HCSGD entry for CASP3
1. General information
| Official gene symbol | CASP3 |
|---|---|
| Entrez ID | 836 |
| Gene full name | caspase 3, apoptosis-related cysteine peptidase |
| Other gene symbols | CPP32 CPP32B SCA-1 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0001782 | B cell homeostasis | IEA | biological_process |
| GO:0001836 | Release of cytochrome c from mitochondria | IEA | biological_process |
| GO:0004190 | Aspartic-type endopeptidase activity | EXP IEA | molecular_function |
| GO:0004197 | Cysteine-type endopeptidase activity | IDA IEA TAS | molecular_function |
| GO:0004861 | Cyclin-dependent protein serine/threonine kinase inhibitor activity | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0005739 | Mitochondrion | IDA | cellular_component |
| GO:0005829 | Cytosol | IDA TAS | cellular_component |
| GO:0005886 | Plasma membrane | TAS | cellular_component |
| GO:0006309 | Apoptotic DNA fragmentation | IEA TAS | biological_process |
| GO:0006508 | Proteolysis | IDA IEA | biological_process |
| GO:0006915 | Apoptotic process | IEA TAS | biological_process |
| GO:0006921 | Cellular component disassembly involved in execution phase of apoptosis | TAS | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | IEA | biological_process |
| GO:0007507 | Heart development | IEA | biological_process |
| GO:0007605 | Sensory perception of sound | IEA | biological_process |
| GO:0008233 | Peptidase activity | IDA | molecular_function |
| GO:0008625 | Extrinsic apoptotic signaling pathway via death domain receptors | IEA | biological_process |
| GO:0008631 | Intrinsic apoptotic signaling pathway in response to oxidative stress | IEA | biological_process |
| GO:0008635 | Activation of cysteine-type endopeptidase activity involved in apoptotic process by cytochrome c | TAS | biological_process |
| GO:0009411 | Response to UV | IEA | biological_process |
| GO:0009611 | Response to wounding | IEA | biological_process |
| GO:0016485 | Protein processing | IEA | biological_process |
| GO:0030216 | Keratinocyte differentiation | IEA | biological_process |
| GO:0030218 | Erythrocyte differentiation | IDA TAS | biological_process |
| GO:0030220 | Platelet formation | TAS | biological_process |
| GO:0030889 | Negative regulation of B cell proliferation | IEA | biological_process |
| GO:0034349 | Glial cell apoptotic process | IEA | biological_process |
| GO:0034612 | Response to tumor necrosis factor | TAS | biological_process |
| GO:0035329 | Hippo signaling | TAS | biological_process |
| GO:0042981 | Regulation of apoptotic process | TAS | biological_process |
| GO:0043029 | T cell homeostasis | IEA | biological_process |
| GO:0043065 | Positive regulation of apoptotic process | TAS | biological_process |
| GO:0043066 | Negative regulation of apoptotic process | IGI | biological_process |
| GO:0043281 | Regulation of cysteine-type endopeptidase activity involved in apoptotic process | TAS | biological_process |
| GO:0043525 | Positive regulation of neuron apoptotic process | IEA | biological_process |
| GO:0045165 | Cell fate commitment | IEA | biological_process |
| GO:0045736 | Negative regulation of cyclin-dependent protein serine/threonine kinase activity | IEA | biological_process |
| GO:0046007 | Negative regulation of activated T cell proliferation | IEA | biological_process |
| GO:0048011 | Neurotrophin TRK receptor signaling pathway | TAS | biological_process |
| GO:0051402 | Neuron apoptotic process | IEA | biological_process |
| GO:0071310 | Cellular response to organic substance | IEA | biological_process |
| GO:0097153 | Cysteine-type endopeptidase activity involved in apoptotic process | IMP | molecular_function |
| GO:0097190 | Apoptotic signaling pathway | TAS | biological_process |
| GO:0097192 | Extrinsic apoptotic signaling pathway in absence of ligand | IEA | biological_process |
| GO:0097193 | Intrinsic apoptotic signaling pathway | TAS | biological_process |
| GO:0097194 | Execution phase of apoptosis | IDA IMP | biological_process |
| GO:0097200 | Cysteine-type endopeptidase activity involved in execution phase of apoptosis | IEA IMP | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0060827362 | 0.9949889252 | 0.2058181234 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Up | 0.2172803131 |
| GSE13712_SHEAR | Up | 0.3667133150 |
| GSE13712_STATIC | Up | 0.1128241094 |
| GSE19018 | Up | 1.3852947130 |
| GSE19899_A1 | Up | 0.3722897895 |
| GSE19899_A2 | Up | 0.8623998138 |
| PubMed_21979375_A1 | Up | 0.7807943331 |
| PubMed_21979375_A2 | Up | 0.3523391385 |
| GSE35957 | Up | 0.2198638652 |
| GSE36640 | Up | 0.0359231321 |
| GSE54402 | Up | 0.3627146978 |
| GSE9593 | Up | 0.2774860842 |
| GSE43922 | Up | 0.2392948739 |
| GSE24585 | Up | 0.5641437697 |
| GSE37065 | Up | 0.1107469781 |
| GSE28863_A1 | Up | 0.0743955645 |
| GSE28863_A2 | Up | 0.3223314739 |
| GSE28863_A3 | Up | 0.1100665137 |
| GSE28863_A4 | Down | -0.0562621304 |
| GSE48662 | Down | -0.2935508249 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Minocycline | DB01017 | APRD00547 |
| 5-[4-(1-Carboxymethyl-2-Oxo-Propylcarbamoyl)-Benzylsulfamoyl]-2-Hydroxy-Benzoic Acid | DB03124 | EXPT00045 |
| IDN-6556 | DB05408 | - |
| 2-HYDROXY-5-(2-MERCAPTO-ETHYLSULFAMOYL)-BENZOIC ACID | DB06862 | - |
| methyl (3S)-3-[(tert-butoxycarbonyl)amino]-4-oxopentanoate | DB07696 | - |
| 1-METHYL-5-(2-PHENOXYMETHYL-PYRROLIDINE-1-SULFONYL)-1H-INDOLE-2,3-DIONE | DB08213 | - |
| [N-(3-DIBENZYLCARBAMOYL-OXIRANECARBONYL)-HYDRAZINO]-ACETIC ACID | DB08229 | - |
| 4-[5-(2-CARBOXY-1-FORMYL-ETHYLCARBAMOYL)-PYRIDIN-3-YL]-BENZOIC ACID | DB08251 | - |
| (1S)-2-oxo-1-phenyl-2-[(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-5-yl)amino]ethyl acetate | DB08497 | - |
| (1S)-1-(3-chlorophenyl)-2-oxo-2-[(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-5-yl)amino]ethyl acetate | DB08498 | - |
| N-[3-(2-fluoroethoxy)phenyl]-N'-(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-6-yl)butanediamide | DB08499 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-30d-5p | MIMAT0000245 | MIRT006240 | Luciferase reporter assay//Western blot | Functional MTI | 22058146 |
| hsa-let-7a-5p | MIMAT0000062 | MIRT005292 | Luciferase reporter assay//Western blot | Functional MTI | 18758960 |
| hsa-miR-138-5p | MIMAT0000430 | MIRT006864 | Luciferase reporter assay | Functional MTI | 22921398 |
| hsa-miR-375 | MIMAT0000728 | MIRT019884 | qRT-PCR;Microarray | Functional MTI (Weak) | 20584986 |
| hsa-miR-128-3p | MIMAT0000424 | MIRT021992 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-221-3p | MIMAT0000278 | MIRT024157 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-26b-5p | MIMAT0000083 | MIRT029617 | Microarray | Functional MTI (Weak) | 19088304 |
| hsa-miR-196a-5p | MIMAT0000226 | MIRT048249 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-let-7a-5p | MIMAT0000062 | NA | hsa-let-7a | {Western blot} | {overexpression by miRNA precursor transfection} | 18758960 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 61 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27294914 | This study explored the protective effect of ginsenoside Rg1 on Sca-1(+) hematopoietic stem/progenitor cells (HSC/HPCs) in a mouse model of d-galactose-induced aging |
| 27294914 | Compared with those in the d-gal administration alone group, ginsenoside Rg1 protected Sca-1(+) HSC/HPCs by decreasing SA-beta-Gal and enhancing the colony forming unit-mixture (CFU-Mix), and adjusting oxidative stress indices like reactive oxygen species (ROS), total anti-oxidant (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-px) and malondialdehyde (MDA) |
| 27294914 | X), 8-OHdG, p16(Ink4a), Rb, p21(Cip1/Waf1) and p53 in senescent Sca-1(+) HSC/HPCs |
| 27294914 | Our findings indicated that ginsenoside Rg1 can improve the resistance of Sca-1(+) HSC/HPCs in a mouse model of d-galactose-induced aging through the suppression of oxidative stress and excessive activation of the Wnt/beta-catenin signaling pathway, and reduction of DNA damage response, p16(Ink4a)-Rb and p53-p21(Cip1/Waf1) signaling |
| 27259496 | The effect peptides KE, KED, AED and AEDG on proliferation (Ki-67), regeneration and aging (CD98hc), apoptosis (caspase-3), and extracellular matrix remodeling (MMP-9) in skin fibroblasts during their aging in culture were studied by immunofluorescent confocal microscopy |
| 27212655 | This resistance occurred via caspase-9 and caspase-3 rather than via caspase-8 |
| 26895377 | Consistently, procaspase-3 protein, but not mRNA decreased in the presence of miR-30e, whereas expression of the cyclin-dependent kinase inhibitor p21 increased both at the mRNA and protein level |
| 26895377 | Performing luciferase reporter gene assays, we identified the 3'-UTR of the caspase-3 mRNA as a direct miR-30e target |
| 26895377 | Interestingly, despite suppressing procaspase-3 expression, miR-30e was unable to protect RKO colon carcinoma cells from DNA damage-induced death or to induce senescence, as miR-30e completely fails to upregulate p21 in these cells |
| 26586345 | Moreover, LGX818 downregulated CyclinD1 in a glycogen synthase kinase 3beta-independent manner and induced cell cycle arrest in the G1 phase, Surprisingly, LGX818 triggered cellular senescence in BRAFV600E melanoma cells, as evidenced by increased beta-galactosidase staining, while no appreciable induction of apoptosis was detected, as determined by Annexin V and propidium iodide staining and immunoblot analysis of caspase-3 processing and poly (ADP-ribose) polymerase cleavage |
| 26515130 | Ad5-CMV-CCN1 induced HSC apoptosis that was evident by proteolytic cleavage of caspase-12, caspase-9 and the executor caspase-3 and positive TUNEL stain |
| 26224580 | On a negative side, statins impaired the osteogenic and chondrogenic differentiation potential of MSCs and increased cell senescence and apoptosis, as indicated by upregulation of p16, p53 and Caspase 3, 8, and 9 |
| 26106432 | Study on the Dynamic Biological Characteristics of Sca-1(+) Hematopoietic Stem and Progenitor Cell Senescence |
| 26084179 | METHOD: Sca-1 + HSC/HPC was isolated by magnetic cell sorting (MACS) and divided into five groups: the normal control group, the aging group, the positive control group, the Rg1 anti-senescence group, and the Rg1-treated group |
| 26084179 | Senescence-associated beta-galactosidase (SA-beta-Gal) staining, cell cycle analysis and hemopoietic progenitor cell mix (CFU-Mix) were adopted to determine the effect Rg1 in delaying or treating Sca-1 + HSC/HPC senescence biology |
| 26084179 | CONCLUSION: Rg, may inhibit Sca-1 + HSC/HPC senescence induced by t-BHP by regulating SIRT6/NF-KB signal path |
| 25962658 | Quantitative analysis of the expression of caspase 3 and caspase 9 in different types of atherosclerotic lesions in the human aorta |
| 25962658 | This study was undertaken to evaluate the levels of the expression of key apoptosis-related genes, namely, caspase 3 (CASP3) and caspase 9 (CASP9) in the normal (non-atherosclerotic) intima of the human aorta in comparison with those in different types of atherosclerotic lesions |
| 25962658 | The study revealed that the expressions of CASP3 and CASP9 genes were changed in different types of atherosclerotic lesions in course of the progression of the disease, but not in a unanimous way |
| 25962658 | The fall in CASP3 expression may be associated with cellular senescence as well as with the domination of necrotic processes in atherosclerotic lesions, as shown by electron microscopic analysis |
| 25962658 | Our study provides novel quantitative data on the expression of CASP3 and CASP9 genes in different atherosclerotic lesions in the human aorta and thus, might assist in better understanding of the processes occurring during the development of lesions in human atherogenesis |
| 25790295 | Unlike WT mice, p66Shc-/- mice did not develop emphysema, showing protection toward oxidative damage to DNA and apoptosis as revealed by a trivial 8-hydroxyguanosine staining and faint TUNEL and caspase-3 positivity on alveolar epithelial cells |
| 25777063 | The 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 |
| 25472717 | This upregulates the downstream proteins CEBPB, FAK, N-cadherin, vimentin, Oct4 and Sca-1 (also known as stem cell antigen-1), and downregulates E-cadherin |
| 25407160 | In the mouse hind limb ischemia model, TUDCA promoted blood perfusion by enhancing angiogenesis through recruitment of Flk-1(+) /CD34(+) and Sca-1(+) /c-kit(+) progenitors into damaged tissue |
| 25363496 | Western blot assay was compared for p53, bax, cleaved caspase 3, rH2AX, and APE1 |
| 25363496 | All the checked variables were significantly increased with aging: 1) increased p53, bax, and caspase 3 may activate the apoptotic pathway, 2) increased rH2AX and 8-OHdG immunolocalization in the proximal convoluted tubules might mean augmented DNA damage, and 3) increased APE1 might be caused by the immunoreactivity in the distal convoluted tubules while decreased in the proximal convoluted tubules |
| 25360110 | Interestingly, markers indicating cellular senescence or oxidative stress (SNCA, CASP3, CAT, SOD2, and TERT) were largely unchanged within the ENS |
| 25341032 | Extended ligation period resulted in the caspase-3 activation and acinar cell death, which was delayed by Atg5 knockout |
| 25017491 | LLFE induced apoptosis in Bel-7402 cells accompanied by activation of caspase-3, -8 and -9 |
| 24839934 | The apoptosis-related proteins, caspase 3, 8 and 9, were detected by western blotting |
| 24839934 | Finally, we detected the protein and mRNA levels of PinX1 and caspase 3, 8 and 9 in colorectal cancer specimens and confirmed that levels of PinX1 and caspase 3, 8 and 9 expression were closely linked to the poor prognosis of colorectal cancer |
| 24793880 | The results clearly demonstrated that the exposure of DU145 cells to 17 inhibits cell proliferation and induces apoptosis by activation of caspase-3 and -9 |
| 24782600 | Activation of egr-1, in turn, upregulates the dual specificity phosphatase, phosphatase and tensin homologue deleted on chromosome ten (PTEN) resulting in activation of pro-apoptotic caspase-3 and caspase-9 and reduced expression of the anti-apoptosis protein, survivin |
| 24750067 | Expression of neurodegenerative disease-related proteins and caspase-3 in glioneuronal tumours |
| 24750067 | Sections were processed for immunohistochemistry using markers for the evaluation of caspase-3 and neurodegeneration-related proteins/pathways and their expression was correlated with the tumour features and the clinical history of epilepsy |
| 24750067 | Expression of APP, DR6, pTau (in GG and DNT) and caspase-3 (in GG) positively correlated with duration of epilepsy |
| 24616707 | The contribution of oxidative stress to the removal of RBCs by macrophages involves caspase-3 activation, which requires oxidative stress |
| 24461061 | SA-beta-Gal, acridine orange (AO)/ethidium bromide (EB) double staining, caspase-3 measurements and comet assay results revealed that cell death induced by pyocyanin involved DNA damage and activation of caspase-3, accelerating cell senescence and apoptosis |
| 24335839 | Sca-1(+) HSC/HPCs were isolated and purified from their bone marrow using MACS |
| 24335839 | RESULTS: The irradiation caused dramatic reduction in the number of Sca-1(+) HSC/HPCs on d 1 and the number barely recovered until d 7 compared to the sham-irradiated group |
| 24335839 | The irradiation significantly decreased SOD activity, increased MDA contents and caused DNA damage in Sca-1(+) HSC/HPCs |
| 24335839 | Moreover, the irradiation significantly increased SA-beta-gal staining, reduced CFU-mix forming, increased the expression of P16(INK4a) and P21(Cip1/Waf1) in the core positions of the cellular senescence signaling pathways and caused G1 phase arrest of Sca-1(+) HSC/HPCs |
| 24335839 | Administration of ginsenoside Rg1 caused small, but significant recovery in the number of Sca-1(+) HSC/HPCs on d 3 and d 7 |
| 24335839 | Furthermore, ginsenoside Rg1 significantly attenuated all the irradiation-induced changes in Sca-1(+) HSC/HPCs, including oxidative stress reaction, DNA damage, senescence-related markers and cellular senescence signaling pathways and cell cycle, etc |
| 24028184 | Cellular senescence was investigated using beta-galactosidase staining and apoptosis was quantified using a fluorescence-based caspase 3 assay |
| 23807740 | Expression 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 |
| 23722523 | A recombinant matriptase causes an increase in caspase-3 activity in a small-intestinal epithelial IEC-6 line cultured on fibronectin-coated plates |
| 23722523 | 1 muM) caused an increased detachment of and increases in the activity of apoptotic effector caspase-3 in a rat small-intestinal epithelial IEC-6 line cultured on laminin-coated plates and proposed that at sites with its high level of expression, matriptase contributes to promoting shedding and/or detachment-induced death of epithelial cells through a mechanism mediating loss of cell-ECM adhesion |
| 23722523 | In this study, we found that even without increasing cell detachment, a high concentration of r-MatCD causes an increase in caspase-3 activity in IEC-6 cells cultured on fibronectin-coated plates, suggesting that the recombinant matriptase can cause apoptosis by a mechanism unrelated to cell detachment |
| 23624226 | Senescence, assessed by telomere length and enzyme-betagalactosidase (beta-gal), reactive oxygen species (ROS), mitochondrial depolarization (JC-1 probe), caspase 3, and apoptosis were determined by flow cytometry |
| 23611899 | To determine whether these effects were due to altered chondrocyte growth and survival, we assayed the expression of cell proliferation marker Ki67, cell cycle arrest markers p21 and p53, and apoptosis marker caspase 3 |
| 23238821 | The apoptosis and senescence of NP cells was investigated by terminal deoxyribonucleotidyl transferase (TDT)-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay, immunohistochemistry, and Western blot for caspase3, caspase8, caspase9, and p16lnk4A (increased in cellular senescence) |
| 23238821 | Diabetes increased apoptosis of NP cells and led to activations of initiators of intrinsic (caspases-9) and extrinsic (caspase-8) pathways as well as their common executioner (caspase-3) |
| 22919441 | Both SIPS and senescent HDFs shared similar apoptotic changes such as increased Annexin V-FITC positive cells, increased cytochrome c release and increased activation of caspase-9 and caspase-3 (P < 0 |
| 22919441 | GTT treatment resulted in a significant reduction of Annexin V-FITC positive cells, inhibited cytochrome c release and decreased activation of caspase-9 and caspase-3 (P < 0 |
| 22919441 | These findings suggested that GTT inhibits apoptosis by modulating the upstream apoptosis cascade, causing the inhibition of cytochrome c release from the mitochondria with concomitant suppression of caspase-9 and caspase-3 activation |
| 22911222 | In mice bearing LuCaP xenograft tumors in vivo, surgical castration similarly increased SA-beta-gal staining, increased expression of p27(Kip1) and HP1gamma, and decreased expression of the proliferation marker KI-67, with minimal induction of apoptosis identified by detection of cleaved caspase 3 and TUNEL |
| 22898871 | Preventing apoptosis by caspase inhibition decreases annexin V-positive cells, caspase-3 cleavage and increases the SA-beta-Gal-positive cell population |
| 22783411 | Effects of gambogic acid on the activation of caspase-3 and downregulation of SIRT1 in RPMI-8226 multiple myeloma cells via the accumulation of ROS |
| 22375401 | METHOD: Sca-1(+) HSC was isolated by magnetic cell sorting(MACS) and divided into five groups: the control group, the aged model group, the Rg1 group, the Rg1 treated aged group and the Rg1 delayed aged group |
| 22375401 | Cell cycle assay and culture of mixed hematopoietic progenitor cell were used to investigate the effect of ginsenoside Rg1 to delay Sca-1(+) HSC senescence |
| 22375401 | CONCLUSION: Activation of telomerase and prolonging of telomere length might be involved in the process of ginsenoside Rg1 to delay and treat the senescence of Sca-1(+) HSC |
| 22267761 | The lung tissue in which type II cells contained higher numbers of gammaH2AX foci per cell had higher percentages of type II cells that expressed p16(INK4a) (p16), phosphorylated nuclear factor (NF)-kappaB and interleukin (IL)-6, and of alveolar wall cells that expressed active caspase-3 |
| 22266010 | After exposure the treatment effects were measured according to certain end points, including changes in urothelial cell viability, reactive oxygen species formation, caspase-3 activity, basal and stimulated adenosine triphosphate release, SA-beta-gal activity and detection of acidic vesicular organelles |
| 22266010 | RESULTS: The 24-hour pyocyanin treatment resulted in a concentration dependent decrease in cell viability at concentrations of 25 muM or greater, and increases in reactive oxygen species formation and caspase-3 activity at 25 muM or greater |
| 22266010 | This effect was not evident at 100 muM pyocyanin and may have been due to apoptotic cell death, as indicated by increased caspase-3 activity |
| 22266010 | CONCLUSIONS: Exposure to pyocyanin alters urothelial cell viability, reactive oxygen species production and caspase-3 activity |
| 21657082 | METHOD: Sca-1 + HSC was isolated by magnetic cell sorting (MACS) and divided into five groups |
| 21657082 | To Rg1 delay aging group, Sca-1 + HSC were established aging model after pretreatment of Rg1 (final concentration is 10 micromol x L(-1)) |
| 21657082 | To Rg1 treat aging group, Sca-1 + HSC gave Rg1 (final concentration is 10 micromol x L(-1)) antiaging treatment after the aging model was established |
| 21657082 | CONCLUSION: Rg1 can significantly delay and treat the senescence of Sca-1 + HSC |
| 21518171 | Apoptosis was assayed on western probed for p53, p21, and caspase-3 and -9 |
| 21471201 | The subsequent treatment of stabilized SCCs with rapamycin decreased tumor size and induced caspase-3 activation |
| 21334198 | Consistently, nutlin-3 elicited apoptosis only in wild-type p53 cells, as assessed by caspase-3 activity assay and flow cytometric analyses of mitochondrial depolarisation and DNA fragmentation |
| 19937729 | FACS investigations, caspase-3 activation, and Sytox Green immunofluorescent assay showed that pathological concentrations of oxysterols induced necrosis (30-50%) after 48 h of treatment |
| 19801829 | The inhibition of H(2)O(2)-induced cell death by clitocybins was mediated by the reduction of caspase 3 and 9 activation, cytochrome c release from mitochondria and the degradation of IkappaB-alpha and IkappaB-beta, which could be resulted in the prevention of cellular senescence |
| 19595526 | The FSS analysis was performed after decalcification and standard histological study, respectively with immunohistochemistry (Factor Von Willebrand antibody) VWF and (TdT-mediated dUTP nick end labelling) TUNEL method and caspase-3 immunohistochemical expression |
| 19251986 | The caspase-like activity DEVDase was measured by using the fluorescent substrate Ac-DEVD-AMC and antibodies against the human caspase-3 active enzyme cross-reacted with bands, the intensity of which paralleled the activity |
| 19251986 | The irreversible caspase-3 inhibitor Z-DEVD-FMK completely inhibited the enzymatic activity whereas serine and aspartyl proteases inhibitors did not |
| 19238475 | Derangement of erythrocytic AE1 in beta-thalassemia by caspase 3: pathogenic mechanisms and implications in red blood cell senescence |
| 19238475 | Since redox-mediated injury is an important pathway in the destruction of beta-thalassemic RBCs, we studied the anion transport and the activity of caspase 3 in the absence and presence of t-butylhydroperoxide in order to evaluate the effect of an increase of cellular oxidative stress |
| 19238475 | These findings led us to formulate a hypothesis about the metabolic characteristics of beta-thalassemic erythrocytes, outlining that one of the main targets of caspase 3 in RBCs is the cytoplasmic domain of band 3 protein |
| 18952756 | Expression of downstream apoptotic/stress markers, including caspase-3, caspase-6, Bax, and HSP-25, was also observed in telomerase-null, but not wild-type, AEC2 |
| 18385095 | Apoptosis was quantified by a caspase-3 assay, and cellular senescence was quantified by beta-galactosidase staining |
| 18385095 | Hydrogen peroxide-induced activation of caspase-3 was reduced by 50 microM quercetin, from 1 |
| 18060755 | Also, 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 |
| 17972103 | Our results indicate that, during take-over, caspase-3 activity in haemocyte lysates increases |
| 17972103 | In addition, about 20%-30% of haemocytes express phosphatidylserine on the outer leaflet of their plasma membrane, show DNA fragmentation and are immunopositive for caspase-3 |
| 17145870 | Here, we report that IR induced caspase-9 and caspase-3 activation and subsequent apoptosis only in p21-deficient colon carcinoma cells, whereas similar treated wild-type cells were permanently arrested in the G(2)-M phase, correlating with the induction of cellular senescence |
| 17145870 | In addition, p21 did neither interact with caspase-3 or caspase-9, suggesting that these events are not required for the observed protection |
| 17145870 | In addition, in vitro caspase activation assays yielded higher caspase-3 activities in extracts of irradiated p21-deficient cells compared with extracts of similar treated wild-type cells |
| 16904918 | The apoptotic markers caspase-3 and cytochrome c were both found to increase in senescent cells |
| 16319532 | Significant activation of caspase-2 and caspase-3 was only observed in MDA-MB-231 cells treated with doxorubicin but not with WP631, indicating that caspases may be not mandatory for the occurrence of cell death through mitotic catastrophe |
| 16319532 | In MCF-7/VP cells, which do not express functional caspase-3, mitotic catastrophe was also induced |
| 14580868 | We now demonstrate that cell death occurs by apoptosis, characterized by activation of caspase 3 |
| 12743603 | Specific molecular markers such as p21/WAF1, activated caspase-3 and activated Akt were associated with these death modes |
| 12743603 | The pan-caspase inhibitor (Q-VD-OPH) greatly reduced doxorubicin-induced caspase-3 activation but did not protect cells against drug toxicity |
| 11850025 | Apoptotic cells in prolonged cultures of senescent PAEC increased from 5 to 35% as determined by protein mass, DNA breakage, and caspase-3 activation |
| 11491387 | Long-term treatment of hepatocytes with NAME also produced a reduction in caspase 3 activation and in the percentage of spontaneous apoptotic cells, and an increase in cell survival and transcriptional activity as shown by attached cellular protein content and the protein-DNA ratio respectively |
| 11261835 | In addition, we present evidence of morphological and biochemical signs of senescence, as shown by the staining for senescence associated beta-galactosidase activity, and induction of programmed cell death, as demonstrated by an increase of caspase-3 activity, in tumor cells exposed to AZT |
| 11163759 | Moreover, we found that hydroxyl radical-induced apoptosis in telomerase-expressing and control fibroblasts was caspase-3 independent |
| 11163759 | These findings have revealed a new type of interrelation between telomerase and caspase-3, which may indicate that in this case the expressed telomerase may inhibit apoptosis at a site not related to the caspase-3 cascade |
| 10530789 | We now document that in response to treatment with apoptotic stimuli, senescent CD8+ T-cell cultures show reduced apoptosis and diminished caspase 3 activity compared with quiescent early passage cultures from the same donor |
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