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Validated All-in-One™ qPCR Primer for CASP3(NM_032991.2) Search again
Product ID:
HQP054409
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CPP32, CPP32B, SCA-1
Gene Description:
caspase 3
Target Gene Accession:
NM_032991.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce two subunits, large and small, that dimerize to form the active enzyme. This protein cleaves and activates caspases 6, 7 and 9, and the protein itself is processed by caspases 8, 9 and 10. It is the predominant caspase involved in the cleavage of amyloid-beta 4A precursor protein, which is associated with neuronal death in Alzheimer's disease. Alternative splicing of this gene results in two transcript variants that encode the same protein. [provided by RefSeq].
Gene References into function
- A soluble proform of caspase 3 containing a fortuitous mutation (W206R) is inactive when incubated with recombinant human caspase 8 and therefore can serve as a useful reagent to test the efficacy of caspase 8 inhibitors.
- Enzyme activation of caspase-3 was observed in apoptosis of K562 human cell line.
- caspase-3 may participate in the regulation mechanism of lymphoma cel apoptosis.
- Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells.
- caspase 3-mediated focal adhesion kinase processing in human ovarian cancer cells: possible regulation by X-linked inhibitor of apoptosis protein
- investigation of molecular mechanism of MPO-mediated apoptosis and caspase-3 activation
- These data suggest that D4-GDI of Rho family GTPase may be regulated during apoptosis through the caspase-3 mediated cleavage of the GDI protein.
- Clinical significance of caspase-3 expression in pathologic-stage I, nonsmall-cell lung cancer
- translation of some IRES-containing mRNAs is regulated by proteolytic cleavage of PTB during apoptosis
- results suggest that IGF-1/PI-3 kinase inhibited C2-ceramide-induced apoptosis due to relieving oxidative damage, which resulted from the inhibition of catalase by activated caspase-3
- Expression levels of apoptosis-related proteins caspase 3, Bcl-2, and PI9 predict clinical outcome in anaplastic large cell lymphoma.
- Identification of high caspase-3 mRNA expression as a unique signature profile for extremely old individuals
- The significant expression of caspase-3 that occurs in monocytes during serum-deprived induction of apoptosis can be down-regulated to baseline levels by addition of platelets.
- High numbers of active caspase 3-positive Reed-Sternberg cells in pretreatment biopsy specimens of patients with Hodgkin disease predict favorable clinical outcome.
- Caspase-cleaved amyloid precursor protein and activated caspase-3 are co-localized in the granules of granulovacuolar degeneration in Alzheimer's disease and Down's syndrome brain.
- Selective inhibition of dipeptidyl peptidase I, not caspases, prevents the partial processing of procaspase-3 in CD3-activated human CD8(+) T lymphocytes
- Pro-CASP3 moved to the the mitochondria of U937 cells during TPA-induced differentiation.
- caspase 3 cleaves CDC6 during apoptosis, which prevents wounded cell from replicating and facilitates death
- Both oleandrin and radiation share a caspase-3 dependent mechanism of apoptosis in the PC-3 human prostate cacncer cell line.
- Hypoxia-induced cleavage of caspase-3 and DFF45/ICAD in human failed cardiomyocytes.
- Role of nuclear PKC delta in mediating caspase-3-upregulation in Jurkat T leukemic cells exposed to ionizing radiation
- Data show that endoplasmic reticulum stress induced by thapsigargin not only activated the apoptosis effector caspase-3 but also caused a large and prolonged increase in the activity of glycogen synthase kinase-3beta.
- caspase 3-independent function of Bak in the TNF-alpha-induced apoptotic pathway
- The apoptosis resistance of mdr cells is not related to the abnormality of CPP32 but the upstream of caspase, the fact of which indicates promising prospect of the research on reversion of mdr cells using CPP32 as target.
- caspase 3 activation and apoptosis are blocked by LIGHT protein in hepatocytes
- A significant positive correlation between in-situ active caspase-3 in the sperm midpiece and DNA fragmentation was observed in the low motility fractions of patients.
- IFN-gamma-mediated caspase-3 activation and C. burnetii killing depend on the expression of membrane TNF.
- determination of levels of caspase-3 expression in breast tumor samples and to determine whether alterations in its expression can affect their ability to undergo apoptosis
- ceramide increases oxidative damage by inhibition of ROS scavenging ability through caspase-3-dependent proteolysis of catalase
- caspase 3 has a role in damaging mitochondrial function and generating reactive oxygen species after activation by cytochrome c
- Presentation of nitric oxide regulates monocyte survival through effects on this enzyme and caspase-9 activation.
- induction of ceramide accumulation by various triggers of ceramide generation triggered the activation of caspase-3.
- mRNA and protein expression of this enzyme are examined in breast cancer to determine level of apoptosis.
- CASP3 induced by H202 was completely blocked by Z-VAD-fmk.
- caspase-3 is essential for efficient induction of apoptosis by staurosporine, but not for mitochondrial steps that occur earlier in the pathway
- one or more distinct cellular mechanisms regulate Bid cleavage by caspases 8 and 3 in situ.
- caspase-3 was upregulated in a region-specific manner with marked activation in the selectively vulnerable hippocampal after cerebral ischemia
- Data report that human oocytes and fragmenting preimplantation embryos possess transcripts encoding Harakiri and caspase-3.
- caspase-3-mediated proteolysis of FAK, an anti-apoptotic protein, is regulated by hsp72
- in neutrophils, functional expression of caspase-3 in neutrophils may be regulated during ontogeny.
- We conclude that the changes in the level of caspase-3 and survivin play an important role in the transformation from normal gastric mucosa to gastric cancer.
- caspase-3 as a key effector of neuronal apoptosis in pneumococcal meningitis.
- activated by coxsackievirus B3 (CVB3) infections and occurred in cells expressing full length CAR
- the caspase 3 apoptosis program is not required for anti-inflammatory clearance by human macrophages
- Caspase-3 mediates a mitochondrial amplification loop that is required for the optimal release of cytochrome c, mitochondrial permeability shift transition, & cell death during apoptosis induced by treatment with the microtubule-damaging agent paclitaxel
- Caspase 3-mediated cell death is central to the biological control of antigen-independent expansion of recent thymic emigrants from human cord blood.
- CASP3 is activated in the oxidative stress-induced apoptosis in tendon fibroblasts in vitro.
- existence of a regulatory mechanism of protein stability and PTEN-protein interactions during apoptosis, executed by caspase-3 in a PTEN phosphorylation-regulated manner.
- caspase 3 has a role in cell death through apoptosis induced by ursolic acid
- MCF-7 tumor cells are deficient in CASP3 and instead have TNF-alpha-induced apoptosis
- Apoptotic cells secrete chemotactic factors that stimulate the attraction of monocytic cells and primary macrophages. The activation of caspase-3 in the apoptotic cell was found to be required for the release of these chemotactic factors.
- In Kennedy syndrome, phosphorylation of the polyglutamine-expanded form of androgen receptor regulates its cleavage by caspase-3 and enhances cell death.
- The crystal structure of the binding site of caspase-3 reveals critical side chain movements in a hydrophobic pocket. The positions of these side chains may have implications for the directed design of inhibitors of caspase-3 or caspase-7.
- Chemical substances derived from the primary foci and metastatic microenvironment can inhibit the growth of metastatic cells by enhancing Caspase-3 expression and diminishing FasL expression in gastric cancer.
- Data suggest that increased intrathecal release of Fas, but not FasL or caspase 3, in the cerebrospinal fluid of infants with hydrocephalus may serve as an indicator of brain injury from progressive ventricular dilatation.
- Caspase 1 involvement in monocyte lysis induced by Actinobacillus actinomycetemcomitans leukotoxin.
- Caspase 3-mediated inactivation of rac GTPases promotes drug-induced apoptosis in human lymphoma cells
- Caspase 3 has a role in proteolysis of the N-terminal cytoplasmic domain of the human erythroid anion exchanger 1 (band 3)
- Inhibition of the Src-family tyrosine kinases activity by PP2 and of caspase-3 by Z-DEVD-FMK reverses apoptosis
- the cascade of pro-apoptotic events leading to Bax, mitochondria, and caspase-3 activation are regulated by calpastatin and calpain-1
- apoptosis was preceded by proteolytic cleavage of caspases 2, 3, and 7, and wild type STAT1 also induced cleavage of caspase 7
- Doxorubicin-induced cell death of ALK-positive anaplastic large-cell lymphoma (ALCL) cells involves CASP3 activation. CASP3 activation correlates with ALK expression in ALCL tumors.
- caspase-3 activation, mitochondrial respiratory function and cytochrome c release have roles in induction of apoptosis by ceramides
- activation of caspase-3 by the Dot/Icm virulence system of Legionella pneumophila is essential for halting biogenesis of the L. pneumophila-containing phagosome through the endosomal/lysosomal pathway
- Caspase-3 is activated in oxidized low-density lipoprotein (ox-LDL) induces apoptosis in endothelial cells.
- IGF-I activates specific apoptotic pathways (Caspase-3 activation, Annexin-V binding and DNA degradation in an osteosarcoma cell line.
- In Jurkat cells caspase-3 is a component of the death-inducing signaling complex that colocalizes in lipid rafts with caspase-8, where caspase-3 activity is required for complete caspase-8 activation following Fas cross-linking.
- Evidence indicates that casp3 activated by ricin acts on BAT3 at the caspase cleavage site, DEQD(1001) to release a C-terminal fragment designated CTF-131, which induces phosphatidylserine exposure, cell rounding, and chromatin condensation as ricin does
- p38-MAPK can directly phosphorylate and inhibit the activities of caspase-8 and caspase-3 and thereby hinder neutrophil apoptosis, and, in so doing, regulate the inflammatory response.
- IFN-gamma-activated monocytes may induce reactive oxygen metabolites in retinal pigment epithelial(RPE) cells through cell-to-cell contact and promote HRPE cell apoptosis via caspase-3 activation.
- activated in normal erythropoiesis and in erythroblasts in culture
- IL-15 does not increase IL-1alpha or IL-1beta production but induces IL-1Ra release, increases myeloid cell differentiation factor-1 stability, decreases the activity of caspase-3 and caspase-8, resulting in an inhibition of vimentin cleavage
- Caspase-3 activation in human disease can play a prominent role in localized cellular degenerative processes without causing nuclear or cell death.
- Mcl-1L degradation by either GrB or caspase-3 interferes with Bim sequestration by Mcl-1L
- Synthetic activation of inducible caspase-3, but not of caspase-8, resulted in apoptosis in glioma cell lines.
- Dispensable for the execution of apoptosis in a metastatic melanoma cell line.
- glc-oxLDL increases TUNEL positivity and caspase-3 activation of human coronary smooth muscle cells
- Transfected caspase-3 is involved in the reduction of Akt level, and its involvement is mediated through caspase-9 activation.
- Caspase-3 is frequently overexpressed in hepatocellular carcinomas and is associated with high serum levels of alpha-fetoprotein.
- mice overexpressing human caspase 3 are essentially normal, however, they have increased susceptibility to degenerative insults
- Overexpression of antiapoptotic proteins Bcl-2 and Bcl-X(L) and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer.
- granule pools of Zn may be distinct from those regulating activation of procaspase-3 and NF-kappaB.
- caspase-8 and -3 have roles in human mast cell apoptosis induction by Pseudomonas aeruginosa exotoxin A
- required for Parvovirus B19 virus-induced apoptosis in primary hepatocytes and hepatocellular carcinoma cell line HepG2
- results suggest that matrix metalloproteinase-9 and matrix metalloproteinase-2 contribute to caspase-mediated brain endothelial cell death after hypoxia-reoxygenation by disrupting cell-matrix interactions and homeostatic integrin signaling
- Neutrophils isolated from cirrhosis patients exhibited a decreased viability and a marked accelerated apoptosis and significantly higher caspase-3 activity.
- BAP31 and caspase 3 are cleaved in a process involving capsase 8 in the mitochondrial membrane during apoptosis
- induced and utilized by human Astrovirus Yuc8 to promote processing of the capsid precursor and dissemination of the viral particles in CAC0-2 cells.
- hypoxia caused epithelial cell death induced by caspase-3-like activity-dependent apoptosis
- These data suggest that increased proneness to caspase activation in lymphocytes could reflect an ongoing systemic response in neurodegenerative disease with pathogenetic implications.
- CASP3 was expressed in the same tissues as its murine counterpart.
- required for Sars virus 7a protein induction of apoptosis in cell lines from different organs
- granzyme B targets a highly restricted range of substrates and orchestrates cellular demolition largely through activation of caspase-3
- the early and temporary activation of PP2A in neutrophils impaired not only the p38 MAPK-mediated inhibition of caspase 3 but also restored the activity to caspase 3 that had already been phosphorylated and thereby inactivated
- results suggest that active caspase-3 is translocated in association with a substrate-like protein(s) from the cytoplasm into the nucleus during progression through apoptosis
- caspase-3 is crucial for the differentiation of bone marrow stromal stem cells by influencing TGF-beta/Smad2 pathway and cell cycle progression
- results suggest that Anaplasma phagocytophilum inhibits human neutrophil apoptosis via transcriptional upregulation of bfl-1 and inhibition of mitochondria-mediated activation of caspase 3
- removal of N-terminal domains of Bid by caspase-8 and Mcl-1 by caspase-3 enables the maximal mitochondrial perturbation that potentiates TRAIL-induced apoptosis
- Expression correlates with intensity of apoptosis in colorectal adenocarcinoma.
- Gossypol induced complete cytochrome c release from mitochondria amd increased caspases-3 and -9 activity in large cell lymphoma cells.
- The increased ratio of Bax/Bcl-2 proteins after Epigallocatechin-3-gallate may lead to activation of caxpaxe-3, leading to apoptosis.
- Taken together, our data suggested that the JNK/c-Jun signaling cascade plays a crucial role in Cd-induced neuronal cell apoptosis and provides a molecular linkage between oxidative stress and neuronal apoptosis.
- Caspase-3 dependent apoptosis occurs in human granulosa cells and activates when follicles begin to leave the resting pool.
- PKCdelta-dependent phosphorylation of caspase-3 is involved in the regulation of monocyte life span
- Caspase 3 activation associated with cellular prion is closely related to its ability to undergo endocytosis. This is, to our knowledge, the first direct description of an endocytosis-dependent PrP(c)-associated function.
- Stx1 and LPS trigger DNA fragmentation and caspase-3 activation, as evidenced by the cleavage of poly(ADP-ribose) polymerase (PARP).
- Absence of active caspase 3-positive nasopharyngeal carcinoma predicts rapid fatal outcome.
- procaspase-2S-mediated anti-apoptotic effects are associated with inhibition of the processing and activation of procaspase-3 in VP-16-treated cells
- calcium could favour a necrotic mechanism by inducing the generation of a form of caspase 3 insensitive to mitochondrial activation
- caspase 3 exists in microparticles from endothelial cells and may be associated with caspase 3 activation unrelated to apoptosis
- The antiapoptotic property of Hualpha-Syn in neuronal cell lines is associated with the attenuation of caspase-3 activity without affecting the caspase-9 activity or the levels of cleaved, active caspase-3.
- Caspase 3 plays a important role in apoptotic process of mesothelioma cells.
- These findings provide biological evidence showing that (+)-alpha-tocopherol can amplify the apoptotic response by up-regulating the expression of pro-caspase-3.
- The characteristics of the fragment of hPMCA4b produced by caspase-3 are reported.
- cleaved caspase-3 positive cells was found in temporal lobe epilepsy sections but not controls; nuclear localization of apoptosis-inducing factor was limited and restricted to cells that were negative for cleaved caspase-3
- involvement of Fas/caspase 8/caspase 3-dependent signaling in an enucleated cell leading to PS externalization, a central feature of erythrophagocytosis and erythrocyte biology
- the prodomain acts as an intramolecular chaperone during assembly of the (pro)caspase-3 subunits and increases the efficiency of formation of the native conformation
- Caspase 3 activation is a prominent feature in periodontitis-associated tissue injury.
- caspase-3, -8, and -9 activity is enhanced by safrole oxidase in lung cancer cells
- desmoglein 1 is a novel caspase-3 target that regulates apoptosis in keratinocytes
- Thrombin is able to induce activation of caspases 3 and 9 in human platelets and significantly increases the amount in the cytoskeleton of the active forms of both caspases and the procaspases 3 and 9.
- Apoptosis marker activated caspase-3 was analysed by immunohistochemistry, during the production of collagen type II, the adhesion and signal transduction receptor beta1-integrin.
- These results provide evidence for a novel type 1 IFN-mediated pathway that regulates apoptosis of T cells through a mitochondrial-dependent and caspase-dependent and independent pathway.
- tTGase is a new type of caspase 3 inhibitor in THG-mediated apoptosis.
- NFATc2 activity is regulated by caspase-3
- These results demonstrate that SSRP1 degradation during apoptosis is a two-step process coupling caspase cleavage and ubiquitin-dependent proteolysis.
- Blood values increased in untreated Parkinson disease patientes.
- Asymmetric dimethylarginine induces apoptosis of endothelial cell via elevation of intracellular oxidant production, which involves p38 MAPK/caspase-3-dependent signaling pathway.
- 170-kDa P-gp has been reported to counteract apoptosis, its cleavage may be a mechanism aimed at blocking an important cell survival component
- CAD is downregulated at the mRNA and protein level during the erythroid differentiation in TF-1 cells.
- These results suggest that caspases, including caspase 3, can act as substrates for non-caspase proteases in cells primed for necrosis induction.
- Protein-protein interaction of NMTs revealed that m-calpain interacts with NMT1 while caspase-3 interacts with NMT2.
- caspase-3 cleavage of EAAT2 is one mechanism responsible for the impairment of glutamate uptake in mutant SOD1-linked amyotrophic lateral sclerosis
- SUMOylation and activation of ataxia-telangiectasia-mutated protein, PKCdelta, caspase-3, and nuclear factor kappaB signaling pathways modulate salivary adaptive responses to stress in cells exposed to either 1% O(2) or DFO.
- caspase-3 cleavage in the spinous layer of the epidermis is a pathologic event contributing to spongiosis formation in acute atopic dermatitis
- caspase-3 and caspase-9 activation has critical roles in hypoxia/reoxygenation induced apoptosis
- Crystal structures were determined of caspase-3 complexes with the substrate analogs at resolutions of 1.7 A to 2.3 A.
- The atomic resolution (1.06 Angstroms) crystal structure of the caspase-3 reveals the structural basis for substrate selectivity in the S4 pocket.
- Thus, early activation of caspase-3 seems to be a non-apoptotic event required for cellular function.
- AECA subsets in the sera of patients with systemic sclerosis (SSc) and diffuse SSc induce patterns of human dermal endothelial cells gene expression in the setting of apoptosis with increased caspase 3 activity and reexpression of fibrillin 1.
- Expression level of intracellular activated caspase-3 in peripheral T cell subsets increases in patients with active systemic lupus erythematosus (SLE), compared to patients with inactive SLE and healthy controls.
- Data show that decorin protein core inhibits tumor xenograft growth and metabolism by hindering epidermal growth factor receptor function and triggering apoptosis via caspase-3 activation.
- Caspase-3-dependent activation of calcium-independent phospholipase A2 enhances cell migration in non-apoptotic ovarian cancer cells
- HDL prevents endothelial progenitor cell (EPC)apoptosis through inhibition of caspase-3 activity suggesting a possible mechanism for its positive effects on circulating EPC numbers
- These data imply that confluent cells undergo spontaneous cell death mediated by cathepsin B; Lipopolysaccharides may accelerate this caspase-independent cell death through release of mitochondrial contents and reactive oxygen species.
- Activated caspase-3-positive cells were present in glomeruli of 88.2% of lupus nephritis cases, observed in the glomerular tuft and cellular and fibrocellular crescents
- peroxynitrite-mediated inhibition of human caspase-3 is impaired by CO2
- Active caspase 3-positive Reed-Sternberg cells were detected in 47 of 70 cases.
- Results indicate that caspase-3 mRNA antisense oligodeoxynucleotides prevent HL-60 cells from apoptosis induced by gamma-radiation,and reduce expression of caspase-3 and its mRNA.
- CASP3 was overexpressed in 40.8% of the 210 invasive ductal breast carcinomas studied
- ROCK-1-dependent caspase-3 activation was coupled with the activation of PTEN and the subsequent inhibition of protein kinase B (Akt) activity, all of which was attenuated by siRNA directed against ROCK-1 expression.
- This study demonstrates FHOD1 is cleaved by caspase-3 at the SVPD(616) site during apoptosis and the C-terminal FHOD1 cleavage product has the ability to inhibit RNA polymerase I transcription.
- These data indicate that, in addition to its function as an effector caspase, caspase-3 plays an important role in maximizing the activation of apical caspases and crosstalk between the two major apoptotic pathways.
- Collectively, these data suggest that cathepsin D activation of caspase 3/7 may be required for inducing one of the death pathways elicited by E. coli.
- Immunoreactivities indicating single-stranded DNA and cleaved caspase-3 were higher in moyamoya disease than in controls and were located in smooth muscle cells of media.
- Cell death in the penumbra of subacute infarcts is partially caspase-3 independent and may be attributed to nitric oxide.
- Single nucleotide polymorphismsin caspase 3 is associated with non-Hodgkin lymphoma
- Taken together, our results indicate that IL-4 inhibits caspase activity during the initial stages of human Th2 cell differentiation by regulating expression of several key players in the Fas-induced pathway.
- Interaction of Ramos cells with immobilized alpha2,6-linked sialic acid suppresses cas[ase-3 activity and inhibits Igm-induced apoptosis.
- p53-dependent staurosporine-induced caspase-3 activation is affected by the C-terminal products of cellular prion protein processing, C1 and C2
- expression of FasL is upregulated in testes of patients with Sertoli cell-only syndrome & maturation arrest, suggesting that it may be associated with apoptotic elimination or altered maturation of Fas-expressing germ cells by activation of caspase-3.
- These data demonstrate that huntingtin inhibits caspase-3 activity.
- PTP-PEST actively contributes to the cellular apoptotic response and reveal the importance of caspases as regulators of PTPs in apoptosis.
- The role of high gammaGT activity in HepG2 cells can be connected with production of reactive oxygen species and with S-thiolation with Cys and Cys-Gly that can influence activity of caspase 3.
- Results discuss caspase-3 immunohistochemical expression as a marker of apoptosis, increased grade and early recurrence in intracranial meningiomas.
- in erythroid precursors undergoing terminal differentiation, Hsp70 prevents active caspase-3 from cleaving GATA-1 and inducing apoptosis
- Human tumor xenograft in nude mice is suppressed significantly by the treatment with a hTERT/re-Caspase-3 system.
- Adult stem cell injections into blastocysts is influenced by apoptosis as shown by high caspase-3 activity.
- Pro-caspase 3 appears to be a substrate of SAG/ROC-(beta-TCRP) E3 ubiquitin ligase, which protects cells from apoptosis by reducing the basal level of pro-caspase-3.
- Data show that caspase-3 antisense oligodeoxynucleotides inhibit apoptosis in gamma-irradiated human leukemia HL-60 cells.(
- The expression of Caspase 3 in peripheral blood mononuclear cells was significantly increased in SLE patients.
- While polyploid, mature megakaryocytes from healthy subjects or myelodysplastic syndromes patients manifested caspase-3 activation during terminal differentiation, freshly isolated, immature MK from MDS died without caspase-3 activation
- In this review, reversible glutathiolation of procaspase-3 by glutaredoxin provides further mechanistic insight into the role of reactive oxygen species in TNF-alpha-induced apoptosis.
- Caspase-3 and the p38alpha MAP kinase were activated during TIMP-1-induced UT-7 cells erythroid differentiation.
- Caspase 3 was found to be activated by elaidic acid and palmitic acid.
- calcineurin B potentiates the activation of procaspase-3 by accelerating its proteolytic maturation
- Comparing SIDS to non-SIDS cases, increased active caspase-3 expression was restricted to four nuclei in the caudal pons and two nuclei in the rostral medulla.
- caspases-3 and caspase-9 play novel roles in transcription by regulating polycomb protein function through direct cleaving of Ring1B.
- Cystatin A suppresses UVB-induced apoptosis of keratinocytes by the inhibition of caspase 3 activation.
- In this test set, cyclooxygenase 2 and Caspase 3 seem to be immunohistochemical markers with prognostic significance for vulva cancer.
- An 8.94-fold and 6.73-fold increase in expression of caspase-3mRNA in intracranial aneurysm and AAA, respectively, were obtained relative to the normal vessels.
- A 3-fold increase in caspase-3 activity was observed in cells treated with TAC-101 colon cancer cells in comparison to the control cells.
- Results demonstrate that cleavage by caspase 3 does not activate caspase 9, but enhances apoptosis by alleviating XIAP inhibition of the apical caspase.
- NF-kappa-B inhibition enhances CASP3 degradation of Akt1 and apoptosis in response to campogthecin.
- EXEL-0862 induced apoptotic death in EOL-1 cells and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells, and resulted in significant downregulation of the antiapoptotic protein Mcl-1 through a caspase-3 dependent mechanism.
- Survivin-DeltaEx3 plays a key role in the inhibition of caspase-3 activity.
- CASP3 expression was higher in the helicobacter pylori infection (HP+) group, HP+ with intestinal metaplasia, and HP+ with dysplasia groups.
- Akt1 is cleaved in vitro at the caspase-3 consensus site DQDD(456).
- Caspase 3 regulated the biochemical, morphological, and functional changes in cells undergoing staurosporine-induced apoptosis. Full-length Dsg2 was processed to a 70-kDa fragment which was released into the cytosol.
- caspase-3 prodomain binding to heat shock protein 27 regulates monocyte apoptosis by inhibiting caspase-3 proteolytic activation
- cleaved caspase-3 is an activated form of caspase-3 that has a role in preventing progression of gliomas
- A specific transnitrosation reaction between procaspase-3 and thioredoxin-1 (Trx) occurs in cultured human T cells and prevents apoptosis.
- RbAp48-mediated transformation of HPV16 is probably because of the regulation by RbAp48 of tumor suppressors retinoblastoma and p53, apoptosis-related enzymes caspase-3 and caspase-8, E6, E7, cyclin D1 (CCND1), and c-MYC.
- demonstrate the cellular mechanisms of neuronal cell degeneration induced via c-Jun-N-terminal kinases and caspase-dependent signaling
- caspase-3 is a key regulator of apoptosis in response to combined genistein and TRAIL in human gastric adenocarcinoma AGS cells through the activation of DR5 and mitochondrial dysfunction
- Thimerosal caused Ca2+-independent apoptosis of gastric cancer cells via phosphorylation of p38 MAPK and caspase-3 activation.
- S100A6 might be involved in the processing of apoptosis by modulating the transcriptional regulation of caspase-3.
- XIAP homotrimerizes via its C-terminal Ring domain, making its inhibitory activity toward caspase-3 more susceptible to Smac.
- Report caspase-3 activity, response to chemotherapy and clinical outcome in patients with colon cancer.
- These findings suggest that caspase-7 facilitates the execution of apoptosis through down-regulation of the 26S proteasome, which regulates the turnover of proteins involved in the apoptotic process.
- Caspase-3 may have a role in local recurrence in rectal cancer
- Gastrins activate members of Rho family G proteins which in turn regulate different proteins of the Bcl-2 family leading to changes in caspase 3 activity.
- Results describe the role of carbohydrate moiety of bleomycin-A2 in caspase-3 activation and internucleosomal chromatin fragmentation in apoptosis of laryngeal carcinoma cells.
- These data indicate that cytosolic PDI is a substrate of caspase-3 and -7, and that it has an anti-apoptotic action.
- bcl2 and Caspase-3 have roles in Shikonin analogue (SA) 93/637 induced apoptosis of human U937 cells
- Two novel homozygously deleted genes in hepatocellular carcinomas are caspase 3 and CHES1.
- constitutively and overexpressed AML1-ETO protein was cleaved to four fragments of 70, 49, 40 and 25 kDa by activated caspase-3 during apoptosis induction by extrinsic mitochondrial and death receptor signaling pathways.
- release of caspase 3-containing microparticles may contribute to endothelial cell survival
- apoE expression modulates capase-3 activity, but this has no significant impact on sensitivity to apoptosis and only a moderate impact on basal cholesterol efflux.
- Enteropathogenic Escherichia coli induced apoptosis in T84 intestinal epithelial cells via induction of caspases-3, -8, and -9.
- caspase-3 could be involved in recruitment of ischemic brain tissue being a marker of infarct growth.
- Single nucleotide polymorphisms in the Caspase-3 gene is associated with lung cancer
- For the first time our data demonstrate that CSN-mediated deneddylation can be regulated by active Casp3 and that the CSN executes a specific function during the apoptotic process.
- HSP105 appears to chaperone the responses to endoplasmic reticulum (ER) stress through its interactions with GRP78 and GSK3, and without HSP105 cell death following ER stress proceeds by a non-caspase-3-dependent process.
- Melatonin maintains mitochondrial membrane potential and attenuates activation of initiator (casp-9) and effector caspases (casp-3/casp-7) and PARP in UVR-exposed HaCaT keratinocytes
- Increased social interaction in mice deficient of the striatal medium spiny neuron-specific phosphodiesterase 10A2.
- Activation of caspase-3 by hydrogen peroxide and progesterone suggest mitochondrial apoptosis is dependent on calcium signaling.
- The experiments revealed that N induces the intrinsic apoptotic pathway, resulting in processing of N at residues 400 and 403 by caspase-6 and/or caspase-3.
- caspase-3 activation by RSVL is required for PARP degradation and induction of apoptosis
- The basal caspase activity is accompanied by a constant cleavage of the motility-associated gelsolin protein, which may contribute to the caspase-mediated promotion of migration and invasiveness in glioblastoma cells
- Triggering of cytosolic RNA recognition pathway with poly(I:C) transfection or influenza A virus infection resulted in caspase-1- and -3-mediated proteolytic processing of pro-IL-18 and secretion of biologically active IL-18.
- The low frequency of apoptotic phenomena (caspase-3 and Bax) in epithelial cells of oral lichen planus may create a favourable substrate for malignant transformation.
- Survivin and caspase-3 expression correlate with poor prognostic parameters (higher histologic grade and high proliferation), but not with outcome, in breast carcinoma patients.
- Sharp inhibition of apoptosis and changes in the levels of cell proliferation in tumor cells were paralleled by decreased expression of peripheral benzodiazepine receptor in patients with squamous cell carcinoma & skin melanoma.
- Data show that diallyl sulfide induces apoptosis in human colon cancer cells, and that caspase-3, NF-kappaB, and ERK-2 are involved.
- The role of multinucleated giant cells may thus be different from epithelioid cells by virtue of higher MPT64, more TGF-beta, and reduced caspase 3 which may contribute towards persistence of infection
- IL-32-induced monocyte-to-macrophage differentiation is mediated through nonapoptotic, caspase-3-dependent mechanisms
- Western blotting suggests that vinorelbine cleaves caspase-3, -9 and -8 and reduces the amount of mitochondrial cytochrome c.
- We show that human PLD1b and PLD2a contain functional caspase 3 cleavage sites and identify the critical aspartate residues within PLD1b that affect its activation by phorbol esters.
- analysis of how active caspase-3 causes apoptosis
- SP1-like sequences mediate human CASP3 promoter activation by p73 and cisplatin.
- It is concluded that P. aeruginosa can induce apoptosis with an up-regulated expression of Bax and a down-regulated expression of Bcl-2, which resulted in increased levels of cytochrome c release and increased caspase-3 and -9 in human U937 cells.
- The distribution of the bcl-2, bax and caspase-3 proteins was investigated in the cells of developing human spinal ganglia.
- These results show that the Fas/FasL-system mediated by caspase-3 activation plays a role in Clonorchis sinensis-infected hepatocyte apoptosis.
- caspase 3 cleavage of Rad51 resulted in a functional decrease in Rad51 strand exchange activity and that inhibition of caspase 3 activity increased Rad51 protein levels and Rad51 foci
- insulin stimulation reversed the camptothecin induced increase of caspase-3 activity
- inhibitor-3 is an in vivo target of caspase-3 and participates in the apoptotic response
- The positive expression rates of Fas, caspase-8 and caspase-3 in somatostatin high and moderate expression groups were higher than that in low expression group.
- study provides evidence that during T cell proliferation the intracellular caspase inhibitor X-linked inhibitor-of-apoptosis protein (XIAP) interacts with caspases-3/-7, thereby blocking their full activation, substrate cleavage, and cell death
- Fas+CD8+ T cells preferentially underwent apoptosis and showed high caspase-3 activation in gastric cancer.
- eIF3k, originally identified as the smallest subunit of eukaryotic translation initiation factor 3 (eIF3) complexes, also localizes to keratin intermediate filaments and physically associates with K18 in epithelial cells.
- identification of O-GlcNAcase as a caspase-3 substrate with a novel caspase-3 cleavage site and provide insight about O-GlcNAcase regulation during apoptosis.
- caspase-3 induces ERK activation through a ceramide-dependant, protease activity-independent mechanism
- Caspase-3 activation triggers extracellular cathepsin L release and endorepellin proteolysis.
- hMTH1 plays an important role in protecting cells against H(2)O(2)-induced apoptosis via a Noxa- and caspase-3/7-mediated signaling pathway, thus conferring a survival advantage through the inhibition of oxidative-stress-induced DNA damage
- Describe caspase-3 expression in developing pituitary gland.
- Caspase-3 and caspase-7 exhibit differential activity toward multiple substrate proteins, including Bid, XIAP, gelsolin, caspase-6, and cochaperone p23.
- We suggest that caspase-3 may function as an indicator of the prognosis of BL/BLL
- Caspase-3 independently associates with coronary calcium, aortic wall thickness, and compliance, suggesting a link between apoptosis and atherosclerosis.
- Isoquinoline-1,3,4-trione derivatives inactivate caspase-3 by generation of reactive oxygen species
- Results describe the immunohistochemical distribution of caspase 3, 9 and Bax in intracranial U87 glioblastoma xenografts, and show that xenografts contain cells positive for caspase-3, caspase-9, and Bax.
- These data demonstrate for the first time the preferential localization and increase of caspase-3 in the postsynaptic density fractions in Alzheimer's disease and suggest an important role for caspase 3 in synapse degeneration during disease progression.
- significant correlations were observed between caspase-3 mRNA expression and the parameters tested were a direct one with both the Bax and a variant of the X-chromosome RBM10 gene, and an inverse one with the angiogenesis-associated CD105 (endoglin) gene
- Downmodulation of BAG3 protein levels allows caspase-3 activation by HIV-1 infection in human primary microglial cells.
- genetic variation in CASP3 may contribute to risk of squamous cell carcinoma of the head and neck
- Overexpression of FLIP reduced TRAIL and TNF-alpha-induced apoptosis in ML-1 cells. However, while FLIPL completely abrogated apoptosis, FLIPS allowed for BID cleavage and caspase-3 activation.
- results indicate that the apoptosis markers Fas receptor and caspase-3 might play a significant role in glaucoma neuropathy at the stage of absolute glaucoma
- These data suggest a mechanism for maintaining NF-kappaB activity in human T cells through the binding of the Caspase-3-generated carboxy-terminal fragment of p65/RelA to IkappaBalpha in order to protect wild-type p65/RelA from IkappaBalpha inhibition.
- Extracellular adenosine induces apoptosis in Caco-2 cells by activating caspase-9 and the downstream effector caspase caspase-3 in association with mitochondrial damage via A(2a) adenosine receptors.