HCSGD entry for PTK2


1. General information

Official gene symbolPTK2
Entrez ID5747
Gene full nameprotein tyrosine kinase 2
Other gene symbolsFADK FAK FAK1 FRNK PPP1R71 p125FAK pp125FAK
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000226Microtubule cytoskeleton organizationIEAbiological_process
GO:0001525AngiogenesisIEA TASbiological_process
GO:0001570VasculogenesisIEAbiological_process
GO:0001764Neuron migrationIEAbiological_process
GO:0001890Placenta developmentTASbiological_process
GO:0001934Positive regulation of protein phosphorylationIMPbiological_process
GO:0003007Heart morphogenesisTASbiological_process
GO:0003779Actin bindingIDAmolecular_function
GO:0004672Protein kinase activityIEA TASmolecular_function
GO:0004713Protein tyrosine kinase activityIEAmolecular_function
GO:0004715Non-membrane spanning protein tyrosine kinase activityIDAmolecular_function
GO:0004871Signal transducer activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005524ATP bindingIEAmolecular_function
GO:0005634NucleusIDA IEAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005815Microtubule organizing centerIEAcellular_component
GO:0005829CytosolIDA TAScellular_component
GO:0005856CytoskeletonIEA TAScellular_component
GO:0005925Focal adhesionIDA IEAcellular_component
GO:0005938Cell cortexIEAcellular_component
GO:0006915Apoptotic processTASbiological_process
GO:0006921Cellular component disassembly involved in execution phase of apoptosisTASbiological_process
GO:0007172Signal complex assemblyIEAbiological_process
GO:0007229Integrin-mediated signaling pathwayIMP TASbiological_process
GO:0007411Axon guidanceTASbiological_process
GO:0007596Blood coagulationTASbiological_process
GO:0008284Positive regulation of cell proliferationIEA ISSbiological_process
GO:0008360Regulation of cell shapeIMPbiological_process
GO:0008432JUN kinase bindingIDAmolecular_function
GO:0009790Embryo developmentTASbiological_process
GO:0010594Regulation of endothelial cell migrationTASbiological_process
GO:0014068Positive regulation of phosphatidylinositol 3-kinase signalingIMPbiological_process
GO:0016324Apical plasma membraneIEAcellular_component
GO:0018108Peptidyl-tyrosine phosphorylationIDAbiological_process
GO:0019901Protein kinase bindingIPImolecular_function
GO:0021955Central nervous system neuron axonogenesisIEAbiological_process
GO:0022408Negative regulation of cell-cell adhesionIDAbiological_process
GO:0030010Establishment of cell polarityTASbiological_process
GO:0030027LamellipodiumIEAcellular_component
GO:0030168Platelet activationTASbiological_process
GO:0030198Extracellular matrix organizationIEAbiological_process
GO:0030335Positive regulation of cell migrationIDAbiological_process
GO:0032319Regulation of Rho GTPase activityTASbiological_process
GO:0033628Regulation of cell adhesion mediated by integrinIDAbiological_process
GO:0038007Netrin-activated signaling pathwayTASbiological_process
GO:0038096Fc-gamma receptor signaling pathway involved in phagocytosisTASbiological_process
GO:0040023Establishment of nucleus localizationIEAbiological_process
GO:0042127Regulation of cell proliferationIMPbiological_process
GO:0042169SH2 domain bindingIPImolecular_function
GO:0043066Negative regulation of apoptotic processIMPbiological_process
GO:0043542Endothelial cell migrationIEAbiological_process
GO:0043552Positive regulation of phosphatidylinositol 3-kinase activityTASbiological_process
GO:0045087Innate immune responseTASbiological_process
GO:0045667Regulation of osteoblast differentiationIMPbiological_process
GO:0045860Positive regulation of protein kinase activityIMPbiological_process
GO:0046621Negative regulation of organ growthIEAbiological_process
GO:0046777Protein autophosphorylationIDA IEAbiological_process
GO:0048013Ephrin receptor signaling pathwayIDAbiological_process
GO:0048870Cell motilityTASbiological_process
GO:0050771Negative regulation of axonogenesisIEAbiological_process
GO:0051493Regulation of cytoskeleton organizationTASbiological_process
GO:0051893Regulation of focal adhesion assemblyTASbiological_process
GO:0051897Positive regulation of protein kinase B signalingIMPbiological_process
GO:0051964Negative regulation of synapse assemblyIEAbiological_process
GO:0060396Growth hormone receptor signaling pathwayIDAbiological_process
GO:2000060Positive regulation of protein ubiquitination involved in ubiquitin-dependent protein catabolic processIEA ISSbiological_process
GO:2000811Negative regulation of anoikisIMPbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.11584720190.93503088790.69872002751.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.0973232332
GSE13712_SHEARUp0.3449308586
GSE13712_STATICUp0.1530823981
GSE19018Up0.2314578131
GSE19899_A1Up0.0825430184
GSE19899_A2Up0.5380605648
PubMed_21979375_A1Up0.4983173407
PubMed_21979375_A2Up0.3763173599
GSE35957Down-0.1216073572
GSE36640Up0.1684755092
GSE54402Up0.4247541954
GSE9593Up0.3708760896
GSE43922Down-0.0186684245
GSE24585Up0.0460009030
GSE37065Up0.1532356685
GSE28863_A1Up0.2047364301
GSE28863_A2Up0.0136662856
GSE28863_A3Down-0.4396404034
GSE28863_A4Up0.0680132206
GSE48662Down-0.3676168964

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL201511CHEMBL26959Q05397
CHEMBL1934352CHEMBL26959Q05397
CHEMBL103667CHEMBL26959Q05397
CHEMBL565612CHEMBL26959Q05397
CHEMBL1934338CHEMBL26959Q05397
CHEMBL103667CHEMBL26959Q05397
CHEMBL1934335CHEMBL26959Q05397
CHEMBL1934353CHEMBL26959Q05397
CHEMBL514554CHEMBL26959Q05397
CHEMBL513909CHEMBL26959Q05397
CHEMBL514554CHEMBL26959Q05397
CHEMBL1721885CHEMBL26959Q05397
CHEMBL1908392CHEMBL26959Q05397
CHEMBL535CHEMBL26959Q05397
CHEMBL1721885CHEMBL26959Q05397
CHEMBL1934341CHEMBL26959Q05397
CHEMBL509032CHEMBL26959Q05397
CHEMBL1908397CHEMBL26959Q05397
CHEMBL1934339CHEMBL26959Q05397
CHEMBL1934347CHEMBL26959Q05397
CHEMBL1934337CHEMBL26959Q05397
CHEMBL1934348CHEMBL26959Q05397
CHEMBL514409CHEMBL26959Q05397
CHEMBL535CHEMBL26959Q05397
CHEMBL1934335CHEMBL26959Q05397
CHEMBL1934345CHEMBL26959Q05397
CHEMBL514554CHEMBL26959Q05397
CHEMBL1934344CHEMBL26959Q05397
CHEMBL1934343CHEMBL26959Q05397
CHEMBL1934334CHEMBL26959Q05397
CHEMBL1934342CHEMBL26959Q05397
CHEMBL1934343CHEMBL26959Q05397
CHEMBL514554CHEMBL26959Q05397
CHEMBL464552CHEMBL26959Q05397
CHEMBL1934352CHEMBL26959Q05397
CHEMBL162CHEMBL26959Q05397
CHEMBL475251CHEMBL26959Q05397
CHEMBL1908393CHEMBL26959Q05397
CHEMBL603469CHEMBL26959Q05397
CHEMBL1934338CHEMBL26959Q05397
CHEMBL1934340CHEMBL26959Q05397
CHEMBL1934336CHEMBL26959Q05397
CHEMBL1908395CHEMBL26959Q05397
CHEMBL601719CHEMBL26959Q05397
CHEMBL1934337CHEMBL26959Q05397
CHEMBL1934353CHEMBL26959Q05397
CHEMBL1934336CHEMBL26959Q05397
CHEMBL180022CHEMBL26959Q05397
CHEMBL1287853CHEMBL26959Q05397
CHEMBL450786CHEMBL26959Q05397
CHEMBL1934351CHEMBL26959Q05397
CHEMBL1934344CHEMBL26959Q05397
CHEMBL514554CHEMBL26959Q05397
CHEMBL162CHEMBL26959Q05397
CHEMBL288441CHEMBL26959Q05397
CHEMBL1934339CHEMBL26959Q05397
CHEMBL1934350CHEMBL26959Q05397
CHEMBL1934341CHEMBL26959Q05397
CHEMBL1822511CHEMBL26959Q05397
CHEMBL379655CHEMBL26959Q05397
CHEMBL208939CHEMBL26959Q05397
CHEMBL570647CHEMBL26959Q05397
CHEMBL203020CHEMBL26959Q05397
CHEMBL381161CHEMBL26959Q05397
CHEMBL208042CHEMBL26959Q05397
CHEMBL206853CHEMBL26959Q05397
CHEMBL207499CHEMBL26959Q05397
CHEMBL6246CHEMBL26959Q05397
CHEMBL205098CHEMBL26959Q05397
CHEMBL382608CHEMBL26959Q05397
CHEMBL378811CHEMBL26959Q05397
CHEMBL205095CHEMBL26959Q05397
CHEMBL207259CHEMBL26959Q05397
CHEMBL437693CHEMBL26959Q05397
CHEMBL207834CHEMBL26959Q05397
CHEMBL489083CHEMBL26959Q05397
CHEMBL207605CHEMBL26959Q05397
CHEMBL378596CHEMBL26959Q05397
CHEMBL205584CHEMBL26959Q05397
CHEMBL379279CHEMBL26959Q05397
CHEMBL453336CHEMBL26959Q05397
CHEMBL377708CHEMBL26959Q05397
CHEMBL380424CHEMBL26959Q05397
CHEMBL207820CHEMBL26959Q05397
CHEMBL207614CHEMBL26959Q05397
CHEMBL488811CHEMBL26959Q05397
CHEMBL517956CHEMBL26959Q05397
CHEMBL207721CHEMBL26959Q05397
CHEMBL383263CHEMBL26959Q05397
CHEMBL208000CHEMBL26959Q05397
CHEMBL570369CHEMBL26959Q05397
CHEMBL439154CHEMBL26959Q05397
CHEMBL378964CHEMBL26959Q05397
CHEMBL207935CHEMBL26959Q05397
CHEMBL382192CHEMBL26959Q05397
CHEMBL208370CHEMBL26959Q05397
CHEMBL208368CHEMBL26959Q05397
CHEMBL207147CHEMBL26959Q05397
CHEMBL425599CHEMBL26959Q05397
CHEMBL162CHEMBL26959Q05397
CHEMBL207131CHEMBL26959Q05397
CHEMBL208384CHEMBL26959Q05397
CHEMBL206524CHEMBL26959Q05397
CHEMBL568729CHEMBL26959Q05397
CHEMBL509435CHEMBL26959Q05397
CHEMBL201511CHEMBL26959Q05397
CHEMBL206255CHEMBL26959Q05397
CHEMBL205942CHEMBL26959Q05397
CHEMBL208419CHEMBL26959Q05397
CHEMBL570846CHEMBL26959Q05397
CHEMBL204686CHEMBL26959Q05397
CHEMBL456936CHEMBL26959Q05397
CHEMBL204933CHEMBL26959Q05397
CHEMBL206322CHEMBL26959Q05397
CHEMBL207161CHEMBL26959Q05397
CHEMBL206890CHEMBL26959Q05397
CHEMBL203178CHEMBL26959Q05397
CHEMBL207961CHEMBL26959Q05397
CHEMBL383300CHEMBL26959Q05397
CHEMBL206876CHEMBL26959Q05397
CHEMBL377957CHEMBL26959Q05397
CHEMBL1922224CHEMBL26959Q05397
CHEMBL206977CHEMBL26959Q05397
CHEMBL529217CHEMBL26959Q05397
CHEMBL206731CHEMBL26959Q05397
CHEMBL205316CHEMBL26959Q05397
CHEMBL383241CHEMBL26959Q05397
CHEMBL535CHEMBL26959Q05397
CHEMBL378018CHEMBL26959Q05397
CHEMBL585927CHEMBL26959Q05397
CHEMBL203676CHEMBL26959Q05397
CHEMBL207787CHEMBL26959Q05397
CHEMBL207491CHEMBL26959Q05397
CHEMBL208468CHEMBL26959Q05397
CHEMBL381609CHEMBL26959Q05397
CHEMBL426131CHEMBL26959Q05397
CHEMBL529663CHEMBL26959Q05397
CHEMBL207232CHEMBL26959Q05397
CHEMBL382809CHEMBL26959Q05397
CHEMBL207444CHEMBL26959Q05397
CHEMBL488646CHEMBL26959Q05397
CHEMBL381262CHEMBL26959Q05397
CHEMBL426311CHEMBL26959Q05397
CHEMBL207084CHEMBL26959Q05397
CHEMBL380226CHEMBL26959Q05397
CHEMBL205588CHEMBL26959Q05397
CHEMBL207875CHEMBL26959Q05397
CHEMBL379969CHEMBL26959Q05397
CHEMBL383006CHEMBL26959Q05397
CHEMBL206978CHEMBL26959Q05397
CHEMBL382452CHEMBL26959Q05397
CHEMBL205098CHEMBL26959Q05397
CHEMBL519590CHEMBL26959Q05397
CHEMBL383834CHEMBL26959Q05397
CHEMBL209044CHEMBL26959Q05397
CHEMBL208734CHEMBL26959Q05397
CHEMBL381374CHEMBL26959Q05397
CHEMBL382637CHEMBL26959Q05397
CHEMBL381308CHEMBL26959Q05397
CHEMBL207737CHEMBL26959Q05397
CHEMBL206797CHEMBL26959Q05397
CHEMBL207053CHEMBL26959Q05397
CHEMBL380683CHEMBL26959Q05397
CHEMBL607707CHEMBL26959Q05397
CHEMBL380312CHEMBL26959Q05397
CHEMBL207015CHEMBL26959Q05397
CHEMBL1922225CHEMBL26959Q05397
CHEMBL378661CHEMBL26959Q05397
CHEMBL207615CHEMBL26959Q05397
CHEMBL206927CHEMBL26959Q05397
CHEMBL379118CHEMBL26959Q05397
CHEMBL382354CHEMBL26959Q05397
CHEMBL488645CHEMBL26959Q05397
CHEMBL207126CHEMBL26959Q05397
CHEMBL425418CHEMBL26959Q05397
CHEMBL518060CHEMBL26959Q05397
CHEMBL208322CHEMBL26959Q05397
CHEMBL383672CHEMBL26959Q05397
CHEMBL379837CHEMBL26959Q05397
CHEMBL380515CHEMBL26959Q05397
CHEMBL511152CHEMBL26958Q05397
CHEMBL1783837CHEMBL26958Q05397
CHEMBL519418CHEMBL26958Q05397
CHEMBL471357CHEMBL26958Q05397
CHEMBL482968CHEMBL26958Q05397
CHEMBL470317CHEMBL26958Q05397
CHEMBL471698CHEMBL26958Q05397
CHEMBL452340CHEMBL26958Q05397
CHEMBL1783839CHEMBL26958Q05397
CHEMBL1783845CHEMBL26958Q05397
CHEMBL487227CHEMBL26958Q05397
CHEMBL401930CHEMBL26958Q05397
CHEMBL471526CHEMBL26958Q05397
CHEMBL453649CHEMBL26958Q05397
CHEMBL1783842CHEMBL26958Q05397
CHEMBL509485CHEMBL26958Q05397
CHEMBL488247CHEMBL26958Q05397
CHEMBL452341CHEMBL26958Q05397
CHEMBL564417CHEMBL26958Q05397
CHEMBL472212CHEMBL26958Q05397
CHEMBL470314CHEMBL26958Q05397
CHEMBL518905CHEMBL26958Q05397
CHEMBL1783838CHEMBL26958Q05397
CHEMBL514554CHEMBL26958Q05397
CHEMBL519418CHEMBL26958Q05397
CHEMBL1783843CHEMBL26958Q05397
CHEMBL455680CHEMBL26958Q05397
CHEMBL535CHEMBL26958Q05397
CHEMBL1240703CHEMBL26958Q05397
CHEMBL162CHEMBL26958Q05397
CHEMBL455677CHEMBL26958Q05397
CHEMBL513744CHEMBL26958Q05397
CHEMBL520059CHEMBL26958Q05397
CHEMBL1084546CHEMBL26958Q05397
CHEMBL470316CHEMBL26958Q05397
CHEMBL472212CHEMBL26958Q05397
CHEMBL509485CHEMBL26958Q05397
CHEMBL487246CHEMBL26958Q05397
CHEMBL487057CHEMBL26958Q05397
CHEMBL472211CHEMBL26958Q05397
CHEMBL288441CHEMBL26958Q05397
CHEMBL1254007CHEMBL26958Q05397
CHEMBL488089CHEMBL26958Q05397
CHEMBL471520CHEMBL26958Q05397
CHEMBL488446CHEMBL26958Q05397
CHEMBL472212CHEMBL26958Q05397
CHEMBL487229CHEMBL26958Q05397
CHEMBL535CHEMBL26958Q05397
CHEMBL452340CHEMBL26958Q05397
CHEMBL603469CHEMBL26958Q05397
CHEMBL1684800CHEMBL26958Q05397
CHEMBL529889CHEMBL26958Q05397
CHEMBL1783846CHEMBL26958Q05397
CHEMBL453649CHEMBL26958Q05397
CHEMBL509485CHEMBL26958Q05397
CHEMBL445162CHEMBL26958Q05397
CHEMBL103667CHEMBL26958Q05397
CHEMBL201307CHEMBL26958Q05397
CHEMBL475817CHEMBL26958Q05397
CHEMBL1257912CHEMBL26958Q05397
CHEMBL460746CHEMBL26958Q05397
CHEMBL1257795CHEMBL26958Q05397
CHEMBL459729CHEMBL26958Q05397
CHEMBL1257911CHEMBL26958Q05397
CHEMBL1258821CHEMBL26958Q05397
CHEMBL1288582CHEMBL26958Q05397
CHEMBL454440CHEMBL26958Q05397
CHEMBL401930CHEMBL26957Q05397
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  • Drugs

Name

Drug

Accession number

7-PYRIDIN-2-YL-N-(3,4,5-TRIMETHOXYPHENYL)-7H-PYRROLO[2,3-D]PYRIMIDIN-2-AMINEDB07248 -
2-({5-CHLORO-2-[(2-METHOXY-4-MORPHOLIN-4-YLPHENYL)AMINO]PYRIMIDIN-4-YL}AMINO)-N-METHYLBENZAMIDEDB07460 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-138-5pMIMAT0000430MIRT006388Luciferase reporter assay//Western blotFunctional MTI21444814
hsa-miR-193a-3pMIMAT0000459MIRT004001Luciferase reporter assay//qRT-PCR//Western blotNon-Functional MTI18381414
hsa-miR-7-5pMIMAT0000252MIRT006900Immunoblot//Immunohistochemistry//Luciferase reporter assay//qRT-PCRFunctional MTI22876288
hsa-miR-21-5pMIMAT0000076MIRT030918MicroarrayFunctional MTI (Weak)18591254
hsa-let-7e-5pMIMAT0000066MIRT051491CLASHFunctional MTI (Weak)23622248
hsa-let-7c-5pMIMAT0000064MIRT051867CLASHFunctional 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-193a-3pMIMAT0000459NAhsa-miR-193a-3p{Western blot}{overexpression by miRNA precursor transfection}18381414
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6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 6 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26873092We found that circ-Foxo3 was mainly distributed in the cytoplasm, where it interacted with the anti-senescent protein ID-1 and the transcription factor E2F1, as well as the anti-stress proteins FAK and HIF1alpha
26873092CONCLUSION: We conclude that ID-1, E2F1, FAK, and HIF1alpha interact with circ-Foxo3 and are retained in the cytoplasm and could no longer exert their anti-senescent and anti-stress roles, resulting in increased cellular senescence
25693733Fucoidan also promoted the expression of cell cycle-associated proteins (cyclin E, Cdk2, cyclin D1, and Cdk4) in senescent ECFCs, significantly reversed cellular senescence, and increased the proliferation of ECFCs via the FAK, Akt, and ERK signaling pathways
25472717This upregulates the downstream proteins CEBPB, FAK, N-cadherin, vimentin, Oct4 and Sca-1 (also known as stem cell antigen-1), and downregulates E-cadherin
24041229The interaction between FAK, MYCN, p53 and Mdm2 in neuroblastoma
24041229This review focuses on the individual protein tyrosine kinase, focal adhesion kinase (FAK) and its interaction with the transcription factors, MYCN, p53, and Mdm2, and how their interactions modulate the growth and malignancy of neuroblastomas
16523241We showed that focal adhesion kinase (FAK) expression and its phosphorylation at Tyr397, autophosphorylation site for focal adhesion formation, and Tyr577, Src-dependent phosphorylation site, were both increased in senescent cells
16523241Moreover, FAK was inactivated proteolytically by apoptotic stimuli in young cells, but not in senescent cells
16523241Interestingly dephosphorylation at Tyr577 of FAK by PP2 treatment, Src-family kinase inhibitor, induced the apoptosis by staurosporine in senescent cells but dephosphorylation at Tyr397 by downregulation of caveolin-1 was not affected
16523241These data suggest that FAK might differently regulate apoptosis and focal adhesion formation through site-specific tyrosine phosphorylation in senescent cells
15263006We observed that the expression integrin beta(1) and focal adhesion kinase (FAK) were increased and that the phosphorylations of FAK and paxillin, hallmarks of focal adhesion formation, were also increased in senescent human diploid fibroblast cells
15263006Interestingly, caveolin-1 knock-out senescent cells, achieved by using small interfering RNA and antisense oligonucleotide, showed disrupted focal adhesion formation and actin stress fibers via the inactivation of FAK, which resulted in morphological adjustment to the young cell-like small spindle shape
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