (ICAM1) is released from senescent cells by microvesicles independently of ADAM17
23451255In contrast, the high levels of ICAM1 expression and ROS production, which characterize these senescent mesothelial cells, enhanced the tumor cell adhesion
23375186After adjustment for demographics, traditional risk factors, and inflammatory markers including high-sensitivity C-reactive protein, interleukin-6, and soluble intercellular adhesion molecule-1, those in the middle tertile had significantly elevated risk for incident CHD (hazard ratio 1
23201774Further examination of SIRT6-depleted HUVEC demonstrated higher intercellular-adhesion molecule-1 (ICAM-1) and plasminogen-activator inhibitor-1 mRNA, lower levels of endothelial nitric oxide synthase mRNA and protein, higher ICAM-1 surface expression, and up-regulation of p21
22928666Silencing Arg-II in senescent cells suppresses eNOS-uncoupling, several senescence markers such as senescence-associated-beta-galactosidase activity, p53-S15, p21, and expression of vascular adhesion molecule-1 (VCAM1) and intercellular adhesion molecule-1 (ICAM1)
22814745Likewise, exposure of mouse aortic explants or cultured human endothelial cells to UCMVs augmented the adhesion of human monocytes by several fold and increased endothelial cell intercellular adhesion molecule-1 via nuclear factor-kappaB activation
21698300These effects were accompanied by a marked reduction of the basal expression of VCAM-1 and ICAM-1
20139322The inhibition of hTERT resulted in the upregulation of HIV-1-induced overexpression of intercellular adhesion molecule-1 via the nuclear factor-kappaB-regulated mechanism and induced the transendothelial migration of HIV-1-infected monocytic U937 cells
19904754Oxidative stress-dependent increase in ICAM-1 expression promotes adhesion of colorectal and pancreatic cancers to the senescent peritoneal mesothelium
19904754Intercellular adhesion molecule-1 (ICAM-1) has been implicated in adhesion of colorectal and pancreatic cancer cells (of the SW480 and PSN-1 line, respectively) to the peritoneal mesothelium
19904754It has been demonstrated that ICAM-1 expression increases with senescence in some cell types, however, the significance of this phenomenon in the context of malignant dissemination remains elusive
19904754In this report we show that the adherence of SW480 and PSN-1 cells to senescent human omentum-derived mesothelial cells (HOMCs) in vitro is greater than to early-passage cells and that the effect is mediated by ICAM-1
19904754Senescent HOMCs display increased expression of ICAM-1 mRNA and cell surface protein
19904754The augmented ICAM-1 expression in HOMCs can be reduced by culturing cells with antioxidants; in contrast, exposure of HOMCs to an oxidant, t-BHP, leads to cellular senescence and increased ICAM-1 expression
19904754These results indicate that increased oxidative stress and increased expression of ICAM-1 in senescent HOMCs may facilitate peritoneal adhesion of selected colorectal and pancreatic cancers
16930678Clonal senescence alters endothelial ICAM-1 function
16930678In this report, ICAM-1 accumulates in late passage endothelial cells when compared to early passage endothelial cells, yet ICAM-1 protein expression is attenuated when senescent cells are challenged by TNF-alpha (10ng/ml)
16930678Importantly, age alters ICAM-1 dynamic properties from directed to random receptor motion within the membrane
16930678Single particle tracking reveals that the average ICAM-1 mobility is 44% less in late than early passage cells after its motion is stimulated by the Protein Kinase C (PKC) activator, phorbol myristate acetate (PMA)
16930678The mechanism for altered ICAM-1 mobility partly can be explained by a reduced rate of alpha-actinin linking with ICAM-1 in late passage Human Pulmonary Artery Endothelial Cells (HPAECs)
16930678Furthermore, tyrosine phosphorylation of alpha-actinin, a requirment for ICAM-1 clustering, is markedly reduced in senescent cells
16930678These findings support a hypothesis that senescence results in changes of ICAM-1 activation and clustering, thus resulting in an age-dependent transmembrane signaling disorder
16930678Therefore, further understanding of age-dependent disturbances of ICAM-1 regulation during inflammation can provide important clues as to appropriate targets for therapeutic interventions and prevention of vascular disorders in elderly at the level of the endothelial surface membrane
15711569Among the molecules involved in the inflammatory response that are overexpressed in senescent cells and aged tissues is intercellular adhesion molecule-1 (ICAM-1)
15711569Furthermore, ICAM-1 is overexpressed in atherosclerosis, an age-related, chronic inflammatory disease
15711569We have recently reported that the transcriptional activator p53 can trigger ICAM-1 expression in an nuclear factor-kappa B (NF-kappaB)-independent manner (Gorgoulis et al, EMBO J
15711569As p53 exhibits an increased transcriptional activity in senescent cells, we investigated whether p53 activation is responsible for the senescence-associated ICAM-1 overexpression
15711569Here, we present evidence from both cell systems to support a p53-mediated ICAM-1 overexpression in senescent cells that is independent of NF-kappaB
15711569We also demonstrate in atherosclerotic lesions the presence of cells coexpressing activated p53, ICAM-1, and stained with the senescence-associated beta-galactosidase, a biomarker of replicative senescence
15247038The proinflammatory phenotype of senescent cells: the p53-mediated ICAM-1 expression
15247038Intercellular adhesion molecule-1 (ICAM-1) is one of the molecules involved in inflammatory response that is overexpressed in senescent cells and aged tissues
15247038Although the role of the nuclear factor-kappa B (NF-kappa B) signaling cascade is crucial in ICAM-1 activation, we have shown that p53 directly activates the expression of ICAM-1 in an NF-kappa B-independent manner
12564113Senescent HAECs exhibited increased ICAM-1 expression and decreased eNOS activity, both of which are alterations implicated in atherogenesis
11927518To determine whether endothelial cell senescence causes endothelial dysfunction, we induced senescence in human aortic endothelial cells (HAECs) by inhibiting telomere function and examined the expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) activity
11927518Senescent HAECs exhibited increased ICAM-1 expression and decreased eNOS activity, both of which are alterations implicated in atherogenesis
10722838Chronic exposure of endothelial cells to homocysteine also increases the expression of two surface molecules linked to vascular disease, intracellular adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1)
10722838Interestingly, the level of expression of both ICAM-1 and PAI-1 correlates with the degree of endothelial senescence
8359220Here we show that (i) senescence enhances monoblastoid U937 cell adhesion to the endothelial monolayer; (ii) the enhanced interaction between senescent endothelial cells and U937 cells is mediated, at least in part, by the overexpression of ICAM-1; and (iii) LPS and interleukin 1 alpha, but not tumor necrosis factor alpha, are unable to stimulate the adhesion of U937 to senescent endothelial cells
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