Amino Acid Chloromethyl Ketones
Cysteine Proteinase Inhibitors
Proto-Oncogene Proteins c-bcl-2
Cytochrome c Group
X-Linked Inhibitor of Apoptosis Protein
Apoptotic Protease-Activating Factor 1
bcl-2-Associated X Protein
Inhibitor of Apoptosis Proteins
In Situ Nick-End Labeling
BH3 Interacting Domain Death Agonist Protein
Apoptosis Regulatory Proteins
Fas-Associated Death Domain Protein
Apoptosis Inducing Factor
Tumor Cells, Cultured
CASP8 and FADD-Like Apoptosis Regulating Protein
Membrane Potential, Mitochondrial
TNF-Related Apoptosis-Inducing Ligand
Reactive Oxygen Species
Tumor Necrosis Factor-alpha
CRADD Signaling Adaptor Protein
Intracellular Signaling Peptides and Proteins
Death Domain Receptor Signaling Adaptor Proteins
Dose-Response Relationship, Drug
CARD Signaling Adaptor Proteins
bcl-2 Homologous Antagonist-Killer Protein
Tumor Suppressor Protein p53
Receptor-Interacting Protein Serine-Threonine Kinases
Antineoplastic Agents, Phytogenic
RNA, Small Interfering
Amino Acid Sequence
Receptors, Tumor Necrosis Factor
Receptors, TNF-Related Apoptosis-Inducing Ligand
bcl-Associated Death Protein
Molecular Sequence Data
JNK Mitogen-Activated Protein Kinases
Adaptor Proteins, Signal Transducing
Protein Structure, Tertiary
Reverse Transcriptase Polymerase Chain Reaction
Receptor-Interacting Protein Serine-Threonine Kinase 2
Protein Synthesis Inhibitors
Myeloid Cell Leukemia Sequence 1 Protein
Protein Processing, Post-Translational
Mitogen-Activated Protein Kinases
Receptors, Death Domain
Proto-Oncogene Proteins c-akt
Drug Screening Assays, Antitumor
Receptors, Tumor Necrosis Factor, Type I
p38 Mitogen-Activated Protein Kinases
Disease Models, Animal
Proteasome Endopeptidase Complex
Drug Resistance, Neoplasm
Gene Expression Regulation
Endoplasmic Reticulum Stress
Recombinant Fusion Proteins
Cell Line, Transformed
Sequence Homology, Amino Acid
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Protein Kinase C-delta
Gene Expression Regulation, Enzymologic
Lamin Type B
MAP Kinase Signaling System
Xenograft Model Antitumor Assays
Mitogen-Activated Protein Kinase 8
Bcl-2 regulates amplification of caspase activation by cytochrome c. (1/8107)Caspases, a family of specific proteases, have central roles in apoptosis . Caspase activation in response to diverse apoptotic stimuli involves the relocalisation of cytochrome c from mitochondria to the cytoplasm where it stimulates the proteolytic processing of caspase precursors. Cytochrome c release is controlled by members of the Bcl-2 family of apoptosis regulators  . The anti-apoptotic members Bcl-2 and Bcl-xL may also control caspase activation independently of cytochrome c relocalisation or may inhibit a positive feedback mechanism    . Here, we investigate the role of Bcl-2 family proteins in the regulation of caspase activation using a model cell-free system. We found that Bcl-2 and Bcl-xL set a threshold in the amount of cytochrome c required to activate caspases, even in soluble extracts lacking mitochondria. Addition of dATP (which stimulates the procaspase-processing factor Apaf-1  ) overcame inhibition of caspase activation by Bcl-2, but did not prevent the control of cytochrome c release from mitochondria by Bcl-2. Cytochrome c release was accelerated by active caspase-3 and this positive feedback was negatively regulated by Bcl-2. These results provide evidence for a mechanism to amplify caspase activation that is suppressed at several distinct steps by Bcl-2, even after cytochrome c is released from mitochondria. (+info)
Caspase-mediated cleavage of p21Waf1/Cip1 converts cancer cells from growth arrest to undergoing apoptosis. (2/8107)The cyclin-dependent kinase inhibitor p21waf1/Cip1 is a downstream effector of the p53-dependent cell growth arrest. We report herein that p21 was cleaved by caspase-3/CPP32 at the site of DHVD112L during the DNA damage-induced apoptosis of cancer cells. The cleaved p21 fragment could no more arrest the cells in G1 phase nor suppress the cells undergoing apoptosis because it failed to bind to the proliferating cell nuclear antigen (PCNA) and lost its capability to localize in the nucleus. Thus, caspase-3-mediated cleavage and inactivation of p21 protein may convert cancer cells from growth arrest to undergoing apoptosis, leading to the acceleration of chemotherapy-induced apoptotic process in cancer cells. (+info)
Caspase 3 inactivation to suppress Fas-mediated apoptosis: identification of binding domain with p21 and ILP and inactivation machinery by p21. (3/8107)The death mediator caspase acts as the dominant regulator during cell death induction. The CPP32 subfamily, including caspase 3 (CPP32/Yama/Apopain), is essential for the cell death signaling. We recently reported that activation of caspase 3 is regulated by complex formation with p21 or ILP. In the present study, we investigated the binding domain with p21 and ILP to further characterize the caspase 3 inactivation machinery. Our results show that caspase 3 contains p21 binding domain in the N-terminus and ILP binding domain in the active site. Further, the caspase 3 binding domain in p21 was independent of the Cdk- or PCNA-binding domain. We also found caspase 3 protection by p21 from the p3-site cleavage serineproteinase contributes to the suppression machinery. Here, we propose the caspase 3 inactivation system by p21 and ILP as new essential system in the regulation of cell death. (+info)
Activation of stress-activated protein kinase/c-Jun NH2-terminal kinase and p38 kinase in calphostin C-induced apoptosis requires caspase-3-like proteases but is dispensable for cell death. (4/8107)Apoptosis was induced in human glioma cell lines by exposure to 100 nM calphostin C, a specific inhibitor of protein kinase C. Calphostin C-induced apoptosis was associated with synchronous down-regulation of Bcl-2 and Bcl-xL as well as activation of caspase-3 but not caspase-1. The exposure to calphostin C led to activation of stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK) and p38 kinase and concurrent inhibition of extracellular signal-regulated kinase (ERK). Upstream of ERK, Shc was shown to be activated, but its downstream Raf1 and ERK were inhibited. The pretreatment with acetyl-Tyr-Val-Ala-Asp-aldehyde, a relatively selective inhibitor of caspase-3, or benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD.fmk), a broad spectrum caspase inhibitor, similarly inhibited calphostin C-induced activation of SAPK/JNK and p38 kinase as well as apoptotic nuclear damages (chromatin condensation and DNA fragmentation) and cell shrinkage, suggesting that caspase-3 functions upstream of SAPK/JNK and p38 kinase, but did not block calphostin C-induced surface blebbing and cell death. On the other hand, the inhibition of SAPK/JNK by transfection of dominant negative SAPK/JNK and that of p38 kinase by SB203580 induced similar effects on the calphostin C-induced apoptotic phenotypes and cell death as did z-VAD.fmk and acetyl-Tyr-Val-Ala-Asp-aldehyde, but the calphostin C-induced PARP cleavage was not changed, suggesting that SAPK/JNK and p38 kinase are involved in the DNA fragmentation pathway downstream of caspase-3. The present findings suggest, therefore, that the activation of SAPK/JNK and p38 kinase is dispensable for calphostin C-mediated and z-VAD.fmk-resistant cell death. (+info)
Role of hypoxia-induced Bax translocation and cytochrome c release in reoxygenation injury. (5/8107)We investigated mechanisms of cell death during hypoxia/reoxygenation of cultured kidney cells. During glucose-free hypoxia, cell ATP levels declined steeply resulting in the translocation of Bax from cytosol to mitochondria. Concurrently, there was cytochrome c release and caspase activation. Cells that leaked cytochrome c underwent apoptosis after reoxygenation. ATP depletion induced by a mitochondrial uncoupler resulted in similar alterations even in the presence of oxygen. Moreover, inclusion of glucose during hypoxia prevented protein translocations and reoxygenation injury by maintaining intracellular ATP. Thus, ATP depletion, rather than hypoxia per se, was the cause of protein translocations. Overexpression of Bcl-2 prevented cytochrome c release and reoxygenation injury without ameliorating ATP depletion or Bax translocation. On the other hand, caspase inhibitors did not prevent protein translocations, but inhibited apoptosis during reoxygenation. Nevertheless, they could not confer long-term viability, since mitochondria had been damaged. Omission of glucose during reoxygenation resulted in continued failure of ATP production, and cell death with necrotic morphology. In contrast, cells expressing Bcl-2 had functional mitochondria and remained viable during reoxygenation even without glucose. Therefore, Bax translocation during hypoxia is a molecular trigger for cell death during reoxygenation. If ATP is available during reoxygenation, apoptosis develops; otherwise, death occurs by necrosis. By preserving mitochondrial integrity, BCL-2 prevents both forms of cell death and ensures cell viability. (+info)
Phosphatidylinositol 3-kinase and protein kinase C are required for the inhibition of caspase activity by epidermal growth factor. (6/8107)The mechanism by which growth factors exert an anti-apoptotic function on many cell types is not well understood. This issue is addressed in relation to epidermal growth factor (EGF) which inhibits apoptosis induced by staurosporine or wortmannin in an epithelial tumour cell line (CNE-2). The presence of EGF substantially reduced the in vitro Ac-DEVD-AMC hydrolytic activity and almost completely suppressed the intracellular cleavage of poly(ADP-ribose) polymerase in staurosporine- or wortmannin-treated cells. Staurosporine but not wortmannin caused the intracellular proteolytic processing of pro-caspase-3 and this event was transiently inhibited by EGF. Staurosporine-induced apoptosis was not inhibited by EGF in the presence of wortmannin or LY294002. Similarly, EGF failed to inhibit wortmannin-induced apoptosis in the presence of staurosporine, chelerythrine chloride or Go6850. These results suggest that phosphatidylinositol 3-kinase and protein kinase C play a role in the survival function of EGF but the reduction of cellular caspase activity cannot be satisfactorily explained by a lack of pro-caspase-3 activation. (+info)
p27Kip1 induces drug resistance by preventing apoptosis upstream of cytochrome c release and procaspase-3 activation in leukemic cells. (7/8107)The cyclin-dependent kinase inhibitor p27Kip1 has been implicated as a drug resistance factor in tumor cells grown as spheroids or confluent monolayers. Here, we show that p27Kip1 overexpression also induces resistance to drug-induced apoptosis and cytotoxicity in human leukemic cells growing in suspension. The anti-apoptotic effect of p27Kip1 is not restricted to DNA-damaging agents but extends to the tubulin poison vinblastin, agonistic anti-Fas antibodies and macromolecule synthesis inhibitors. To further identify at which level this protein interferes with the cell death pathway, we investigated its influence on caspase activation and mitochondrial changes. Exposure of mock-transfected U937 cells to 50 microm etoposide activates procaspase-3 and the long isoform of procaspase-2 and induces mitochondrial potential decrease and cytochrome c release from mitochondria to the cytosol. All these events are prevented by p27Kip1 overexpression. p27Kip1 does not modulate Bcl-2, Bcl-X(L), Mcl-1 and Bax protein level in leukemic cells but suppresses Mcl-1 expression decrease observed in mock-transfected U937 cells undergoing etoposide-induced cell death. We conclude that p27Kip1 prevents cell death upstream of the final pathway common to many apoptotic stimuli that involves cytochrome c release from mitochondria and activation of downstream caspases. (+info)
MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (8/8107)Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited. (+info)
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Loss of appetite
* Weight loss
* Bone pain
* Swelling in the abdomen or neck
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Death regulator Nedd2-like caspase
Autoimmune lymphoproliferative syndrome
Nerve tissue protein
Clostridium difficile toxin A
Death Domain database
HLA-B associated transcript 3
Proto-oncogene tyrosine-protein kinase Src
Fragmentation (cell biology)
Pattern recognition receptor
Caspase-3, human recombinant proteinase | E1003 | APExBIO
Commentary | Leukemia
Caspase-3 inhibitor Z-DEVD-FMK - LubioScience
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Caspase-3 DEVD-R110 Fluorometric HTS Assay Kit | Technique alternative | 01018551680 - caspase-3.com
Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation - CSHL Scientific Digital Repository
La Caspase-3 est-elle impliquée dans la différenciation des cellules souches adultes ? - Normandie Université
Frontiers | IL-1β and TNFα Differentially Influence NF-κB Activity and FasL-Induced Apoptosis in Primary Murine Hepatocytes...
Hydrogen-rich saline improves survival and neurological outcome after cardiac arrest and cardiopulmonary resuscitation in rats
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Anti-4-1BB Ligand antibody(DM68), Rabbit mAb - PD-L1 ELISA Kit, Dnmt1, Caspase-3, B7-H4 Antibody, PD-1, TCF, TLR Cell Lines
NIOSHTIC-2 Search Results - Full View
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minocycline - Ontology Report - Rat Genome Database
bcl-x Antibody [Unconjugated] (AF800): Novus Biologicals
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ATP-Glo™ Bioluminometric Cell Viability Assay - Biotium
- A constitutively active and uninhibitable caspase-3 zymogen efficiently induces apoptosis. (ncsu.edu)
- The caspase-3 zymogen has essentially zero activity until it is cleaved by initiator caspases during apoptosis. (ncsu.edu)
- Apoptosis is typically considered an anti-oncogenic process since caspase activation can promote the elimination of genetically unstable or damaged cells . (bvsalud.org)
- We report that a central effector of apoptosis , caspase-3 , facilitates rather than suppresses chemical- and radiation -induced genetic instability and carcinogenesis . (bvsalud.org)
- Human and some mouse caspases are active in apoptosis and cell death and even in necrosis and inflammation. (caspase-3.com)
- Using an established in vivo model of Fas-mediated apoptosis, we demonstrate here that elimination of certain caspases was compensated in vivo by the activation of other caspases. (cshl.edu)
- In this paper, we show that during cisplatin-induced apoptosis of human metastatic melanoma cells, calpain activation, as measured in intact cells by two different fluorescent substrates, is an early event, taking place well before caspase-3/-7 activation, and progressively increasing during 48 h of treatment. (unisi.it)
- The increase in apoptosis was associated with activation of caspase-3, caspase-7, and poly (ADP-ribose) polymerase-1 (PARP-1). (cdc.gov)
- It helps protect these cells from self-destructing (undergoing apoptosis) by blocking (inhibiting) the action of certain enzymes called caspases, which are necessary for apoptosis. (medlineplus.gov)
- Caspasa de prodominio corto con papel efector en la APOPTOSIS. (bvsalud.org)
- A short pro-domain caspase that plays an effector role in APOPTOSIS. (bvsalud.org)
- Regulator of calcineurin 1 (RCAN1) facilitates neural apoptosis through caspase-3 activation. (bvsalud.org)
Increased caspase-3 activity1
- Whereas TNFα preincubation leads to elevated levels of caspase-3 activity and cell death, pretreatment with IL-1β induces increased caspase-3 activity but keeps cells alive. (frontiersin.org)
- Caspase-3 is a caspase protein encoded by the CASP3 gene that interacts with caspase-9 and caspase-8. (caspase-3.com)
- At 8-72 hr after ischemia, caspase-3 mRNA and protein were induced in the hippocampus and caudate-putamen (CPu), accompanied by increased caspase-3-like protease activity. (unthsc.edu)
- In the hippocampus, caspase-3 mRNA and protein were predominantly increased in degenerating CA1 pyramidal neurons. (unthsc.edu)
- Protein kinase C mediates caspase 3 activation: A role for erythrocyte morphology changes. (unicatt.it)
- Here we extend our previous observations, reporting that RBC morphology is regulated by a series of specific cell signaling events linked to Protein Kinase C (PKC)-mediated activation of caspase 3. (unicatt.it)
- Our data suggests that on initial exposure to influenza virus, host cells upregulate COX6C mRNA expression through silencing miR-4276 and repressed viral replication by inducing the apoptotic protein caspase-9. (cdc.gov)
- Our findings suggest that rather than acting as a broad inhibitor of carcinogenesis , caspase-3 activation may contribute to genome instability and play a pivotal role in tumor formation following damage. (bvsalud.org)
- Furthermore, ventricular infusion of Z-DEVD-FMK, a caspase-3 inhibitor, decreased caspase-3 activity in the hippocampus and significantly reduced cell death and DNA fragmentation in the CA1 sector up to 7 d after ischemia. (unthsc.edu)
- The contribution of different proteolytic systems, in particular calpains and effector caspases, in apoptotic cell death is still controversial. (unisi.it)
- TMT-induced damage to auditory neurons was associated with significant soma shrinkage, nuclear condensation, and activation of caspase-3, biomarkers indicative of apoptotic cell death. (cdc.gov)
- Furthermore, attenuation of EndoG activity significantly reduced radiation -induced DNA damage and oncogenic transformation, identifying EndoG as a downstream effector of caspase-3 in this pathway. (bvsalud.org)
- deficiency in caspases essential for this pathway, caspase-9 or caspase-3, unexpectedly resulted in rapid activation of alternate caspases after injection of Jo2, and therefore failed to protect mice against Jo2 toxicity. (cshl.edu)
- Moreover, both ultraviolet and gamma irradiation, two established inducers of the mitochondrial caspase-activation pathway, also elicited compensatory activation of caspases in cultured caspase-3(-/-) hepatocytes, indicating that the compensatory caspase activation was mediated through the mitochondria. (cshl.edu)
- These data demonstrate that PKC-mediated activation of caspase 3 is an integral and essential part of signaling pathway in RBCs, that may be a regulatory factor of RBC mechanical properties, through regulation of NO metabolism. (unicatt.it)
- Our findings show that TMT is exclusively neurotoxicity in rat cochlear organotypic culture and that TMT-induced auditory neuron death occurs through a caspase-mediated apoptotic pathway. (cdc.gov)
- Inhibition of PKC also completely inhibits PMA mediated caspase-3 activation. (unicatt.it)
- We found that a significant fraction of mammalian cells treated with ionizing radiation can survive despite caspase-3 activation. (bvsalud.org)
- A short recovery period of 6h of cells from SWCNT exposure resulted in reversal of caspase-3 and caspase-7, and a partial reversal of PARP-1 activation. (cdc.gov)
- The results of this study show that the molecular mechanism for raw SWCNT-mediated toxicity in BEAS-2B cells is through the activation of caspase-3, caspase-7, and PARP-1. (cdc.gov)
- Within the first 3 h of infection with influenza virus, significant down-regulation of hsa-miRNA-4276 (miRNA-4276) is followed by a 2-fold increase in cytochrome c oxidase VIC (COX6C) mRNA was found to occur in human alveolar and bronchial epithelial cells. (cdc.gov)
- Double-label experiments detected DNA fragmentation in the majority of CA1 neurons and selective CPu neurons that overexpressed caspase-3. (unthsc.edu)
- The direct activation of procaspase-3 through a conformational switch rather than by chain cleavage may lead to novel therapeutic strategies for inducing cell death. (ncsu.edu)
- Moreover, this sublethal activation of caspase-3 promoted persistent DNA damage and oncogenic transformation. (bvsalud.org)
- Our findings provide direct experimental evidence for compensatory pathways of caspase activation. (cshl.edu)
- The treatment of hepatocytes with the BMDM supernatant, which contains both IL-1β and TNFα, sensitized to FasL-induced caspase-3 activation and cell death. (frontiersin.org)
- Proteolytic activation of the caspase-3 precursor was detected in hippocampus and CPu but not in cortex at 4-72 hr after ischemia. (unthsc.edu)
- Calpain activation proves to be an early and crucial event in the apoptotic machinery, as demonstrated by the significant protection of cell death in samples co-treated with the calpain inhibitors, MDL 28170, calpeptin and PD 150606, where a variable but significant reduction of both caspase-3/-7 activity and cell detachment is observed. (unisi.it)
- Organic solvent-induced proximal tubular cell toxicity via caspase-3 activation. (cdc.gov)
- The activation of PARP-1, caspase-3, and caspase-7 was only partially diminished after a recovery of 6h from the exposure to crocidolite. (cdc.gov)
- Cell viability, cell morphology, chromatin condensation, cPARP - 1 level, and caspase - 3 activation, and the expression of p21 WAF1/Cip1 were analyzed. (who.int)
- A mutation in the allosteric site of the caspase 3 dimer interface of Val266 to histidine abolishes activity of the enzyme, and models predict that the mutation mimics the action of small molecule allosteric inhibitors by preventing formation of the active site. (ncsu.edu)
- This issue should therefore be considered in developing caspase inhibitors for therapeutic applications. (cshl.edu)
- the expression of specific CNS enzyme (enolase), proinflammatory cytokines MIF and apoptotic marker caspase-3 in the umbilical blood of infants delivered for Covid positive mothers. (who.int)
- The results demonstrate that considering allosteric inhibition of caspase 3 as a shift between discrete ‘off-state’ or ‘on-state’ conformations is insufficient. (ncsu.edu)
- and (4) studied the effect of caspase-3 inhibition on cell survival and DNA fragmentation in the hippocarnpus in a rat model of transient global ischemia. (unthsc.edu)
- On the other hand, caspase 3 inhibition, lessens the PMA induced-effects on the appearance of RBC morphology alterations, although it enhances PMA-mediated effects on nitric oxide (NO) derived metabolites levels. (unicatt.it)
- XN significantly increased the level of cPARP - 1, active caspase - 3, and the expression of p21WAF/CIP mRNA. (who.int)
- In addition, hydrogen-rich saline treatment reduced caspase-3 activity in cortex and hippocampus after cardiac arrest/resuscitation. (nih.gov)
- Prognostic Impact of Polymorphisms in the CASPASE Genes on Survival of Patients with Colorectal Cancer. (cdc.gov)
- Stability measurements show that only the K242A single mutant decreases stability of the dimer, whereas both single mutants and the double mutant demonstrate much lower activity compared to wild-type caspase-3. (ncsu.edu)
- On average, dengue becomes symptomatic after a 4- to 10-day incubation period (range, 3-14 days). (medscape.com)
- After the There is plasma leakage into the serous cavities bite, there is an incubation period of 3 to 14 also and hepatomegaly with raised liver enzymes days (average 4 to 7 days) followed by the onset is not uncommon. (who.int)
- Caspase-3 promotes genetic instability and carcinogenesis. (bvsalud.org)
- In addition, chemically induced skin carcinogenesis was significantly reduced in mice genetically deficient in caspase-3 . (bvsalud.org)
- This study is limited as blood lead was present at background environmental levels and reflected exposure in recent past (3 months). (who.int)
- Conversely, formation of the K242–E246 salt bridge in caspase-3 is needed for an accurate, stable conformation of loop L4 and proper active site formation in the mature enzyme. (ncsu.edu)
- The 1.63 Å (1 Å = 0.1 nm) structure of the variant demonstrates that the mutation is accommodated at the dimer interface to generate an enzyme with substantially the same activity and specificity as wild-type caspase-3. (ncsu.edu)
- These data strongly suggest that caspase-3 activity contributes to delayed neuronal death after transient ischemia. (unthsc.edu)
- Interactions between loops 2, 2′ and 4, known as the loop bundle, stabilize the active site of caspase-3. (ncsu.edu)
- as a single species, A . phagocytophilum (Figure 2) (1,3). (cdc.gov)
- Overall, the results suggest E246 and K242 are important in procaspase-3 for their interaction with neighboring residues, not with one another. (ncsu.edu)
- Intracellular hyperthermia using magnetite nanoparticles (10-100 nm-sized Fe 3 O 4 ) may be another choice to overcome the difficult challenges for melanoma treatment. (hindawi.com)
- Structural studies of the caspase-3 variants show the involvement of K242 in hydrophobic interactions that stabilize helix 5, near the dimer interface, and the role of E246 appears to be to neutralize the positive charge of K242 within the hydrophobic cluster. (ncsu.edu)
- A more comprehensive view of allosteric regulation of caspase 3 requires the representation of an ensemble of inactive states and shows that subtle structural changes lead to the population of the inactive ensemble. (ncsu.edu)
- 17% of subjects were exposed to inorganic lead, while 3% were exposed to organic lead. (who.int)
- Shortly after the fever breaks (3-7 days after symptom onset or sometimes within 24 hours before), signs of plasma leakage appear, along with the development of hemorrhagic symptoms such as bleeding from sites of trauma, gastrointestinal bleeding, and hematuria. (medscape.com)
- Renal excretion of excess dietary phosphate intake ensures maintenance of phosphate homeostasis, maintaining serum phosphate at a level of approximately 3-4 mg/dL in the serum. (medscape.com)
- Over the last three years The Ottawa Hospital held an average rank of #3 among hospitals for CIHR funding. (ohri.ca)