HCSGD entry for BCL2

1. General information

Official gene symbolBCL2
Entrez ID596
Gene full nameB-cell CLL/lymphoma 2
Other gene symbolsBcl-2 PPP1R50
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:0000209Protein polyubiquitinationIDAbiological_process
GO:0001101Response to acidIEAbiological_process
GO:0001503OssificationIEAbiological_process
GO:0001541Ovarian follicle developmentIEAbiological_process
GO:0001656Metanephros developmentIEAbiological_process
GO:0001658Branching involved in ureteric bud morphogenesisIEAbiological_process
GO:0001662Behavioral fear responseIEAbiological_process
GO:0001782B cell homeostasisIEAbiological_process
GO:0001836Release of cytochrome c from mitochondriaISS NASbiological_process
GO:0001952Regulation of cell-matrix adhesionIEAbiological_process
GO:0002020Protease bindingIDAmolecular_function
GO:0002320Lymphoid progenitor cell differentiationIEAbiological_process
GO:0002326B cell lineage commitmentIEAbiological_process
GO:0002931Response to ischemiaIEAbiological_process
GO:0003014Renal system processIEAbiological_process
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005739MitochondrionIDAcellular_component
GO:0005741Mitochondrial outer membraneIDA TAScellular_component
GO:0005783Endoplasmic reticulumIDAcellular_component
GO:0005789Endoplasmic reticulum membraneIEAcellular_component
GO:0005829CytosolIEAcellular_component
GO:0006470Protein dephosphorylationIEAbiological_process
GO:0006582Melanin metabolic processIEAbiological_process
GO:0006808Regulation of nitrogen utilizationIEAbiological_process
GO:0006915Apoptotic processTASbiological_process
GO:0006959Humoral immune responseTASbiological_process
GO:0006974Cellular response to DNA damage stimulusIMPbiological_process
GO:0007015Actin filament organizationIEAbiological_process
GO:0007409AxonogenesisIEAbiological_process
GO:0007565Female pregnancyNASbiological_process
GO:0007569Cell agingIEAbiological_process
GO:0008134Transcription factor bindingIEAmolecular_function
GO:0008219Cell deathIDAbiological_process
GO:0008584Male gonad developmentIEAbiological_process
GO:0008625Extrinsic apoptotic signaling pathway via death domain receptorsIDAbiological_process
GO:0008630Intrinsic apoptotic signaling pathway in response to DNA damageIBAbiological_process
GO:0008631Intrinsic apoptotic signaling pathway in response to oxidative stressIEAbiological_process
GO:0009314Response to radiationNASbiological_process
GO:0009636Response to toxic substanceIDAbiological_process
GO:0009791Post-embryonic developmentIEAbiological_process
GO:0010039Response to iron ionIDAbiological_process
GO:0010224Response to UV-BIEAbiological_process
GO:0010332Response to gamma radiationIEAbiological_process
GO:0010507Negative regulation of autophagyTASbiological_process
GO:0010523Negative regulation of calcium ion transport into cytosolIEAbiological_process
GO:0010559Regulation of glycoprotein biosynthetic processIEAbiological_process
GO:0014031Mesenchymal cell developmentIEAbiological_process
GO:0014042Positive regulation of neuron maturationIEAbiological_process
GO:0014911Positive regulation of smooth muscle cell migrationIEAbiological_process
GO:0015267Channel activityIDAmolecular_function
GO:0016020MembraneIDAcellular_component
GO:0016049Cell growthIEAbiological_process
GO:0016248Channel inhibitor activityIDAmolecular_function
GO:0016337Cell-cell adhesionIEAbiological_process
GO:0018105Peptidyl-serine phosphorylationIEAbiological_process
GO:0018107Peptidyl-threonine phosphorylationIEAbiological_process
GO:0021747Cochlear nucleus developmentIEAbiological_process
GO:0022612Gland morphogenesisIEAbiological_process
GO:0022898Regulation of transmembrane transporter activityIDAbiological_process
GO:0030279Negative regulation of ossificationIEAbiological_process
GO:0030307Positive regulation of cell growthIDAbiological_process
GO:0030308Negative regulation of cell growthIEAbiological_process
GO:0030318Melanocyte differentiationIEAbiological_process
GO:0030336Negative regulation of cell migrationIEAbiological_process
GO:0030890Positive regulation of B cell proliferationIMPbiological_process
GO:0031069Hair follicle morphogenesisIEAbiological_process
GO:0031103Axon regenerationIEAbiological_process
GO:0031625Ubiquitin protein ligase bindingIPImolecular_function
GO:0031647Regulation of protein stabilityIEAbiological_process
GO:0031965Nuclear membraneIDAcellular_component
GO:0032469Endoplasmic reticulum calcium ion homeostasisTASbiological_process
GO:0032835Glomerulus developmentIEAbiological_process
GO:0032848Negative regulation of cellular pH reductionIDAbiological_process
GO:0033033Negative regulation of myeloid cell apoptotic processIEAbiological_process
GO:0033077T cell differentiation in thymusIEAbiological_process
GO:0033138Positive regulation of peptidyl-serine phosphorylationIEAbiological_process
GO:0033689Negative regulation of osteoblast proliferationIEAbiological_process
GO:0034097Response to cytokineIDAbiological_process
GO:0035094Response to nicotineIDAbiological_process
GO:0035265Organ growthIEAbiological_process
GO:0035872Nucleotide-binding domain, leucine rich repeat containing receptor signaling pathwayTASbiological_process
GO:0040018Positive regulation of multicellular organism growthIEAbiological_process
GO:0042100B cell proliferationIDAbiological_process
GO:0042149Cellular response to glucose starvationIEAbiological_process
GO:0042493Response to drugIDA IMPbiological_process
GO:0042542Response to hydrogen peroxideIEAbiological_process
GO:0042802Identical protein bindingIPImolecular_function
GO:0042803Protein homodimerization activityIPImolecular_function
GO:0043029T cell homeostasisIEAbiological_process
GO:0043066Negative regulation of apoptotic processIDA IEA IMPbiological_process
GO:0043085Positive regulation of catalytic activityIEAbiological_process
GO:0043209Myelin sheathIEAcellular_component
GO:0043375CD8-positive, alpha-beta T cell lineage commitmentIEAbiological_process
GO:0043496Regulation of protein homodimerization activityIDAbiological_process
GO:0043497Regulation of protein heterodimerization activityIDAbiological_process
GO:0043524Negative regulation of neuron apoptotic processIDAbiological_process
GO:0043565Sequence-specific DNA bindingIDAmolecular_function
GO:0043583Ear developmentIEAbiological_process
GO:0045069Regulation of viral genome replicationIEAbiological_process
GO:0045087Innate immune responseTASbiological_process
GO:0045636Positive regulation of melanocyte differentiationIEAbiological_process
GO:0045930Negative regulation of mitotic cell cycleIEAbiological_process
GO:0046671Negative regulation of retinal cell programmed cell deathIEAbiological_process
GO:0046902Regulation of mitochondrial membrane permeabilityISSbiological_process
GO:0046930Pore complexIDAcellular_component
GO:0046982Protein heterodimerization activityIPImolecular_function
GO:0048041Focal adhesion assemblyIEAbiological_process
GO:0048536Spleen developmentIEAbiological_process
GO:0048538Thymus developmentIEAbiological_process
GO:0048546Digestive tract morphogenesisIEAbiological_process
GO:0048589Developmental growthIEAbiological_process
GO:0048599Oocyte developmentIEAbiological_process
GO:0048743Positive regulation of skeletal muscle fiber developmentIEAbiological_process
GO:0048753Pigment granule organizationIEAbiological_process
GO:0048873Homeostasis of number of cells within a tissueIEAbiological_process
GO:0050853B cell receptor signaling pathwayIMPbiological_process
GO:0051384Response to glucocorticoidIEAbiological_process
GO:0051402Neuron apoptotic processTASbiological_process
GO:0051434BH3 domain bindingIPImolecular_function
GO:0051607Defense response to virusIDAbiological_process
GO:0051721Protein phosphatase 2A bindingIEAmolecular_function
GO:0051881Regulation of mitochondrial membrane potentialISSbiological_process
GO:0051902Negative regulation of mitochondrial depolarizationTASbiological_process
GO:0051924Regulation of calcium ion transportIDAbiological_process
GO:0055085Transmembrane transportIDAbiological_process
GO:0070059Intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressIDAbiological_process
GO:0071310Cellular response to organic substanceIEAbiological_process
GO:0071456Cellular response to hypoxiaIEAbiological_process
GO:0072593Reactive oxygen species metabolic processIEAbiological_process
GO:0097192Extrinsic apoptotic signaling pathway in absence of ligandIEAbiological_process
GO:0097193Intrinsic apoptotic signaling pathwayTASbiological_process
GO:1900740Positive regulation of protein insertion into mitochondrial membrane involved in apoptotic signaling pathwayTASbiological_process
GO:2000134Negative regulation of G1/S transition of mitotic cell cycleIEAbiological_process
GO:2000811Negative regulation of anoikisIMPbiological_process
GO:2001234Negative regulation of apoptotic signaling pathwayIMPbiological_process
GO:2001240Negative regulation of extrinsic apoptotic signaling pathway in absence of ligandIGIbiological_process
GO:2001243Negative regulation of intrinsic apoptotic signaling pathwayIDAbiological_process
GO:2001244Positive regulation of intrinsic apoptotic signaling pathwayTASbiological_process
Entries Per Page
Displaying Page of

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.96915630110.09305642640.99999024730.5809625712

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

Data sourceUp or downLog fold change
GSE11954Down-0.0160366161
GSE13712_SHEARDown-0.1634935574
GSE13712_STATICDown-0.1134116342
GSE19018Up0.0344740342
GSE19899_A1Up0.0319000596
GSE19899_A2Down-0.1380993379
PubMed_21979375_A1Down-0.2545400904
PubMed_21979375_A2Down-0.2998400245
GSE35957Up0.0684299009
GSE36640Down-0.4815283369
GSE54402Down-0.1206334611
GSE9593Up0.1951049146
GSE43922Up0.0331802168
GSE24585Down-1.0810074286
GSE37065Down-0.0629539289
GSE28863_A1Down-0.1514889125
GSE28863_A2Down-0.1085914272
GSE28863_A3Up0.1331353191
GSE28863_A4Up0.0043604868
GSE48662Down-0.0095496806

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL1689142CHEMBL48609P10415
CHEMBL387142CHEMBL48609P10415
CHEMBL221856CHEMBL48609P10415
CHEMBL221708CHEMBL48609P10415
CHEMBL221218CHEMBL48609P10415
CHEMBL1689141CHEMBL48609P10415
CHEMBL374941CHEMBL48609P10415
CHEMBL385119CHEMBL48609P10415
CHEMBL376254CHEMBL48609P10415
CHEMBL373713CHEMBL48609P10415
CHEMBL222069CHEMBL48609P10415
CHEMBL375841CHEMBL48609P10415
CHEMBL595134CHEMBL48609P10415
CHEMBL1689146CHEMBL48609P10415
CHEMBL218408CHEMBL48609P10415
CHEMBL375842CHEMBL48609P10415
CHEMBL385101CHEMBL48609P10415
CHEMBL385104CHEMBL48609P10415
CHEMBL374270CHEMBL48609P10415
CHEMBL376696CHEMBL48609P10415
CHEMBL376408CHEMBL48609P10415
CHEMBL375770CHEMBL48609P10415
CHEMBL374271CHEMBL48609P10415
CHEMBL373577CHEMBL48609P10415
CHEMBL437146CHEMBL48609P10415
CHEMBL373544CHEMBL48609P10415
CHEMBL376921CHEMBL48609P10415
CHEMBL1689145CHEMBL48609P10415
CHEMBL386955CHEMBL48609P10415
CHEMBL1689143CHEMBL48609P10415
CHEMBL1689139CHEMBL48609P10415
CHEMBL268908CHEMBL48609P10415
CHEMBL439495CHEMBL48609P10415
CHEMBL221750CHEMBL48609P10415
CHEMBL192571CHEMBL48609P10415
CHEMBL387141CHEMBL48609P10415
CHEMBL1689144CHEMBL48609P10415
CHEMBL437148CHEMBL48609P10415
CHEMBL375628CHEMBL48609P10415
CHEMBL376659CHEMBL48609P10415
CHEMBL1689140CHEMBL48609P10415
CHEMBL374214CHEMBL48609P10415
CHEMBL1672081CHEMBL48609P10415
CHEMBL374303CHEMBL48609P10415
CHEMBL373712CHEMBL48609P10415
CHEMBL373631CHEMBL48609P10415
CHEMBL426558CHEMBL48609P10415
CHEMBL242340CHEMBL48609P10415
CHEMBL406312CHEMBL48609P10415
CHEMBL219775CHEMBL48609P10415
CHEMBL376055CHEMBL48609P10415
CHEMBL1096755CHEMBL48609P10415
CHEMBL258819CHEMBL48609P10415
CHEMBL1824188CHEMBL48609P10415
CHEMBL1672080CHEMBL48609P10415
CHEMBL243190CHEMBL48609P10415
CHEMBL1672069CHEMBL48609P10415
CHEMBL242339CHEMBL48609P10415
CHEMBL437577CHEMBL48609P10415
CHEMBL595134CHEMBL48609P10415
CHEMBL51483CHEMBL48609P10415
CHEMBL1824189CHEMBL48609P10415
CHEMBL219775CHEMBL48609P10415
CHEMBL1672071CHEMBL48609P10415
CHEMBL259034CHEMBL48609P10415
CHEMBL226678CHEMBL48609P10415
CHEMBL1672082CHEMBL48609P10415
CHEMBL1095309CHEMBL48609P10415
CHEMBL404899CHEMBL48609P10415
CHEMBL241897CHEMBL48609P10415
CHEMBL1672070CHEMBL48609P10415
CHEMBL242969CHEMBL48609P10415
CHEMBL1824190CHEMBL48609P10415
CHEMBL51483CHEMBL48609P10415
CHEMBL1097075CHEMBL48609P10415
CHEMBL1824187CHEMBL48609P10415
CHEMBL226578CHEMBL48609P10415
CHEMBL389660CHEMBL48609P10415
CHEMBL272974CHEMBL48609P10415
CHEMBL1824186CHEMBL48609P10415
CHEMBL439400CHEMBL48609P10415
CHEMBL270646CHEMBL48609P10415
CHEMBL376055CHEMBL48609P10415
CHEMBL481409CHEMBL48609P10415
CHEMBL259033CHEMBL48609P10415
CHEMBL269836CHEMBL48609P10415
CHEMBL243203CHEMBL48609P10415
CHEMBL243190CHEMBL48609P10415
CHEMBL220055CHEMBL48609P10415
CHEMBL220055CHEMBL48609P10415
CHEMBL1672068CHEMBL48609P10415
CHEMBL220055CHEMBL48609P10415
CHEMBL242126CHEMBL48609P10415
CHEMBL397906CHEMBL48609P10415
CHEMBL241895CHEMBL48609P10415
CHEMBL595134CHEMBL48609P10415
CHEMBL1095310CHEMBL48609P10415
CHEMBL270268CHEMBL48609P10415
CHEMBL1098324CHEMBL48609P10415
CHEMBL214839CHEMBL48609P10415
CHEMBL454406CHEMBL48608P10415
CHEMBL508211CHEMBL48608P10415
CHEMBL51483CHEMBL48608P10415
CHEMBL192571CHEMBL48608P10415
CHEMBL503783CHEMBL48608P10415
CHEMBL509760CHEMBL48608P10415
CHEMBL503783CHEMBL48608P10415
CHEMBL452892CHEMBL48608P10415
CHEMBL376408CHEMBL48608P10415
CHEMBL595134CHEMBL48608P10415
CHEMBL503783CHEMBL48608P10415
CHEMBL454411CHEMBL48608P10415
CHEMBL452586CHEMBL48608P10415
CHEMBL1269110CHEMBL48608P10415
CHEMBL1271021CHEMBL48608P10415
CHEMBL500866CHEMBL48608P10415
CHEMBL473446CHEMBL48608P10415
CHEMBL1940668CHEMBL48608P10415
CHEMBL1940662CHEMBL48608P10415
CHEMBL1269075CHEMBL48608P10415
CHEMBL1269077CHEMBL48608P10415
CHEMBL467309CHEMBL48608P10415
CHEMBL1270819CHEMBL48608P10415
CHEMBL446802CHEMBL48608P10415
CHEMBL508392CHEMBL48608P10415
CHEMBL1269070CHEMBL48608P10415
CHEMBL1272170CHEMBL48608P10415
CHEMBL1271331CHEMBL48608P10415
CHEMBL509208CHEMBL48608P10415
CHEMBL1269076CHEMBL48608P10415
CHEMBL466801CHEMBL48608P10415
CHEMBL502454CHEMBL48608P10415
CHEMBL510332CHEMBL48608P10415
CHEMBL446607CHEMBL48608P10415
CHEMBL481581CHEMBL48608P10415
CHEMBL480009CHEMBL48608P10415
CHEMBL504480CHEMBL48608P10415
CHEMBL481581CHEMBL48608P10415
CHEMBL1269107CHEMBL48608P10415
CHEMBL513318CHEMBL48608P10415
CHEMBL538616CHEMBL48608P10415
CHEMBL446802CHEMBL48608P10415
CHEMBL467508CHEMBL48608P10415
CHEMBL1271230CHEMBL48608P10415
CHEMBL498873CHEMBL48608P10415
CHEMBL503454CHEMBL48608P10415
CHEMBL1269503CHEMBL48608P10415
CHEMBL503454CHEMBL48608P10415
CHEMBL1940669CHEMBL48608P10415
CHEMBL1940667CHEMBL48608P10415
CHEMBL1940665CHEMBL48608P10415
CHEMBL1269012CHEMBL48608P10415
CHEMBL1272170CHEMBL48608P10415
CHEMBL1272224CHEMBL48608P10415
CHEMBL481775CHEMBL48608P10415
CHEMBL1269504CHEMBL48608P10415
CHEMBL517577CHEMBL48608P10415
CHEMBL1940679CHEMBL48608P10415
CHEMBL1269110CHEMBL48608P10415
CHEMBL470541CHEMBL48608P10415
CHEMBL551288CHEMBL48608P10415
CHEMBL1940666CHEMBL48608P10415
CHEMBL1094366CHEMBL48608P10415
CHEMBL1269503CHEMBL48608P10415
CHEMBL1269076CHEMBL48608P10415
CHEMBL453466CHEMBL48608P10415
CHEMBL464268CHEMBL48608P10415
CHEMBL473446CHEMBL48608P10415
CHEMBL449546CHEMBL48608P10415
CHEMBL501871CHEMBL48608P10415
CHEMBL1940663CHEMBL48608P10415
CHEMBL1940664CHEMBL48608P10415
CHEMBL541496CHEMBL48608P10415
CHEMBL481775CHEMBL48608P10415
CHEMBL1269075CHEMBL48608P10415
CHEMBL448237CHEMBL48608P10415
CHEMBL1940670CHEMBL48608P10415
CHEMBL1271332CHEMBL48608P10415
CHEMBL1269072CHEMBL48608P10415
CHEMBL51483CHEMBL48608P10415
CHEMBL516633CHEMBL48608P10415
CHEMBL469305CHEMBL48608P10415
CHEMBL1270714CHEMBL48608P10415
CHEMBL1271440CHEMBL48608P10415
CHEMBL1269074CHEMBL48608P10415
CHEMBL502211CHEMBL48608P10415
CHEMBL480010CHEMBL48608P10415
CHEMBL1094250CHEMBL48608P10415
CHEMBL552735CHEMBL48608P10415
CHEMBL518858CHEMBL48608P10415
CHEMBL467229CHEMBL48608P10415
CHEMBL22150CHEMBL48608P10415
CHEMBL1272224CHEMBL48608P10415
CHEMBL541004CHEMBL48608P10415
CHEMBL464440CHEMBL48608P10415
CHEMBL541427CHEMBL48608P10415
CHEMBL453380CHEMBL48608P10415
CHEMBL501763CHEMBL48608P10415
CHEMBL450954CHEMBL48608P10415
CHEMBL509472CHEMBL48608P10415
CHEMBL451856CHEMBL48608P10415
CHEMBL553474CHEMBL48608P10415
CHEMBL1270617CHEMBL48608P10415
CHEMBL520607CHEMBL48608P10415
CHEMBL501793CHEMBL48608P10415
CHEMBL449546CHEMBL48608P10415
CHEMBL510828CHEMBL48608P10415
CHEMBL1269506CHEMBL48608P10415
CHEMBL451196CHEMBL48608P10415
CHEMBL1269074CHEMBL48608P10415
CHEMBL1269012CHEMBL48608P10415
CHEMBL539481CHEMBL48608P10415
CHEMBL552287CHEMBL48608P10415
CHEMBL1270616CHEMBL48608P10415
CHEMBL504480CHEMBL48608P10415
CHEMBL1940678CHEMBL48608P10415
CHEMBL554545CHEMBL48608P10415
CHEMBL518649CHEMBL48608P10415
CHEMBL467709CHEMBL48608P10415
CHEMBL1269070CHEMBL48608P10415
CHEMBL1269072CHEMBL48608P10415
CHEMBL450954CHEMBL48608P10415
CHEMBL510724CHEMBL48608P10415
CHEMBL480008CHEMBL48608P10415
CHEMBL460173CHEMBL48608P10415
CHEMBL1270820CHEMBL48608P10415
CHEMBL1094250CHEMBL48608P10415
CHEMBL1270922CHEMBL48608P10415
CHEMBL500574CHEMBL48608P10415
CHEMBL460173CHEMBL48608P10415
CHEMBL520607CHEMBL48608P10415
CHEMBL502066CHEMBL48608P10415
CHEMBL1269077CHEMBL48608P10415
CHEMBL1269505CHEMBL48608P10415
CHEMBL1940680CHEMBL48608P10415
CHEMBL514298CHEMBL48608P10415
CHEMBL538616CHEMBL48608P10415
CHEMBL444140CHEMBL48608P10415
CHEMBL1269107CHEMBL48608P10415
CHEMBL467229CHEMBL48608P10415
CHEMBL509788CHEMBL48608P10415
CHEMBL1094366CHEMBL48608P10415
CHEMBL513318CHEMBL48608P10415
CHEMBL1271231CHEMBL48608P10415
CHEMBL1269073CHEMBL48608P10415
CHEMBL1269073CHEMBL48608P10415
CHEMBL509208CHEMBL48608P10415
CHEMBL1940671CHEMBL48608P10415
CHEMBL449695CHEMBL48608P10415
CHEMBL509788CHEMBL48608P10415
CHEMBL1269507CHEMBL48608P10415
CHEMBL446480CHEMBL48608P10415
CHEMBL506763CHEMBL48608P10415
CHEMBL51483CHEMBL48608P10415
CHEMBL506360CHEMBL48608P10415
CHEMBL51483CHEMBL48607P10415
CHEMBL202964CHEMBL48607P10415
CHEMBL370837CHEMBL48607P10415
CHEMBL443221CHEMBL48607P10415
CHEMBL204822CHEMBL48607P10415
CHEMBL217223CHEMBL48607P10415
CHEMBL201670CHEMBL48607P10415
CHEMBL379895CHEMBL48607P10415
CHEMBL214965CHEMBL48607P10415
CHEMBL370836CHEMBL48607P10415
CHEMBL334590CHEMBL48607P10415
CHEMBL383229CHEMBL48607P10415
CHEMBL217354CHEMBL48607P10415
CHEMBL380433CHEMBL48607P10415
CHEMBL337153CHEMBL48607P10415
CHEMBL380709CHEMBL48607P10415
CHEMBL203620CHEMBL48607P10415
CHEMBL434952CHEMBL48607P10415
CHEMBL135934CHEMBL48607P10415
CHEMBL436605CHEMBL48607P10415
CHEMBL217354CHEMBL48607P10415
CHEMBL202540CHEMBL48607P10415
CHEMBL214839CHEMBL48607P10415
CHEMBL340270CHEMBL48607P10415
CHEMBL216213CHEMBL48607P10415
CHEMBL371861CHEMBL48607P10415
CHEMBL202798CHEMBL48607P10415
CHEMBL382648CHEMBL48607P10415
CHEMBL371861CHEMBL48607P10415
CHEMBL383399CHEMBL48607P10415
CHEMBL378808CHEMBL48607P10415
CHEMBL335265CHEMBL48607P10415
CHEMBL214965CHEMBL48607P10415
CHEMBL382018CHEMBL48607P10415
CHEMBL370835CHEMBL48607P10415
CHEMBL372834CHEMBL48607P10415
CHEMBL540363CHEMBL48607P10415
CHEMBL51483CHEMBL48607P10415
CHEMBL201947CHEMBL48607P10415
CHEMBL344184CHEMBL48607P10415
CHEMBL214839CHEMBL48607P10415
CHEMBL137800CHEMBL48607P10415
CHEMBL201669CHEMBL48607P10415
CHEMBL192571CHEMBL48607P10415
CHEMBL380502CHEMBL48607P10415
CHEMBL217223CHEMBL48607P10415
CHEMBL344184CHEMBL48607P10415
CHEMBL137135CHEMBL48607P10415
CHEMBL378820CHEMBL48607P10415
CHEMBL198903CHEMBL48607P10415
CHEMBL379013CHEMBL48607P10415
CHEMBL1253484CHEMBL48604P10415
Entries Per Page
Displaying Page of

  • Drugs

Name

Drug

Accession number

DocetaxelDB01248 APRD00932
RasagilineDB01367 EXPT02758
E7389DB04940 -
S-8184DB05281 -
DHA-paclitaxelDB05297 -
ABT-263DB05764 -
VenetoclaxDB11581 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-34b-5pMIMAT0000685MIRT000065qRT-PCR//Luciferase reporter assay//Western blotFunctional MTI18803879
hsa-miR-21-5pMIMAT0000076MIRT000159Luciferase reporter assayFunctional MTI17072344
hsa-miR-21-5pMIMAT0000076MIRT000159qRT-PCR//Western blotNon-Functional MTI22528454
hsa-miR-21-5pMIMAT0000076MIRT000159Western blotFunctional MTI21468550
hsa-miR-21-5pMIMAT0000076MIRT000159Western blot;OtherFunctional MTI20048743
hsa-miR-204-5pMIMAT0000265MIRT000192Luciferase reporter assayFunctional MTI19074899
hsa-miR-153-3pMIMAT0000439MIRT000290Luciferase reporter assay//Western blot//Reporter assayFunctional MTI19676043
hsa-let-7a-5pMIMAT0000062MIRT000418Microarray//qRT-PCRFunctional MTI (Weak)17260024
hsa-miR-15a-5pMIMAT0000068MIRT000815qRT-PCR//proteomics analysisFunctional MTI (Weak)18362358
hsa-miR-15a-5pMIMAT0000068MIRT000815Luciferase reporter assayFunctional MTI17707831
hsa-miR-15a-5pMIMAT0000068MIRT000815Luciferase reporter assayFunctional MTI19478946
hsa-miR-15a-5pMIMAT0000068MIRT000815Western blotFunctional MTI20876285
hsa-miR-15a-5pMIMAT0000068MIRT000815Microarray//qRT-PCRFunctional MTI (Weak)17260024
hsa-miR-15a-5pMIMAT0000068MIRT000815Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI16166262
hsa-miR-15a-5pMIMAT0000068MIRT000815Western blotFunctional MTI19903841
hsa-miR-15b-5pMIMAT0000417MIRT000978Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay//Reporter assay;OtherFunctional MTI18449891
hsa-miR-365a-3pMIMAT0000710MIRT006243Luciferase reporter assay//Western blotFunctional MTI22072615
hsa-miR-365a-3pMIMAT0000710MIRT006243Western blotFunctional MTI21640710
hsa-miR-16-5pMIMAT0000069MIRT001800Luciferase reporter assayFunctional MTI17877811
hsa-miR-16-5pMIMAT0000069MIRT001800Luciferase reporter assay//qRT-PCR//Western blot//Reporter assayFunctional MTI18449891
hsa-miR-16-5pMIMAT0000069MIRT001800qRT-PCR//proteomics analysisFunctional MTI (Weak)18362358
hsa-miR-16-5pMIMAT0000069MIRT001800Luciferase reporter assayFunctional MTI17351108
hsa-miR-16-5pMIMAT0000069MIRT001800Luciferase reporter assayFunctional MTI17707831
hsa-miR-16-5pMIMAT0000069MIRT001800Immunohistochemistry//Microarray//Western blotFunctional MTI20643754
hsa-miR-16-5pMIMAT0000069MIRT001800Western blotFunctional MTI20876285
hsa-miR-16-5pMIMAT0000069MIRT001800Luciferase reporter assay//Western blotFunctional MTI19269153
hsa-miR-16-5pMIMAT0000069MIRT001800Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI16166262
hsa-miR-16-5pMIMAT0000069MIRT001800Western blotFunctional MTI19903841
hsa-miR-16-5pMIMAT0000069MIRT001800SequencingFunctional MTI (Weak)20371350
hsa-miR-34a-5pMIMAT0000255MIRT002298Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;qRT-PCR;OtherFunctional MTI19683563
hsa-miR-34a-5pMIMAT0000255MIRT002298qRT-PCR//Western blot//Luciferase reporter assayFunctional MTI18505919
hsa-miR-34a-5pMIMAT0000255MIRT002298qRT-PCR//Luciferase reporter assay//Western blotFunctional MTI18803879
hsa-miR-34a-5pMIMAT0000255MIRT002298Luciferase reporter assayFunctional MTI19461653
hsa-miR-34a-5pMIMAT0000255MIRT002298Luciferase reporter assay//Western blot//MicroarrayFunctional MTI17914404
hsa-miR-34a-5pMIMAT0000255MIRT002298Luciferase reporter assay//Microarray//Western blotFunctional MTI17656095
hsa-miR-34a-5pMIMAT0000255MIRT002298Flow//Immunoblot//Luciferase reporter assay//Reporter assayFunctional MTI20598588
hsa-miR-34a-5pMIMAT0000255MIRT002298Reporter assay;OtherFunctional MTI21399894
hsa-miR-34a-5pMIMAT0000255MIRT002298ProteomicsFunctional MTI (Weak)21566225
hsa-miR-20a-5pMIMAT0000075MIRT003011Luciferase reporter assayFunctional MTI19666108
hsa-miR-17-5pMIMAT0000070MIRT003014Luciferase reporter assayFunctional MTI19666108
hsa-miR-29c-3pMIMAT0000681MIRT003289Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20041405
hsa-miR-29b-3pMIMAT0000100MIRT003290Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20041405
hsa-miR-29a-3pMIMAT0000086MIRT003291Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20041405
hsa-miR-181a-5pMIMAT0000256MIRT003501Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;OtherFunctional MTI20162574
hsa-miR-181a-5pMIMAT0000256MIRT003501Luciferase reporter assayFunctional MTI22285729
hsa-miR-181a-5pMIMAT0000256MIRT003501Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI22209977
hsa-miR-181a-5pMIMAT0000256MIRT003501Immunoblot//Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI21958558
hsa-miR-181a-5pMIMAT0000256MIRT003501Luciferase reporter assayFunctional MTI22610076
hsa-miR-181b-5pMIMAT0000257MIRT003500Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;OtherFunctional MTI20162574
hsa-miR-181b-5pMIMAT0000257MIRT003500Luciferase reporter assayFunctional MTI22610076
hsa-miR-181c-5pMIMAT0000258MIRT003499Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;OtherFunctional MTI20162574
hsa-miR-181d-5pMIMAT0002821MIRT003498Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;OtherFunctional MTI20162574
hsa-miR-181d-5pMIMAT0002821MIRT003498FACS//Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI22207524
hsa-miR-125b-5pMIMAT0000423MIRT006253Luciferase reporter assay//Western blotFunctional MTI22293115
hsa-miR-34c-5pMIMAT0000686MIRT003979qRT-PCR//Luciferase reporter assay//Western blotFunctional MTI18803879
hsa-miR-192-5pMIMAT0000222MIRT004844Luciferase reporter assay//qRT-PCR//Reporter assay;Microarray;OtherFunctional MTI19074876
hsa-miR-195-5pMIMAT0000461MIRT005362Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20727858
hsa-miR-630MIMAT0003299MIRT005578Immunoblot//Luciferase reporter assay//qRT-PCRFunctional MTI21274007
hsa-miR-451aMIMAT0001631MIRT005744qRT-PCR//Western blotFunctional MTI20816946
hsa-miR-449aMIMAT0001541MIRT006445ChIP-seq//Luciferase reporter assayFunctional MTI21569010
hsa-miR-200b-3pMIMAT0000318MIRT006670Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI21993663
hsa-miR-200c-3pMIMAT0000617MIRT006673Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI21993663
hsa-miR-429MIMAT0001536MIRT006674Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI21993663
hsa-miR-136-5pMIMAT0000448MIRT006868Luciferase reporter assayFunctional MTI22967897
hsa-miR-7-5pMIMAT0000252MIRT006904GFP reporter assay//Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;qRT-PCR;OtherFunctional MTI21750649
hsa-miR-148a-3pMIMAT0000243MIRT006975Luciferase reporter assayFunctional MTI21455217
hsa-miR-24-2-5pMIMAT0004497MIRT006977Luciferase reporter assayFunctional MTI21463514
hsa-miR-182-5pMIMAT0000259MIRT007063Flow//Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI22848417
hsa-miR-196b-5pMIMAT0001080MIRT007146ImmunocytochemistryFunctional MTI (Weak)23293219
hsa-miR-143-3pMIMAT0000435MIRT007348Western blotFunctional MTI23276710
hsa-miR-143-3pMIMAT0000435MIRT007348Western blotFunctional MTI19843160
hsa-miR-375MIMAT0000728MIRT019975qRT-PCR;MicroarrayFunctional MTI (Weak)20584986
hsa-miR-215-5pMIMAT0000272MIRT024494MicroarrayFunctional MTI (Weak)19074876
hsa-miR-103a-3pMIMAT0000101MIRT027158SequencingFunctional MTI (Weak)20371350
hsa-miR-96-5pMIMAT0000095MIRT027929SequencingFunctional MTI (Weak)20371350
Entries Per Page
Displaying Page of
  • mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

hsa-miR-15a-5pMIMAT00000681hsa-miR-15a{Western blot}{overexpression by mature miRNA transfection}16166262
hsa-miR-16-5pMIMAT00000691hsa-miR-16{Western blot}{overexpression by mature miRNA transfection}16166262
hsa-miR-16-5pMIMAT00000691hsa-miR-1617877811
hsa-miR-34a-5pMIMAT00002551hsa-miR-34a{Western blot}{underexpression by LNA antisense miRNA oligonucleotides}17656095
hsa-miR-16-5pMIMAT00000691hsa-miR-16{Western blot}{overexpression by miRNA precursor transfection}18449891
hsa-miR-15b-5pMIMAT00004171hsa-miR-15b{Western blot}{overexpression by miRNA precursor transfection}18449891
hsa-miR-15a-5pMIMAT0000068NAhsa-miR-15a18362358
hsa-miR-16-5pMIMAT0000069NAhsa-miR-1618362358
hsa-miR-16-5pMIMAT0000069NAhsa-miR-16proteomics analysisoverexpression18362358
hsa-miR-15a-5pMIMAT0000068NAhsa-miR-15a{phenotypic analysis of target gene}{overexpression}18362358
hsa-miR-34a-5pMIMAT0000255NAhsa-miR-34a{Western blot}{overexpression by miRNA precursor transfection}18834855
hsa-miR-16-5pMIMAT0000069NAhsa-miR-16{Western blot}{overexpression by miRNA precursor transfection}19269153
hsa-miR-296-5pMIMAT0000690NAhsa-miR-296-5p{Western blot}{downregulation}20485139
hsa-miR-181a-5pMIMAT0000256NAhsa-miR-181a{Western blot}{overexpression by miRNA mimics tranfection}20204284
hsa-miR-1MIMAT00004161hsa-miR-1{Western blot}{overexpression}19506341
hsa-miR-143-3pMIMAT00004351hsa-miR-143{Western blot}{overexpression by miRNA precursor transfection}20878132
hsa-miR-143-3pMIMAT00004352hsa-miR-143{Western blot}{overexpression by miRNA precursor transfection}20878132
Entries Per Page
Displaying Page of

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 55 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27212655The oxidative stress-sensitive proteins ataxia-telangiectasia mutated and p53 were phosphorylated, and the expression of apoptosis molecules Bax increased, and Bcl-2 decreased in early passage MSCs; however, the expression of the apoptotic molecules did less change in response to apoptotic stimulation in late-passage MSCs, suggesting that the intrinsic apoptotic signalling pathway was not induced by oxidative stress in long-term-cultured MSCs
27208501Mechanistically, TIS21(/BTG2) regulated posttranslational modification of p53 via enhancing miR34a and Bax expressions as opposed to inhibiting SIRT1 and Bcl2 expression
26711051N targets Bcl-2, Bcl-xl, and Bcl-w, while T targets Bcl-2, Bcl-xl, and Mcl-1
26711051The combination of Bcl-2, Bcl-xl, and Bcl-w siRNAs was senolytic in HUVECs and IMR90 cells, while combination of Bcl-2, Bcl-xl, and Mcl-1 siRNAs was not
26687460PEAM-injected IVDs showed significantly higher BAX/BCL2 ratio vs sham-injected IVDs suggestive of an anti-apoptotic effect of the PEAMs
26657143To test this idea, we screened a collection of compounds and identified ABT263 (a specific inhibitor of the anti-apoptotic proteins BCL-2 and BCL-xL) as a potent senolytic drug
26437300Decreased protein levels of the shelterin subunits, shortened telomere length, over-expressed Ki-67, and Bcl2 as well as mutations in P53 were detected both in MGC and BCC
26437300However, several parameters distinguish MGC from BCC samples: (i) the mRNA level of the shelterin subunits decreased in MGC but it increased in BCC; (ii) P53 was more highly mutated in MGC; (iii) Siah1 mRNA was over-expressed in BCC; (iv) BCC samples contain a higher level of senescent cells; (v) Ki-67 and Bcl2 expression were lower in BCC
25895748Protein expression relating to apoptosis (Bax, Bcl-2, Survivin), autophagy (Beclin-1, LC3B) and cellular senescence (p21, p16) was evaluated using indirect immunofluorescence
25882843Alternately, Mito-Pim1 enhances survival by increasing expression of Bcl-2 and Bcl-XL and decreasing cell death after H2O2 treatment, thereby preserving mitochondrial integrity superior to PimWT
25777063The molecular mechanisms involve substrate competition of tau and beta-catenin for glycogen synthase kinase 3beta (GSK-3beta); activation of Akt; preservation of Bcl-2 and suppression of Bax, cytosolic cytochrome-c, and caspase-3 activity; and upregulation of unfolded protein response (UPR), i
25540416EBNA2 and EBNALP associate with EBV and cell enhancers, up-regulate the EBNA promoter, MYC, and EBV Latent infection Membrane Proteins (LMPs), which up-regulate BCL2 to protect EBV-infected B-cells from MYC proliferation-induced cell death
25540416EBNA3A was at MYC, CDKN2A/B, CCND2, CXCL9/10, and BCL2, together with RUNX3, BATF, IRF4, and SPI1
25481090In addition, the protein levels of p-AKT, p-ERK, Bcl-2, matrix metallopeptidase 9 (MMP-9) and fibronectin (FN) were significantly reduced following quercetin treatment
25440825Apoptotic indices of smooth muscle cells and Bcl-2 were significantly greater at the site of UPJO (5
25333784Expression levels of Bcl-2 and Bax proteins were measured by western blot analysis
25333784LBPs also inhibited H2O2-induced downregulated Bcl-2 and upregulated Bax proteins and increased the levels of SOD and GSH enzyme activity
24673471Beclin-1 was indispensable to Ang II-induced autophagy, and its BH3 domain was required for the interaction with Bcl-2 to attenuate autophagy
24607549Among these, Bcl-2 family members--which are critically involved in maintaining mitochondrial integrity--may play a role in controlling mitochondrial function and dysfunction during cellular aging, also considering that Bcl-2, the master member of the family, is an anti-oxidant and anti-apoptotic factor and regulates mitochondrial fission/fusion and autophagy
24607549This intriguing hypothesis is supported by several observations: i) in endothelial cells undergoing replicative senescence (HUVECs), a well-established model of cell senescence, miR-146a, miR-34a, and miR-181a are over-expressed whereas their target Bcl-2 is down-regulated; ii) IPA of the miR-146a, miR-34a and miR-181a network shows that they are closely linked to each other, to Bcl-2 and to mitochondria; and iii) miR-146a, miR-34a, and miR-181a are involved in important cell functions (growth, proliferation, death, survival, maintenance) and age-related diseases (cancer, skeletal and muscle disorders, neurological, cardiovascular and metabolic diseases)
24475256Surprisingly, under self-renewing culture conditions, some of these senescent cells undergo p53-independent apoptosis, which can be suppressed by caspase inhibition and BCL2 overexpression
24024133Senescent HDFs are more resistant to oxidative stress (exogenous H2O2)-induced apoptosis in comparison to non-senescent (control) HDFs; this is associated with constitutively high levels of the anti-apoptotic gene, Bcl-2, and low expression of the pro-apoptotic gene, Bax
24024133In contrast to Bax gene, chromatin immunoprecipitation studies demonstrate marked enrichment of the Bcl-2 gene with H4K16Ac, and depletion with H4K20Me3, predicting active transcription of this gene in senescent HDFs
23984931After tBHP treatment, Bcl-2 protein expression decreased and Bax protein expression increased
23984931Bax protein expression decreased, but Bcl-2 protein expression increased after AG490 and probucol treatment
23907579Treatment of gastric cancer cells with DHA increased miR-15b and miR-16 expression, caused a downregulation of Bcl-2, resulting in apoptosis of gastric cancer cells
23807740Expression profiles of certain relevant genes and proteins like p53, Akt, Bcl-2, Bax, cytochrome c and caspase 3 also provided evidence of ROS mediated p53 up-regulation and further boost in Bax expression and followed by cytochrome c release and activation of caspase 3
22919441Gene expression analysis showed that GTT treatment down regulated BAX mRNA, up-regulated BCL2A1 mRNA and decreased the ratio of Bax/Bcl-2 protein expression (P < 0
22899934On the other hand, the expression of inhibitory Bcl-2/xL proteins increases with aging
22898871Inhibition of apoptosis by targeting Bim expression or overexpression of Bcl2 potentiates senescence
22898871In contrast, in apoptotic-deficient cells (Bim expression or overexpression of Bcl2), the inhibition of autophagy did not significantly modify the SA-beta-Gal-positive cell population
21909125The expression of apoptosis-associated proteins, such as p53, p21, Bcl-2, and Bax, did not significantly change in the presence of H(2)O(2) (100 mumol/L) or RHL (10 mumol/L)
21730299Here, we report a crucial role of Bcl-2 in the impaired angiogenic functions in senescent endothelial cells (ECs) by modulating the mitochondrial redox state
21730299We identified that Bcl-2 expression was markedly reduced in 3 independent models for senescent ECs, and pharmacological inhibition, as well as small interfering RNA-mediated gene silencing of Bcl-2, significantly impaired the angiogenic functions in young ECs
21730299Bcl-2 has an antioxidative role by locating the glutathione at mitochondria, and we found that mitochondrial oxidative stress was significantly augmented in senescent ECs, in association with reduced mitochondria-associated glutathione
21730299Transfection of Bcl-2 in senescent ECs significantly reduced the mitochondrial oxidative stress, restored the mitochondrial membrane potential, and improved the angiogenic capacity
21730299Furthermore, gene transfer of Bcl-2 using adenovirus significantly improved the in vivo angiogenesis in the Matrigel plugs implanted into aged mice, whereas the Bcl-2 inhibitor reduced the angiogenesis in the Matrigel plugs implanted into young mice
21730299Together, Bcl-2 plays a crucial role in the regulation of the mitochondrial redox state in ECs, and, thus, loss of Bcl-2 during the senescence exacerbates the impaired angiogenesis by augmenting the mitochondrial oxidative stress
21698300Compared to early cultures, late passage HUVECs also exhibited nuclear translocation of NF-kappaB (p65) and reciprocal shifts in BAX and BCL2 protein content resulting in almost 2-fold increase in BAX/BCL2 ratio and 3-fold increase in apoptotic response to TNFalpha exposure (p<0
21212468Remarkably, overexpressed Zfra induces apoptosis via the mitochondrial pathway, which involves suppression of Bcl-2 and Bcl-xL expression (without causing cytochrome c release), counteracting the apoptotic function of tumor suppressor p53 and WWOX, and dissipation of mitochondrial membrane potential for ultimately leading to cell death
21182935Similarly, UVB-induced translocation of Bax and Bcl-2 to mitochondria and cytosol, respectively, was markedly attenuated in cells overexpressing AR
21084274ABT-737, a small molecule cell-permeable Bcl-2 antagonist that acts by mimicking BH3 proteins, induces apoptotic cell death in multiple cancer types
20969773P16INK4a was downregulated, p53 was low expressed and Bax/Bcl-2 ratio was reversed
20729911Unlike PTX, knockdown of TACC3 did not trigger a cell death response, but instead resulted in a progressive loss of the pro-apoptotic Bcl-2 protein Bim that links microtubule integrity to spindle poison-induced cell death
20703098Importantly, p53(R172P) MEFs failed to downregulate anti-apoptotic protein Bcl-2, which has been shown to play an important role in p53-dependent apoptosis
19653337The relative expression level of Bcl-2 dropped to less than 50% of control cells at a sub-apoptotic concentration of chelidonine and subsequently increased to higher than 120% at LD(50)
19147823In contrast, the expression of several proteins involved in the regulation of macroautophagy, notably Beclin-1 and Bcl-2, was found to change with senescence
18694296Both SAHA and MS-275 induced an arrest in the cell cycle along with the induction of apoptotic pathways as evidenced by flow cytometry, annexin assay, detection of activated caspase 9, and molecular analysis of Bax/Bcl-2 expression
18158869METHODS: BMMS-03 cells and hMSC from the bone marrow of a 4-month-old elicited fetus, were transiently transfected with the pcDNA3-hbxip plasmid encoding the HBXIP gene and pSilencer-hbxip plasmid encoding RNA interference (RNAi) targeting HBXIP mRNA, followed by the examination of the hTERT promoter reporter gene by luciferase assay, and the detection of telomerase activity by telomeric repeat amplication protocol, respectively, as well as the expression levels of hTERT, c-Myc, and Bcl-2 by Western blot analysis
18158869RESULTS: The overexpression of HBXIP led to a significant upregulation of hTERT promoter activity, telomerase activity, and the expression levels of hTERT, c-Myc, and Bcl-2 in BMMS-03 cells
18060755Also, DHA and PEDF synergistically activate NPD1 synthesis and antiapoptotic protein expression and decreased proapoptotic Bcl-2 protein expression and caspase 3 activation during oxidative stress
18060755The Bcl-2 pro- and antiapoptotic proteins, neurotrophins, and NPD1, lie along a cell fate-regulatory pathway whose component members are highly interactive, and have potential to function cooperatively in cell survival
17882791By blocking apoptosis, Bcl-2 in p38-dependent manner promotes cell cycle arrest and accelerated senescence after DNA damage and serum withdrawal
17433785Expression of Bcl2 blocked apoptosis in tumor cells, but surprisingly, mice with short telomeres were still resistant to tumor formation
16711390Bcl-2 introduction in E1A + c-Ha-ras-transformants is accompanied by a rise of SA beta-Gal (Senescence Associated beta-Galactosidase) activity, which is commonly considered to be a marker of cell senescence
16711390Co-immunoprecipitation experiments demonstrated the introduction of Bcl-2 to result in formation of Bcl-2 complexes with early region E1A oncoproducts, which are thought to be responsible for proapoptotic susceptibility of E1A-expressing transformants
16711390The data obtained lead to suggestion that bcl-2 transfer to E1A + c-Ha-ras-transformants may induce a switch from the cell death program on the program of senescence after DNA damage, due, presumably, to Bcl-2 interaction with the apoptosis activator the viral oncoprotein E1A
16705698Apoptosis does not appear to be a major determinant of doxorubicin-induced mortality in FU-SY-1 SS or NHDF cultures, but may impact SW982 cells via the overexpression of BAX relative to Bcl-2
16545683Bcl-2 protects against oxidative stress while inducing premature senescence
16545683The former suggests a molecular link between cell cycle regulation and cell survival that could involve regulatory proteins such as Bcl-2
16545683There is strong evidence that, in addition to its well-known effects on apoptosis, Bcl-2 is involved in antioxidant protection and regulation of cell cycle progression
16545683The aim of this work was to determine if the protection against oxidative stress mediated by Bcl-2 could prevent or delay oxidative stress-induced senescence
16545683Fibroblasts overexpressing Bcl-2 were exposed to 75 microM H2O2 for 2 h to induce SIPS
16545683Our results indicate that overexpression of Bcl-2 protected primary fibroblasts against oxidative stress-mediated reduction in cell proliferation, but did not prevent premature senescence
15922292Unknotting the roles of Bcl-2 and Bcl-xL in cell death
15922292The antiapoptotic Bcl-2 family proteins Bcl-2 and Bcl-xL play important roles in inhibiting mitochondria-dependent extrinsic and intrinsic cell death pathways
15922292The overexpression of Bcl-2 is able to inhibit not only apoptotic cell death but also in part nonapoptotic cell death, which has the role of cell cycle arrest in the G1 phase, which may promote cellular senescence
15922292The overexpression of Bcl-2 may also have the ability to enhance cell death in the interaction of Bcl-xL with other factors
15922292This review discusses the previously unexplained aspects of Bcl-2 and Bcl-xL functions associated with cell death, for better understanding of their functions in the regulation
15013668Furthermore, we found that while the pro-apoptotic p53 increased, the anti-apoptotic Bcl-2 declined
14653227Pro-death Bax increased, while anti-death Bcl-2 and Bcl-XL decreased, and apoptotic TUNEL-positive cells were detected in the hippocampus of klotho mutant mice at the age of 7 weeks
12959928Senescent BMP4-treated cells had lower ERK activation, VEGF expression, and Bcl2 expression than wild-type cells, consistent with a less proliferative, less angiogenic phenotype with increased susceptibility to death by apoptosis
12473065Similarities between preparations included: an enhanced ability for both Apo2L/TRAIL preparations to kill a greater relative percentage of HaCaT cells compared with keratinocytes; enhanced cytotoxicity towards keratinocytes that had their NF-B activity inhibited; a dependence of both Apo2L/TRAIL preparations on FADD and caspase activation; triggering of the same caspase cascades including caspase 8 and 3; and an ability to induce apoptosis even when HaCaT cells and keratinocytes were transduced to overexpress either Bcl-2 or Bcl-x(L) (survival factors that reduce susceptibility to UV-light-induced apoptosis)
12473065Moreover, the death receptor pathway triggered by LZ-Apo2L/TRAIL can overcome the apoptotic resistance normally observed in response to UV-light mediated by Bcl-2/Bcl-x(L), as well as by the state of cellular senescence
12469202Bcl-2 in cancer and normal tissue cells as a prediction marker of response to 5-fluorouracil
12469202Bcl-2 in cancer cells was shown to be a potent indicator of 5-FU efficacy, but the protein in normal tissue cells appeared not to be a marker of 5-FU toxicity probably due to the functional alteration of Bcl-2 associated with cell senescence
12469202Transfection analysis of Bcl-2-S and Bcl-2-AS into A549 lung cancer cells revealed that Bcl-2 suppressed cell death induced by 5-FU, and the gene expression level of Bcl-2 was closely correlated with the IC50 for 5-FU in 21 fresh human gastric tumor specimens
12469202Transfection analysis of Bcl-2-S and Bcl-2-AS into MJ90 cells showed that Bcl-2 correlated with the resistance to 5-FU in the transfectants at PDL60 as in A549 cells, but increased Bcl-2 in the PDL72 senescent transfectant did not cause an increase of the resistance to 5-FU
12469202Cell aging was observed in MJ90 cells and Bcl-2 in the cells was found to decrease with the cell senescence
11850025Steady state levels of Bcl-2, an anti-apoptotic protein, in senescent prolonged cultures decreased to less than 20% for all time points compared with young cells
11850025These results indicate that terminal cellular aging enhances apoptosis and the levels of Bcl-2/Bad may be associated with the apoptotic process in porcine lung endothelial cells
11642719Bcl2 expression was mainly seen in medullary thymocytes, reflecting the surviving thymocytes in this region
11557274Senescent cells are resistant to death despite low Bcl-2 level
11557274Bcl-2 is a product of the oncogene, bcl-2, but it may also participate in cellular senescence
11557274To investigate the role of Bcl-2, we analyzed the level of Bcl-2 during aging of normal human fibroblasts by immunoblot analysis and found that its level was highly suppressed in four normal senescent fibroblast strains
11480555Ceramide activation of protein phosphatases has been shown to promote inactivation of a number of pro-growth cellular regulators including the kinases PKC alpha and Akt, Bcl2 and the retinoblastoma protein
10593857Several proto-oncogenes and tumor suppressor genes have been implicated in the regulation of telomerase activity, both directly and indirectly; these include c-Myc, Bcl-2, p21(WAF1), Rb, p53, PKC, Akt/PKB, and protein phosphatase 2A
10438583Effects of differential overexpression of Bcl-2 on apoptosis, proliferation, and telomerase activity in Jurkat T cells
10438583The effects of Bcl-2 overexpression on several of its multifunctional characteristics, which include anti-apoptotic properties, impeding of cell proliferation, and telomerase activity, were examined in four Jurkat T cell clones overexpressing different levels of Bcl-2
10438583When treated with anti-Fas or staurosporine, only three of the four clones showed resistance to apoptosis that correlated with the level of Bcl-2 expression
10438583Surprisingly, the clone having no anti-apoptotic characteristic expressed the highest level of Bcl-2
10438583When all the clones were treated with anti-Fas the processing of caspase-2, -3, and -7 but not -8 was inhibited in the resistant clones to a similar extent by the differential overexpression of Bcl-2
10438583However, with staurosporine treatment the processing of all the caspases examined was inhibited to a similar degree by the different levels of Bcl-2 expression in the resistant clones
10438583These results suggest that Bcl-2 blocked Fas-mediated cell death by acting downstream of caspase-8, which is in contrast to staurosporine-induced apoptosis where Bcl-2 is acting upstream of caspase-8
10438583When the anti-proliferative effect of Bcl-2 was examined, a direct correlation between a decrease in cell proliferation and the level of Bcl-2 overexpressed in the clones was observed
10438583The clone overexpressing the greatest amount of Bcl-2 protein, which had no resistance to apoptosis, had the slowest proliferative rate
10438583This suggests that the anti-apoptotic effect of Bcl-2 can be separated from its anti-proliferative effect
10438583The possible effect of overexpression of Bcl-2 on telomerase activity, which is known to control the proliferative capacity of normal cells and cellular senescence, was also determined
10438583Our results suggest that Bcl-2 had no effect on telomerase activity or telomere length in the clones
10438583In summary, our results further suggest that some properties of Bcl-2, such as anti-apoptotic and inhibition of cell proliferation, are individual features of a multifaceted protein
10066788Overexpression of Bcl-2 and the caspase inhibitor zVAD-fmk protected cells against apoptosis in the presence of telomerase inhibitors, suggesting a site of action of telomerase prior to caspase activation and mitochondrial dysfunction
Entries Per Page
Displaying Page of