Caspase 3
Caspase 9
Caspase Inhibitors
Caspase 8
Caspase 7
Caspases
Caspase 1
Caspase 10
Apoptosis
Amino Acid Chloromethyl Ketones
Cysteine Proteinase Inhibitors
Caspase 12
Caspase 14
Enzyme Activation
DNA Fragmentation
Proto-Oncogene Proteins c-bcl-2
Cytochromes c
Mitochondria
Antigens, CD95
Cytochrome c Group
X-Linked Inhibitor of Apoptosis Protein
Poly(ADP-ribose) Polymerases
Apoptotic Protease-Activating Factor 1
bcl-2-Associated X Protein
Cell Death
Inhibitor of Apoptosis Proteins
Jurkat Cells
Caspases, Initiator
In Situ Nick-End Labeling
Cell Survival
BH3 Interacting Domain Death Agonist Protein
Apoptosis Regulatory Proteins
Signal Transduction
Cysteine Endopeptidases
Fas-Associated Death Domain Protein
Enzyme Inhibitors
bcl-X Protein
Apoptosis Inducing Factor
Blotting, Western
Tumor Cells, Cultured
Cells, Cultured
CASP8 and FADD-Like Apoptosis Regulating Protein
Staurosporine
Annexin A5
Membrane Potential, Mitochondrial
Carrier Proteins
HL-60 Cells
TNF-Related Apoptosis-Inducing Ligand
HeLa Cells
Necrosis
Caspases, Effector
Apoptosomes
Reactive Oxygen Species
Tumor Necrosis Factor-alpha
Transfection
Proteins
CRADD Signaling Adaptor Protein
Intracellular Signaling Peptides and Proteins
Death Domain Receptor Signaling Adaptor Proteins
Dose-Response Relationship, Drug
Flow Cytometry
Phosphatidylserines
CARD Signaling Adaptor Proteins
bcl-2 Homologous Antagonist-Killer Protein
Calpain
Granzymes
Proto-Oncogene Proteins
Mitochondrial Proteins
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
Cytosol
bcl-Associated Death Protein
Molecular Sequence Data
NF-kappa B
Serpins
JNK Mitogen-Activated Protein Kinases
Etoposide
U937 Cells
Genes, bcl-2
Adaptor Proteins, Signal Transducing
Mitochondrial Membranes
Models, Biological
Down-Regulation
Ceramides
Immunoblotting
Neurons
Protein Structure, Tertiary
Cell Cycle
Phosphorylation
Reverse Transcriptase Polymerase Chain Reaction
Microscopy, Fluorescence
Mice, Knockout
Receptor-Interacting Protein Serine-Threonine Kinase 2
Protein Synthesis Inhibitors
Myeloid Cell Leukemia Sequence 1 Protein
Mutation
Up-Regulation
Drosophila Proteins
Substrate Specificity
Membrane Potentials
Cell Nucleus
Neoplasm Proteins
Autophagy
RNA Interference
Protein-Serine-Threonine Kinases
Coumarins
RNA, Messenger
Protein Processing, Post-Translational
Oxidative Stress
Intracellular Membranes
Protein Binding
Immunohistochemistry
Mitogen-Activated Protein Kinases
Propidium
Receptors, Death Domain
Proto-Oncogene Proteins c-akt
Cycloheximide
Membrane Proteins
Rats, Sprague-Dawley
Protease Inhibitors
Drug Screening Assays, Antitumor
Receptors, Tumor Necrosis Factor, Type I
p38 Mitogen-Activated Protein Kinases
Proteolysis
Protein Transport
Serine Endopeptidases
Disease Models, Animal
DNA Damage
Acetylcysteine
Proteasome Endopeptidase Complex
Cell-Free System
Ultraviolet Rays
Fibroblasts
Hydrogen Peroxide
Drug Resistance, Neoplasm
Gene Expression Regulation
Gene Expression
Endoplasmic Reticulum Stress
Epithelial Cells
Recombinant Fusion Proteins
Microscopy, Confocal
Cell Division
Neuroprotective Agents
Cell Line, Transformed
Lamins
Drosophila
Sequence Homology, Amino Acid
Gene Expression Regulation, Neoplastic
Microtubule-Associated Proteins
Cytoplasm
Gene Knockdown Techniques
Permeability
DNA Primers
Nuclear Proteins
Interleukin-1beta
Cathepsin B
Cell Differentiation
Bongkrekic Acid
Hepatocytes
Mice, Transgenic
Doxorubicin
Cytoprotection
Aspartic Acid
L-Lactate Dehydrogenase
Protein Kinase C-delta
Gene Expression Regulation, Enzymologic
Lamin Type B
Isatin
Keratin-18
Neuroblastoma
Glutathione
Leupeptins
MAP Kinase Signaling System
Macrophages
Xenograft Model Antitumor Assays
Mitogen-Activated Protein Kinase 8
Endoplasmic Reticulum
Inhibition of NF-kappa B activity in human T lymphocytes induces caspase-dependent apoptosis without detectable activation of caspase-1 and -3. (1/222)
NF-kappa B is involved in the transcriptional control of various genes that act as extrinsic and intrinsic survival factors for T cells. Our findings show that suppression of NF-kappa B activity with cell-permeable SN50 peptide, which masks the nuclear localization sequence of NF-kappa B1 dimers and prevents their nuclear localization, induces apoptosis in resting normal human PBL. Inhibition of NF-kappa B resulted in the externalization of phosphatidylserine, induction of DNA breaks, and morphological changes consistent with apoptosis. DNA fragmentation was efficiently blocked by the caspase inhibitor Z-VAD-fmk and partially blocked by Ac-DEVD-fmk, suggesting that SN50-mediated apoptosis is caspase-dependent. Interestingly, apoptosis induced by NF-kappa B suppression, in contrast to that induced by TPEN (N,N,N',N'-tetrakis [2-pyridylmethyl]ethylenediamine) or soluble Fas ligand (CD95), was observed in the absence of active death effector proteases caspase-1-like (IL-1 converting enzyme), caspase-3-like (CPP32/Yama/apopain), and caspase-6-like and without cleavage of caspase-3 substrates poly(ADP-ribose) polymerase and DNA fragmentation factor-45. These findings suggest either low level of activation is required or that different caspases are involved. Preactivation of T cells resulting in NF-kappa B nuclear translocation protected cells from SN50-induced apoptosis. Our findings demonstrate an essential role of NF-kappa B in survival of naive PBL. (+info)Alternative, non-secretase processing of Alzheimer's beta-amyloid precursor protein during apoptosis by caspase-6 and -8. (2/222)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder. Although the pathogenesis of AD is unknown, it is widely accepted that AD is caused by extracellular accumulation of a neurotoxic peptide, known as Abeta. Mutations in the beta-amyloid precursor protein (APP), from which Abeta arises by proteolysis, are associated with some forms of familial AD (FAD) and result in increased Abeta production. Two other FAD genes, presenilin-1 and -2, have also been shown to regulate Abeta production; however, studies examining the biological role of these FAD genes suggest an alternative theory for the pathogenesis of AD. In fact, all three genes have been shown to regulate programmed cell death, hinting at the possibility that dysregulation of apoptosis plays a primary role in causing neuronal loss in AD. In an attempt to reconcile these two hypotheses, we investigated APP processing during apoptosis and found that APP is processed by the cell death proteases caspase-6 and -8. APP is cleaved by caspases in the intracellular portion of the protein, in a site distinct from those processed by secretases. Moreover, it represents a general effect of apoptosis, because it occurs during cell death induced by several stimuli both in T cells and in neuronal cells. (+info)Caspase-6 role in apoptosis of human neurons, amyloidogenesis, and Alzheimer's disease. (3/222)
Neuronal cell death, neurofibrillary tangles, and amyloid beta peptide (Abeta) deposition depict Alzheimer's disease (AD) pathology, but neuronal loss correlates best with dementia. We have shown that increased production of Abeta is a consequence of neuronal apoptosis, suggesting that apoptosis activates proteases involved in amyloid precursor protein (APP) processing. Here, we investigate key effectors of cell death, caspases, in human neuronal apoptosis and APP processing. We find that caspase-6 is activated and responsible for neuronal apoptosis by serum deprivation. Caspase-6 activity precedes the time of commitment to neuronal apoptosis by 10 h, indicating possible activity without subsequent apoptosis. Inhibition of caspase-6 activity prevents serum deprivation-mediated increase of Abeta. Caspase-6 directly cleaves APP at the C terminus and generates a C-terminal fragment of 3 kDa (Capp3) and an Abeta-containing 6.5-kDa fragment, Capp6.5, that increases in serum-deprived neurons. A pulse-chase experiment reveals a precursor-product relationship between Capp6.5, intracellular Abeta, and secreted Abeta, indicating a potential alternate amyloidogenic pathway. Caspase-6 proenzyme is present in adult human brain tissue, and the p10 active caspase-6 fragment is detected in AD brain tissue. These results indicate a possible alternate pathway for APP amyloidogenic processing in human neurons and a potential implication for this pathway in the neuronal demise of AD. (+info)Cleavage and inactivation of ATM during apoptosis. (4/222)
The activation of the cysteine proteases with aspartate specificity, termed caspases, is of fundamental importance for the execution of programmed cell death. These proteases are highly specific in their action and activate or inhibit a variety of key protein molecules in the cell. Here, we study the effect of apoptosis on the integrity of two proteins that have critical roles in DNA damage signalling, cell cycle checkpoint controls, and genome maintenance-the product of the gene defective in ataxia telangiectasia, ATM, and the related protein ATR. We find that ATM but not ATR is specifically cleaved in cells induced to undergo apoptosis by a variety of stimuli. We establish that ATM cleavage in vivo is dependent on caspases, reveal that ATM is an efficient substrate for caspase 3 but not caspase 6 in vitro, and show that the in vitro caspase 3 cleavage pattern mirrors that in cells undergoing apoptosis. Strikingly, apoptotic cleavage of ATM in vivo abrogates its protein kinase activity against p53 but has no apparent effect on the DNA binding properties of ATM. These data suggest that the cleavage of ATM during apoptosis generates a kinase-inactive protein that acts, through its DNA binding ability, in a trans-dominant-negative fashion to prevent DNA repair and DNA damage signalling. (+info)Proteolytic cleavage of beta-catenin by caspases: an in vitro analysis. (5/222)
Cleavage of structural proteins by caspases has been associated with the severe morphological changes occurring during the apoptotic process. One of the proteins regulating the connection of the actin filament with cadherins in a cell-cell adhesion complex is beta-catenin. During apoptosis, both an N-terminal and a small C-terminal part are removed from beta-catenin. Removal of the N-terminal part may result in a disconnection of the actin filament from a cadherin cell-cell adhesion complex. We demonstrate that caspase-8, -3 and -6 directly proteolyse beta-catenin in vitro. However, the beta-catenin cleavage products generated by caspase-8 were different from those generated by caspase-3 or caspase-6. Caspase-1, -2, -4/11 and -7 did not or only very inefficiently cleave beta-catenin. These data suggest that activation of procaspase-3, -6 or -8 by different stimuli in the cell might result in a differential proteolysis of beta-catenin. (+info)Caspase-induced proteolysis of the cyclin-dependent kinase inhibitor p27Kip1 mediates its anti-apoptotic activity. (6/222)
The caspase-mediated cleavage of a limited number of cellular proteins is a common feature of apoptotic cell death. This cleavage usually inhibits the function of the target protein or generates peptides that actively contribute to the death process. In the present study, we demonstrate that the cyclin-dependent kinase inhibitor p27Kip1 is cleaved by caspases in human leukemic cells exposed to apoptotic stimuli. We have shown recently that p27Kip1 overexpression delayed leukemic cell death in response to cytotoxic drugs. In transient transfection experiments, the p23 and the p15 N-terminal peptides generated by p27Kip1 proteolysis demonstrate an anti-apoptotic effect similar to that induced by the wild-type protein, whereas cleavage-resistant mutants have lost their protective effect. Moreover, stable transfection of a cleavage-resistant mutant of p27Kip1 sensitizes leukemic cells to drug-induced cell death. Altogether, these results indicate that proteolysis of p27Kip1 triggered by caspases mediates the anti-apoptotic activity of the protein. (+info)Caspase-3 is the primary activator of apoptotic DNA fragmentation via DNA fragmentation factor-45/inhibitor of caspase-activated DNase inactivation. (7/222)
Caspase-3 initiates apoptotic DNA fragmentation by proteolytically inactivating DFF45 (DNA fragmentation factor-45)/ICAD (inhibitor of caspase-activated DNase), which releases active DFF40/CAD (caspase-activated DNase), the inhibitor's associated endonuclease. Here, we examined whether other apoptotic proteinases initiated DNA fragmentation via DFF45/ICAD inactivation. In a cell-free assay, caspases-3, -6, -7, -8, and granzyme B initiated benzoyloxycarbonyl-Asp-Glu-Val-Asp (DEVD) cleaving caspase activity, DFF45/ICAD inactivation, and DNA fragmentation, but calpain and cathepsin D failed to initiate these events. Strikingly, only the DEVD cleaving caspases, caspase-3 and caspase-7, inactivated DFF45/ICAD and promoted DNA fragmentation in an in vitro DFF40/CAD assay, suggesting that granzyme B, caspase-6, and caspase-8 promote DFF45/ICAD inactivation and DNA fragmentation indirectly by activating caspase-3 and/or caspase-7. In vitro, however, caspase-3 inactivated DFF45/ICAD and promoted DNA fragmentation more effectively than caspase-7 and endogenous levels of caspase-7 failed to inactivate DFF45/ICAD in caspase-3 null MCF7 cells and extracts. Together, these data suggest that caspase-3 is the primary inactivator of DFF45/ICAD and therefore the primary activator of apoptotic DNA fragmentation. (+info)Caspase-3 and caspase-7 but not caspase-6 cleave Gas2 in vitro: implications for microfilament reorganization during apoptosis. (8/222)
Apoptosis is characterized by proteolysis of specific cellular proteins by a family of cystein proteases known as caspases. Gas2, a component of the microfilament system, is cleaved during apoptosis and the cleaved form specifically regulates microfilaments and cell shape changes. We now demonstrate that Gas2 is a substrate of caspase-3 but not of caspase-6. Proteolytic processing both in vitro and in vivo is dependent on aspartic residue 279. Gas2 cleavage was only partially impaired in apoptotic MCF-7 cells which lack caspase-3, thus indicating that different caspases can process Gas2 in vivo. In vitro Gas2 was processed, albeit with low affinity, by caspase-7 thus suggesting that this caspase could be responsible for the incomplete Gas2 processing observed in UV treated MCF-7 cells. In vivo proteolysis of Gas2 was detected at an early stage of the apoptotic process when the cells are still adherent on the substrate and it was coupled to the specific rearrangement of the microfilament characterizing cell death. Finally we also demonstrated that Gas2 in vitro binds to F-actin, but this interaction was unaffected by the caspase-3 dependent proteolytic processing. (+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
* Fever
* Loss of appetite
* Weight loss
* Fatigue
* Bone pain
* Swelling in the abdomen or neck
* Constipation
* 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.
Caspase 6
Caspase 3
HIPK2
Jeanne Hardy
PANoptosis
Thirumala-Devi Kanneganti
Caspase 8
Caspase-9
Caspase
Caspase 1
Caspase 11
Caspase 10
Caspase 2
Caspase 14
Caspase 12
Epigenetics of neurodegenerative diseases
NUAK1
Caspase-activated DNase
C15orf52
Death regulator Nedd2-like caspase
Jeff Carroll
Inhibitor of apoptosis
Pyroptosis
TRAIL
THOC1
NLRP
CARD10
Michelle Gray
SATB1
Clinical neurochemistry
Proto-oncogene tyrosine-protein kinase Src
NOL3
GNLY
PSMD7
HSPA1B
TUNEL assay
SFRS2IP
Galectin-9
Histone H2B
SPTAN1
TRADD
Pattern recognition receptor
BCL2L13
ENDOG
HSPA8
Find-me signals
WNK3
Luciferase
Nancy Rothwell
Chromosome 16
NLRP4
Lipid signaling
Goniothalamus macrophyllus
NLRP12
PARP4
Emricasan
Anticancer gene
Unfolded protein response
Caspy, a zebrafish caspase, activated by ASC oligomerization is required for pharyngeal arch development. | J Biol Chem;278(6)...
AbMiner - Antibody Detail | Genomics and Pharmacology Facility
Dr. Nandita Mishra - Amrita Vishwa Vidyapeetham
NIOSHTIC-2 Search Results - Full View
Biomarkers Search
Lysosomal exocytosis of HSP70 stimulates monocytic BMP6 expression in Sjögren's syndrome - PubMed
Person Details: Dr. Michael Karin (Superfund Research Program)
Microglia LPS-Related Module Antibody Sampler Kit | Cell Signaling Technology
Frontiers | IL-1β and TNFα Differentially Influence NF-κB Activity and FasL-Induced Apoptosis in Primary Murine Hepatocytes...
MeSH Browser
Induction of Inflammation by West Nile virus Capsid through the Caspase-9 Apoptotic Pathway - Volume 8, Number 12-December 2002...
NIH Guide: AGING, OXIDATIVE STRESS AND CELL DEATH
Recombinant Anti-Amyloid Precursor Protein antibody [EPR5118-34] KO Tested (ab126732)
Induction of apoptosis of human osteoclasts by the transcription factor decoy approach: relevance for the treatment of...
FAM-FLICA® Caspase-8 Assay Kit
Biomarkers Search
Kallenberger2014 - CD95L induced apoptosis initiated by caspase-8, wild-type HeLa cells (cis/trans-cis/trans variant) |...
Human Caspase-8 Antibody MAB704: R&D Systems
Daniel G. Peterson | Editor | SciTechnol | Journal of Applied Bi
Anticancer effect of involucrasin A on colorectal cancer cells by modulating the Akt/MDM2/p53 pathway
Heterozygous germline BLM mutations increase susceptibility to asbestos and mesothelioma - PubMed
Kelly A. Shipkowski, Ph.D., D.A.B.T. - Office of Program Operations
DeCS
MeSH Browser
Activated-carbon-filled agarose hydrogel as a natural medium for seed germination and seedling growth - BT3 Technologies
Advances in Understanding the Role of Aloe Emodin and Targeted Drug Delivery Systems in Cancer
Pre-symptomatic caspase-1 inhibitor delays cognitive decline in a mouse model of Alzheimer disease and aging | AlzPED
Apoptosis21
- 7. Identification of the novel substrates for caspase-6 in apoptosis using proteomic approaches. (nih.gov)
- 10. A Review on Caspases: Key Regulators of Biological Activities and Apoptosis. (nih.gov)
- 15. Initiator and executioner caspases in salivary gland apoptosis of Rhipicephalus haemaphysaloides. (nih.gov)
- 16. Changes in nuclear morphology during apoptosis correlate with vimentin cleavage by different caspases located either upstream or downstream of Bcl-2 action. (nih.gov)
- 17. In situ trapping of activated initiator caspases reveals a role for caspase-2 in heat shock-induced apoptosis. (nih.gov)
- The results of the current study revealed a number of non-peptide-based caspase inhibitors that may be useful in assessing the role of inhibiting the executioner caspases in minimizing tissue damage in disease conditions characterized by unregulated apoptosis. (nih.gov)
- Brief exposure to the pan-caspase apoptosis inhibitor Z-VAD-FMK restored attachment ability and promoted a differentiated morphology, as well as formation of 3D spheroids. (springer.com)
- 7. Hwang-Heuk-San induces apoptosis in HCT116 human colorectal cancer cells through the ROS-mediated activation of caspases and the inactivation of the PI3K/Akt signaling pathway. (nih.gov)
- 13. Involvement of NLRP3/Caspase-1/GSDMD-Dependent pyroptosis in BPA-Induced apoptosis of human neuroblastoma cells. (nih.gov)
- A short pro-domain caspase that plays an effector role in APOPTOSIS . (nih.gov)
- Further, canagliflozin prevents ISO-induced apoptosis of kidney cells by inhibiting Bax protein upregulation and caspase-3 activation. (nature.com)
- Apoptosis is induced through the mitochondrial pathway resulting in caspase-9 activation and downstream caspase-3 activation. (cdc.gov)
- We observed that the WNV-Cp protein is a pathogenic protein, which drives apoptosis in vitro through the mitochodrial/caspase-9 pathway. (cdc.gov)
- Caspases play important roles in apoptosis and inflammation. (immunochemistry.com)
- ICT's FLICA assay kits are used by researchers seeking to quantitate apoptosis via caspase activity in cultured cells and tissues. (immunochemistry.com)
- Peng, Z;Gillissen, B;Richter, A;Sinnberg, T;Schlaak, MS;Eberle, J. Enhanced Apoptosis and Loss of Cell Viability in Melanoma Cells by Combined Inhibition of ERK and Mcl-1 Is Related to Loss of Mitochondrial Membrane Potential, Caspase Activation and Upregulation of Proapoptotic Bcl-2 Proteins . (immunochemistry.com)
- Apoptosis in response to the ligand CD95L (also known as Fas ligand) is initiated by caspase-8, which is activated by dimerization and self-cleavage at death-inducing signaling complexes (DISCs). (ebi.ac.uk)
- The activation of caspase-8 by combined intra- and interdimeric cleavage ensures weak signaling at low concentrations of CD95L and strongly accelerated activation at higher ligand concentrations, thereby contributing to precise control of apoptosis. (ebi.ac.uk)
- Detects human Caspase-8 precursor in Western blots and a 42 kDa doublet generated during apoptosis. (rndsystems.com)
- Subsequently, flow cytometry and western blotting indicated that involucrasin A induced apoptosis and upregulated the expression levels of apoptosis‑related proteins, such as cleaved‑caspase 6 and cleaved‑caspase 9, in a dose‑dependent manner. (spandidos-publications.com)
- Caspasa de prodominio corto que desempeña una función efectora en la APOPTOSIS. (bvsalud.org)
Inhibitor5
- NCGC-00183434) is the most potent caspase 1 inhibitor reported to date. (nih.gov)
- This in vitro assay employs the fluorescent inhibitor probe FAM-LETD-FMK to label active caspase-8 enzyme in living cells. (immunochemistry.com)
- Inflammatory Caspase-1 has a significant impact on AD-like pathophysiology and Caspase-1 inhibitor, VX-765, reverses cognitive deficits in AD mouse models. (nih.gov)
- The Group III Caspase Inhibitor I controls the biological activity of Group III caspases (caspase-6, -8, -9, and -10). (emdmillipore.com)
- Only caspase 9 inhibitor totally abrogated γTriDAP cytotoxicity. (biomedcentral.com)
Inhibitors6
- A number of these compounds were potent inhibitors of caspase 1 (IC 50 s ≤ 1 nM). (nih.gov)
- It also possesses a unique selectivity pattern relative to other reported caspase inhibitors. (nih.gov)
- Inhibitors of caspase 1 are sought for intervention strategies within ischemic disorders, Huntington's disease, amyotrophic lateral sclerosis (ALS), rheumatoid arthritis, osteoarthritis, inflammatory bowel disease and sepsis. (nih.gov)
- 9. Identification of early intermediates of caspase activation using selective inhibitors and activity-based probes. (nih.gov)
- Isatin sulfonamide analogs containing a Michael addition acceptor: a new class of caspase 3/7 inhibitors. (nih.gov)
- Synthesis and in vitro evaluation of sulfonamide isatin Michael acceptors as small molecule inhibitors of caspase-6. (nih.gov)
CASP81
- Caspase 8 antibody LS-C301799 is an FITC-conjugated rabbit polyclonal antibody to human Caspase 8 (CASP8) (aa217-384). (lsbio.com)
Proteins1
- We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). (hopkinsmedicine.org)
Protein5
- Western blot analysis was performed to investigate the effects of royal jelly on the protein expression levels of Bax, caspase-3 , caspase-6 , Bcl-2, NF-κB, COX-2, and Erk. (bvsalud.org)
- Additionally, the protein expression of caspase-3 , caspase-6 , Bax, and Erk were decreased in fluoride -treated groups and they were significantly increased by RJ treatment compared to the un -treated rats . (bvsalud.org)
- Procaspase 1 is known to associate with several multi-protein complexes capable of responding to numerous external stimuli, suggesting that caspase 1 is a major regulator of the inflammation response. (nih.gov)
- and protein carbonyl, IL-1B, and caspase-1 determination. (cdc.gov)
- For a caspase-9-specific test, 5 μg of pcWNV-Cp-DJY or pcWNV-CpWT was cotransfected with a dominant negative caspase-9 (DN caspase-9) construct, and cleavage of procaspase-9 protein was determined by Western blot analysis with antihuman caspase-9 antibody (MBL, Nagoya, Japan). (cdc.gov)
Apoptotic cascade2
- 18. Bcl-2 regulates a caspase-3/caspase-2 apoptotic cascade in cytosolic extracts. (nih.gov)
- It is known as the initiating caspase for the apoptotic cascade. (rndsystems.com)
Executioner caspases2
Antibody2
- The localization pattern of capsid expression was analyzed by immunofluorescent assay in HeLa, 293-T, RD, or SH-SY5Y cells by using anti-His tag antibody as described ( 6 ). (cdc.gov)
- PVDF membrane was probed with 1 µg/mL of Human Caspase-8 Monoclonal Antibody (Catalog # MAB704), followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF007 ). (rndsystems.com)
Cleavage3
- 2. Cleavage of GSDME by caspase-3 determines lobaplatin-induced pyroptosis in colon cancer cells. (nih.gov)
- Previous work indicated that the degree of substrate cleavage by caspase-8 determines whether a cell dies or survives in response to a death stimulus. (ebi.ac.uk)
- We derived and experimentally validated a minimal model in which cleavage of caspase-8 in the enzymatic domain occurs in an interdimeric manner through interaction between DISCs, whereas prodomain cleavage sites are cleaved in an intradimeric manner within DISCs. (ebi.ac.uk)
Activation8
- Caspase 1, also known as interleukin-converting enzyme or ICE, is responsible for the proteolytic activation of interleukin (IL)-1β and IL-18. (nih.gov)
- Caspase-1 was significantly elevated in the liver at 6 h, to a greater extent in BALB/c mice, suggesting inflammasome pathway activation. (cdc.gov)
- Conclusions: BALB/c mice were more responsive to nanoceria-induced effects, e.g. liver caspase-1 activation, reduced liver vacuolation, and increased spleen cell density. (cdc.gov)
- 3. Death and survival from executioner caspase activation. (nih.gov)
- 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)
- 11. Empagliflozin protects diabetic pancreatic tissue from damage by inhibiting the activation of the NLRP3/caspase-1/GSDMD pathway in pancreatic β cells: in vitro and in vivo studies. (nih.gov)
- 17. Microglial and Neuronal Cell Pyroptosis Induced by Oxygen-Glucose Deprivation/Reoxygenation Aggravates Cell Injury via Activation of the Caspase-1/GSDMD Signaling Pathway. (nih.gov)
- The FAM FLICA Caspase-8 assay probe allows researchers to assess caspase-8 activation. (immunochemistry.com)
C57BL6
- Prior studies showed nanoparticle clearance was different in C57BL/6 versus BALB/c mice, strains prone to Th1 and Th2 immune responses, respectively. (cdc.gov)
- Methods: C57BL/6 and BALB/c female mice were i.p. injected with 10 mg/kg nanoceria or vehicle and terminated 0.5 to 24 h later. (cdc.gov)
- Results: Peripheral organ cerium significantly increased, generally more in C57BL/6 mice. (cdc.gov)
- Light microscopy revealed greater liver vacuolation in C57BL/6 mice and a nanoceria-induced decrease in BALB/c but not C57BL/6 mice vacuolation. (cdc.gov)
- Nanoceria increased spleen lymphoid white pulp cell density in BALB/c but not C57BL/6 mice. (cdc.gov)
- Ferritin accumulation was greatly increased proximal to the nanoceria, forming core-shell-like structures in C57BL/6 but even distribution in BALB/c mice. (cdc.gov)
Specificity1
- Caspases are cysteine proteases with a strict specificity for cleaving peptide sequences C-terminal to aspartic acids residues. (nih.gov)
Signaling pathway1
- 12. Suppression of the caspase-1/GSDMD-mediated pyroptotic signaling pathway through dexamethasone alleviates corneal alkali injuries. (nih.gov)
Initiator1
- These compounds were also observed to have a low potency for inhibiting the initiator caspases, caspase-1 and caspase-8, and caspase-6. (nih.gov)
Humans2
- Currently, 12 caspase isozymes have been identified in humans, with numerous reported activities. (nih.gov)
- Infection with multiple herpes viruses, for instance, is an inextricable part of the human condition , to which more than 90% of humans are subject (6). (oneradionetwork.com)
Vitro1
- A number of isatin sulfonamide analogues were prepared and their potencies for inhibiting caspase-1, -3, -6, -7, and -8 were evaluated in vitro. (nih.gov)
Inhibits2
- 9. Hydrogen inhibits endometrial cancer growth via a ROS/NLRP3/caspase-1/GSDMD-mediated pyroptotic pathway. (nih.gov)
- Also inhibits caspase-1 and caspase-3. (emdmillipore.com)
Inflammation1
- These results suggest that Caspase-1-mediated inflammation occurs early in the disease and raise hope that VX-765, a previously Food and Drug Administration-approved drug for human CNS clinical trials, may be a useful drug to prevent the onset of cognitive deficits and brain inflammation in AD. (nih.gov)
Pathways2
- Royal jelly protects brain tissue against fluoride-induced damage by activating Bcl-2/NF-κB/caspase-3/caspase-6/Bax and Erk signaling pathways in rats. (bvsalud.org)
- This study is aimed at determining whether royal jelly (RJ) which has a powerful antioxidant property prevents fluoride -induced brain tissue damage and exploring whether Bcl-2/NF-κB/ and caspase-3 / caspase-6 /Bax/ Erk pathways play a critical role in the neuroprotective effect of RJ. (bvsalud.org)
Induces4
- 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)
- 1. Secoisolariciresinol diglucoside induces pyroptosis by activating caspase-1 to cleave GSDMD in colorectal cancer cells. (nih.gov)
- 4. Saikosaponin-D induces the pyroptosis of lung cancer by increasing ROS and activating the NF-κB/NLRP3/caspase-1/GSDMD pathway. (nih.gov)
- 6. Triclabendazole Induces Pyroptosis by Activating Caspase-3 to Cleave GSDME in Breast Cancer Cells. (nih.gov)
Cysteine1
- A nitrile-containing propionic acid moiety as an electrophile for covalent attack by the active site cysteine residue of caspase 1 was investigated. (nih.gov)
Cascade1
- DN caspase-9 (provided courtesy of Emad S. Alnmeri, Thomas Jefferson University, Philadelphia, PA) has been reported to inhibit the caspase cascade ( 5 ). (cdc.gov)
Molecular2
- Molecular modeling studies provided further insight into the interaction of this class of compounds with activated caspase-3. (nih.gov)
- Modeling indicated that sustained membrane-bound caspase-8 activity is followed by transient cytosolic activity, which can be interpreted as a molecular timer mechanism reflected by a limited lifetime of active caspase-8. (ebi.ac.uk)
Ligand1
- To determine how a death ligand stimulus is effectively translated into caspase-8 activity, we assessed this activity over time in single cells with compartmentalized probes that are cleaved by caspase-8 and used multiscale modeling to simultaneously describe single-cell and population data with an ensemble of single-cell models. (ebi.ac.uk)
Examination1
- Examination of these small molecules versus a caspase panel demonstrated an impressive degree of selectivity for caspase 1 inhibition. (nih.gov)
Enzyme1
- The remaining green fluorescent signal is a direct measure of the active caspase-8 enzyme activity present in the cell at the time the reagent was added. (immunochemistry.com)
Mechanisms1
- 6. Caspase mechanisms. (nih.gov)
Inflammatory2
Compounds1
- Natural products are a key source of new antitumorigenic agents, as 80-83% of approved anticancer drugs are natural compounds or their derivatives ( 6 ). (spandidos-publications.com)
Roles1
- 11. The enigmatic roles of caspases in tumor development. (nih.gov)
Decrease1
- This effect is associated with an increase of caspase-3 and a decrease of interleukin-6 production. (minervamedica.it)
Cells4
- Caspase 1 is constitutively and inducibly expressed in immune response elements such as T cells, macrophages and neutrophils. (nih.gov)
- 2. Imaging-based methods for assessing caspase activity in single cells. (nih.gov)
- For this purpose, the idea that adding different side chains to the anthraquinone skeleton will increase its therapeutic effects and that new anthraquinone derivatives can prevent the development of resistance in cancer cells has gained importance [ 5 , 6 ]. (hindawi.com)
- Nod1-deficient breast cancer cells (MCF-7) were more resistant to tumor necrosis factor-induced cytotoxicity, and this was accompanied by a reduction in caspase signaling. (biomedcentral.com)
Target1
- 8. Pro-caspase-3 is a major physiologic target of caspase-8. (nih.gov)
Activity1
- Detect caspase-8 activity with the FLICA Caspase-8 Assay Kit. (immunochemistry.com)
Active1
- Association with another p18/p10 heterodimer generates active caspase-8. (rndsystems.com)
Role1
- Recently, several studies have shown that microvascular thrombosis generation also plays a pivotal role in the pathophysiology of AKI, and many antithrombin agents, such as heparin [ 6 ] and antithrombin III (ATIII) [ 7 - 9 ] could mitigate renal IRI. (oncotarget.com)
Cell1
- The FLICA reagent FAM-LETD-FMK enters each cell and irreversibly binds to activated caspase-8. (immunochemistry.com)
Western1
- Detection of Human Caspase‑8 by Western Blot. (rndsystems.com)
Show1
- 13. Caspases from scleractinian coral show unique regulatory features. (nih.gov)