HCSGD entry for CXCR4

1. General information

Official gene symbolCXCR4
Entrez ID7852
Gene full namechemokine (C-X-C motif) receptor 4
Other gene symbolsCD184 D2S201E FB22 HM89 HSY3RR LAP3 LCR1 LESTR NPY3R NPYR NPYRL NPYY3R WHIM
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000187Activation of MAPK activityTASbiological_process
GO:0001569Patterning of blood vesselsIEAbiological_process
GO:0001618Virus receptor activityIEAmolecular_function
GO:0001666Response to hypoxiaIEPbiological_process
GO:0001667Ameboidal cell migrationIEAbiological_process
GO:0001764Neuron migrationIEAbiological_process
GO:0002407Dendritic cell chemotaxisTASbiological_process
GO:0003779Actin bindingIDAmolecular_function
GO:0004930G-protein coupled receptor activityTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005737CytoplasmTAScellular_component
GO:0005764LysosomeIDAcellular_component
GO:0005769Early endosomeIDAcellular_component
GO:0005770Late endosomeIDAcellular_component
GO:0005886Plasma membraneIDA TAScellular_component
GO:0006915Apoptotic processTASbiological_process
GO:0006954Inflammatory responseTASbiological_process
GO:0007186G-protein coupled receptor signaling pathwayIDAbiological_process
GO:0007204Positive regulation of cytosolic calcium ion concentrationTASbiological_process
GO:0007281Germ cell developmentIEAbiological_process
GO:0007420Brain developmentIEAbiological_process
GO:0008045Motor neuron axon guidanceIEAbiological_process
GO:0008354Germ cell migrationIEAbiological_process
GO:0009615Response to virusTASbiological_process
GO:0009897External side of plasma membraneIEAcellular_component
GO:0009986Cell surfaceIDAcellular_component
GO:0015026Coreceptor activityTASmolecular_function
GO:0016021Integral component of membraneIEAcellular_component
GO:0016023Cytoplasmic membrane-bounded vesicleIDAcellular_component
GO:0016032Viral processTASbiological_process
GO:0016494C-X-C chemokine receptor activityNASmolecular_function
GO:0019221Cytokine-mediated signaling pathwayNASbiological_process
GO:0019722Calcium-mediated signalingIMPbiological_process
GO:0019955Cytokine bindingIEAmolecular_function
GO:0030054Cell junctionIEAcellular_component
GO:0030260Entry into host cellTASbiological_process
GO:0030334Regulation of cell migrationIEAbiological_process
GO:0030426Growth coneIEAcellular_component
GO:0031252Cell leading edgeIDAcellular_component
GO:0031410Cytoplasmic vesicleIDAcellular_component
GO:0031625Ubiquitin protein ligase bindingIPImolecular_function
GO:0032027Myosin light chain bindingIDAmolecular_function
GO:0042098T cell proliferationIEAbiological_process
GO:0042119Neutrophil activationIEAbiological_process
GO:0043130Ubiquitin bindingIDAmolecular_function
GO:0043217Myelin maintenanceISSbiological_process
GO:0048714Positive regulation of oligodendrocyte differentiationISSbiological_process
GO:0050920Regulation of chemotaxisIMPbiological_process
GO:0061351Neural precursor cell proliferationIEAbiological_process
GO:0070098Chemokine-mediated signaling pathwayNASbiological_process
GO:0071345Cellular response to cytokine stimulusIDAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00003105510.98816102350.01547924531.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up1.3675433407
GSE13712_SHEARUp0.3143134452
GSE13712_STATICDown-0.1429925150
GSE19018Up0.3061492190
GSE19899_A1Up2.6851459919
GSE19899_A2Up4.0652598516
PubMed_21979375_A1Up7.4251354000
PubMed_21979375_A2Up8.3198430206
GSE35957Up0.0531268637
GSE36640Up1.4893051289
GSE54402Up6.0405422892
GSE9593Down-0.0893437543
GSE43922Up2.0814831377
GSE24585Up0.1225466733
GSE37065Up0.1341957735
GSE28863_A1Down-0.0269998105
GSE28863_A2Down-0.0551146006
GSE28863_A3Up0.1176154436
GSE28863_A4Up0.0807918510
GSE48662Down-0.0386984297

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL462588CHEMBL21079P61073
CHEMBL460299CHEMBL21079P61073
CHEMBL1949732CHEMBL21079P61073
CHEMBL452864CHEMBL21079P61073
CHEMBL452868CHEMBL21079P61073
CHEMBL516630CHEMBL21079P61073
CHEMBL18442CHEMBL21079P61073
CHEMBL460482CHEMBL21079P61073
CHEMBL508054CHEMBL21079P61073
CHEMBL1644080CHEMBL21079P61073
CHEMBL516989CHEMBL21079P61073
CHEMBL541728CHEMBL21079P61073
CHEMBL541728CHEMBL21079P61073
CHEMBL508054CHEMBL21079P61073
CHEMBL454896CHEMBL21079P61073
CHEMBL1092637CHEMBL21079P61073
CHEMBL1949733CHEMBL21079P61073
CHEMBL452864CHEMBL21079P61073
CHEMBL516480CHEMBL21079P61073
CHEMBL1242210CHEMBL21079P61073
CHEMBL462588CHEMBL21079P61073
CHEMBL1682994CHEMBL21079P61073
CHEMBL460491CHEMBL21079P61073
CHEMBL1644082CHEMBL21079P61073
CHEMBL518501CHEMBL21079P61073
CHEMBL461359CHEMBL21079P61073
CHEMBL1682997CHEMBL21079P61073
CHEMBL518041CHEMBL21079P61073
CHEMBL460484CHEMBL21079P61073
CHEMBL577268CHEMBL21079P61073
CHEMBL461359CHEMBL21079P61073
CHEMBL452864CHEMBL21079P61073
CHEMBL1644081CHEMBL21079P61073
CHEMBL1682996CHEMBL21079P61073
CHEMBL506505CHEMBL21079P61073
CHEMBL1682998CHEMBL21079P61073
CHEMBL461358CHEMBL21079P61073
CHEMBL460298CHEMBL21079P61073
CHEMBL1949730CHEMBL21079P61073
CHEMBL1096504CHEMBL21079P61073
CHEMBL518041CHEMBL21079P61073
CHEMBL1091591CHEMBL21079P61073
CHEMBL516480CHEMBL21079P61073
CHEMBL1949675CHEMBL21079P61073
CHEMBL461358CHEMBL21079P61073
CHEMBL1088913CHEMBL21079P61073
CHEMBL518501CHEMBL21079P61073
CHEMBL454689CHEMBL21079P61073
CHEMBL460491CHEMBL21079P61073
CHEMBL454896CHEMBL21079P61073
CHEMBL1949731CHEMBL21079P61073
CHEMBL452868CHEMBL21079P61073
CHEMBL1094864CHEMBL21079P61073
CHEMBL460299CHEMBL21079P61073
CHEMBL1682995CHEMBL21079P61073
CHEMBL454689CHEMBL21079P61073
CHEMBL516630CHEMBL21079P61073
CHEMBL460298CHEMBL21079P61073
CHEMBL373440CHEMBL21079P61073
CHEMBL373636CHEMBL21079P61073
CHEMBL375991CHEMBL21079P61073
CHEMBL375990CHEMBL21079P61073
CHEMBL1093149CHEMBL21079P61073
CHEMBL219135CHEMBL21079P61073
CHEMBL450041CHEMBL21079P61073
CHEMBL518004CHEMBL21079P61073
CHEMBL373637CHEMBL21079P61073
CHEMBL450815CHEMBL21079P61073
CHEMBL436283CHEMBL21079P61073
CHEMBL218806CHEMBL21079P61073
CHEMBL375993CHEMBL21079P61073
CHEMBL508684CHEMBL21079P61073
CHEMBL436536CHEMBL21079P61073
CHEMBL374108CHEMBL21079P61073
CHEMBL480502CHEMBL21079P61073
CHEMBL1093137CHEMBL21079P61073
CHEMBL18442CHEMBL21079P61073
CHEMBL374862CHEMBL21079P61073
CHEMBL518924CHEMBL21079P61073
CHEMBL1088913CHEMBL21079P61073
CHEMBL219474CHEMBL21079P61073
CHEMBL219339CHEMBL21079P61073
CHEMBL426169CHEMBL21079P61073
CHEMBL374421CHEMBL21079P61073
CHEMBL219096CHEMBL21079P61073
CHEMBL443092CHEMBL21079P61073
CHEMBL446868CHEMBL21079P61073
CHEMBL477121CHEMBL21079P61073
CHEMBL376219CHEMBL21079P61073
CHEMBL219075CHEMBL21079P61073
CHEMBL1090509CHEMBL21079P61073
CHEMBL472323CHEMBL21079P61073
CHEMBL387120CHEMBL21079P61073
CHEMBL1089434CHEMBL21079P61073
CHEMBL18442CHEMBL21079P61073
CHEMBL384429CHEMBL21079P61073
CHEMBL375850CHEMBL21079P61073
CHEMBL376811CHEMBL21079P61073
CHEMBL1652605CHEMBL21078P61073
CHEMBL1652605CHEMBL21078P61073
CHEMBL237830CHEMBL21078P61073
CHEMBL18442CHEMBL21078P61073
CHEMBL18442CHEMBL21078P61073
CHEMBL1202230CHEMBL21078P61073
CHEMBL554014CHEMBL21078P61073
CHEMBL538038CHEMBL21078P61073
CHEMBL543895CHEMBL21078P61073
CHEMBL1202231CHEMBL21078P61073
CHEMBL364295CHEMBL21076P61073
CHEMBL366033CHEMBL21076P61073
CHEMBL191914CHEMBL21076P61073
CHEMBL371993CHEMBL21076P61073
CHEMBL193217CHEMBL21076P61073
CHEMBL372422CHEMBL21076P61073
CHEMBL191949CHEMBL21076P61073
CHEMBL436097CHEMBL21076P61073
CHEMBL426635CHEMBL21076P61073
CHEMBL192594CHEMBL21076P61073
CHEMBL191687CHEMBL21076P61073
CHEMBL372874CHEMBL21076P61073
CHEMBL370001CHEMBL21076P61073
CHEMBL192368CHEMBL21076P61073
CHEMBL263704CHEMBL21076P61073
CHEMBL436083CHEMBL21076P61073
CHEMBL192913CHEMBL21076P61073
CHEMBL192685CHEMBL21076P61073
CHEMBL191942CHEMBL21076P61073
CHEMBL424826CHEMBL21076P61073
CHEMBL436283CHEMBL21076P61073
CHEMBL364014CHEMBL21076P61073
CHEMBL191914CHEMBL21076P61073
CHEMBL192345CHEMBL21076P61073
CHEMBL364011CHEMBL21076P61073
CHEMBL191998CHEMBL21076P61073
CHEMBL191639CHEMBL21076P61073
CHEMBL191651CHEMBL21076P61073
CHEMBL370001CHEMBL21076P61073
CHEMBL408062CHEMBL21076P61073
CHEMBL373155CHEMBL21076P61073
CHEMBL192183CHEMBL21076P61073
CHEMBL365952CHEMBL21076P61073
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  • Drugs

Name

Drug

Accession number

FramycetinDB00452 APRD00618
AMD-070DB05501 -
PlerixaforDB06809 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-146a-5pMIMAT0000449MIRT000006qRT-PCR//Luciferase reporter assay//Western blotFunctional MTI18568019
hsa-miR-146a-5pMIMAT0000449MIRT000006MicroarrayFunctional MTI (Weak)20375304
hsa-miR-224-5pMIMAT0000281MIRT000635Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20023705
hsa-miR-150-5pMIMAT0000451MIRT006668FACS//Western blotFunctional MTI22039399
hsa-miR-26b-5pMIMAT0000083MIRT030235MicroarrayFunctional 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-146a-5pMIMAT00004491hsa-miR-146a18568019
hsa-miR-146a-5pMIMAT00004492hsa-miR-146a18568019
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6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 8 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25693733Fucoidan-preconditioning of senescent ECFCs was shown by flow cytometry to restore the expression of functional ECFC surface markers (CD34, c-Kit, VEGFR2, and CXCR4) and stimulate the in vitro tube formation capacity of ECFCs
22721583We adopted granulocyte colony-stimulating factor combined with CXCR4 antagonist AMD3100 to stimulate MSCs to release into blood circulation of the rats
21245959Naturally senescent cells and cells rendered senescent by VEGFR-2 TKIs had reduced VEGFR-2 and CXCR-4 expression and demonstrated reduced migratory ability to VEGF
21198398The increase in HSC expansion is likely attributable to SB-mediated inhibition of HSC apoptosis and senescence and upregulation of HoxB4 and CXCR4
19932479Investigation of molecular mechanisms in bone marrow (BM)-derived progenitor cells from mice revealed that BMC therapy and, more consistently, in combination with MT ameliorated functional activity via decreased cellular senescence and increased telomerase and chemokine CXCR4 activities
19567818An antagonist of the chemokine receptor CXCR4 induces mitotic catastrophe in ovarian cancer cells
19567818The chemokine receptor CXCR4 is expressed by malignant cells in ovarian cancer and is implicated in their growth and spread
19567818We report here a unique mechanism of action of a small peptide antagonist of CXCR4 on ovarian cancer cells: induction of cell death by mitotic catastrophe
19567818We conclude that CTCE-9908 has a unique mechanism of action in ovarian cancer cells that seems to be CXCR4 specific
18049311Therapeutic effects of autologous bone marrow cells and metabolic intervention in the ischemic hindlimb of spontaneously hypertensive rats involve reduced cell senescence and CXCR4/Akt/eNOS pathways
16946301WHIM syndrome myelokathexis reproduced in the NOD/SCID mouse xenotransplant model engrafted with healthy human stem cells transduced with C-terminus-truncated CXCR4
16946301WHIM(warts, hypogammaglobulinemia, recurrent bacterial infection, and myelokathexis) syndrome is a rare immunodeficiency caused in many cases by autosomal dominant C-terminal truncation mutations in the chemokine receptor CXCR4
16946301We transduced healthy human CD34(+) peripheral blood-mobilized stem cells (PBSCs) with retrovirus vector encoding wild-type (wt) CXCR4 or WHIM-type mutated CXCR4 and studied these cells ex vivo in culture and after engraftment in a nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mouse xenograft model
16946301Neither wt CXCR4 nor mutated CXCR4 transgene expression itself enhanced apoptosis of neutrophils arising in transduced PBSC cultures even with stimulation by a CXCR4 agonist, stromal cell-derived factor-1 (SDF-1 [CXCL12])
16946301Excess wt CXCR4 expression by transduced human PBSCs enhanced marrow engraftment, but did not affect bone marrow (BM) apoptosis or the release of transduced leukocytes into PB
16946301However, mutated CXCR4 transgene expression further enhanced BM engraftment, but was associated with a significant increase in apoptosis of transduced cells in BM and reduced release of transduced leukocytes into PB
16946301We conclude that increased apoptosis of mature myeloid cells in WHIM is secondary to a failure of marrow release and progression to normal myeloid cell senescence, and not a direct effect of activation of mutated CXCR4
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