STZ is a broad-spectrum antibiotic that is toxic to the insulin producing β cells of pancreatic islets. It is currently used clinically for the treatment of metastatic islet cell carcinoma of the pancreas [12 ] and has been used investigationally in a wide variety of large and small animal species [2 (link)–5 , 13 (link)–17 (link)]. The method of STZ action in β cell depletion has been studied extensively over the years. It is generally assumed that STZ is taken up via the cell membrane GLUT2 glucose transporter and causes DNA alkylation and eventual β cell death [15 (link), 17 (link)], although streptozotocin’s actions as a protein alkylating agent [18 (link)] and nitric oxide donor may contribute to its cytotoxicity [19 (link)]. Because STZ enters the cell via GLUT2, the toxic action is not specific to β cells and can cause damage to other tissues including the liver and kidney [5 , 15 (link), 17 (link), 19 (link)].
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Cell Function
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Cell Death
Cell Death
Cell death is a fundamental biological process involving the programmed destruction of cells.
It plays a crucial role in development, homeostasis, and disease.
There are several types of cell death, including apoptosis, necrosis, and autophagy, each with distinct mechanisms and implications.
Understanding cell death pathways is essential for research in areas such as cancer, neurodegenerative disorders, and tissue regeneration.
Optimizing cell death research through AI-driven comparative analysis can help identify the best protocols and products, advancing our knowledge and therapuetic interventions in this critical field of biology.
It plays a crucial role in development, homeostasis, and disease.
There are several types of cell death, including apoptosis, necrosis, and autophagy, each with distinct mechanisms and implications.
Understanding cell death pathways is essential for research in areas such as cancer, neurodegenerative disorders, and tissue regeneration.
Optimizing cell death research through AI-driven comparative analysis can help identify the best protocols and products, advancing our knowledge and therapuetic interventions in this critical field of biology.
Most cited protocols related to «Cell Death»
Alkylating Agents
Alkylation
Animals
Antibiotics
Cell Death
Cells
Cytotoxin
Glucose Transporter
Islets of Langerhans
Kidney
Liver
Nitric Oxide Donors
Pancreatic beta Cells
Pancreatic Carcinoma
Plasma Membrane
SLC2A2 protein, human
Staphylococcal Protein A
Tissues
Toxic Actions
Zebrafish were maintained in accordance with UK Home Office regulations, UK Animals (Scientific Procedures) Act 1986, under project licence 80/2192, which was reviewed by The Wellcome Trust Sanger Institute Ethical Review Committee.
Heterozygous F2 fish were randomly incrossed and upon egg collection F2 adults were fin clipped and kept as isolated breeding pairs. For each family we aimed to phenotype 12 pairs, over 3 weeks of breeding. Each clutch of eggs, which was labelled with the breeding pair ID, was sorted into three 10cm petri dishes of ~50 embryos each. Embryos were incubated at 28.5°C. Previous mutagenesis screens were used as a reference for the phenotyping 27 (link),28 (link). Those phenotypes studied were: day 1 – early patterning defects, early arrest, notochord, eye development, somites, patterning and cell death in the brain; day 2 – cardiac defects, circulation of the blood, pigment (melanocytes), eye and brain development; day 3 – cardiac defects, circulation of the blood, pigment (melanocytes), movement and hatching; day 4 – cardiac defects, movement, pigment (melanocytes) and muscle defects; day 5 – behaviour (hearing, balance, response to touch), swim bladder, pigment (melanocytes, xanthophores and iridophores), distribution of pigment, jaw, skull, axis length, body shape, notochord degeneration, digestive organs (intestinal folds, liver and pancreas), left-right patterning. In the first round of the phenotyping, all phenotypic embryos were discarded. At 5 dpf, >48 phenotypically wild-type embryos were harvested. Embryos were fixed in 100% methanol and stored at −20°C until genotyping was initiated. In the second round, F2s that were heterozygous for a suspected causal mutation were re-crossed. All phenotypes observed in those clutches of embryos were counted, documented and photographed. Phenotypic embryos were fixed in 100% methanol and at 5 dpf 48 phenotypically wild-type embryos were also collected. The first round genotyping results were assessed using a Chi-squared test with a p-value cut off of <0.05. If the number of homozygous embryos was above the cut-off (i.e. in the expected 25% ratio), the allele was deemed to not cause a phenotype within the first 5 dpf. If the number of homozygous embryos was below the cut-off, the allele was carried forward into the second round of phenotyping. In the second round, we aimed to genotype 48 embryos for each phenotype, ideally from multiple clutches. An allele was documented as causing a phenotype if the phenotypic embryos were homozygous for the allele. We allowed up to 10% of embryos for a given phenotype to not be homozygous, to account for errors in egg collection. Such alleles were outcrossed for further genotyping with F4 embryos at a later date. Where possible, alleles were also submitted to complementation tests.
Heterozygous F2 fish were randomly incrossed and upon egg collection F2 adults were fin clipped and kept as isolated breeding pairs. For each family we aimed to phenotype 12 pairs, over 3 weeks of breeding. Each clutch of eggs, which was labelled with the breeding pair ID, was sorted into three 10cm petri dishes of ~50 embryos each. Embryos were incubated at 28.5°C. Previous mutagenesis screens were used as a reference for the phenotyping 27 (link),28 (link). Those phenotypes studied were: day 1 – early patterning defects, early arrest, notochord, eye development, somites, patterning and cell death in the brain; day 2 – cardiac defects, circulation of the blood, pigment (melanocytes), eye and brain development; day 3 – cardiac defects, circulation of the blood, pigment (melanocytes), movement and hatching; day 4 – cardiac defects, movement, pigment (melanocytes) and muscle defects; day 5 – behaviour (hearing, balance, response to touch), swim bladder, pigment (melanocytes, xanthophores and iridophores), distribution of pigment, jaw, skull, axis length, body shape, notochord degeneration, digestive organs (intestinal folds, liver and pancreas), left-right patterning. In the first round of the phenotyping, all phenotypic embryos were discarded. At 5 dpf, >48 phenotypically wild-type embryos were harvested. Embryos were fixed in 100% methanol and stored at −20°C until genotyping was initiated. In the second round, F2s that were heterozygous for a suspected causal mutation were re-crossed. All phenotypes observed in those clutches of embryos were counted, documented and photographed. Phenotypic embryos were fixed in 100% methanol and at 5 dpf 48 phenotypically wild-type embryos were also collected. The first round genotyping results were assessed using a Chi-squared test with a p-value cut off of <0.05. If the number of homozygous embryos was above the cut-off (i.e. in the expected 25% ratio), the allele was deemed to not cause a phenotype within the first 5 dpf. If the number of homozygous embryos was below the cut-off, the allele was carried forward into the second round of phenotyping. In the second round, we aimed to genotype 48 embryos for each phenotype, ideally from multiple clutches. An allele was documented as causing a phenotype if the phenotypic embryos were homozygous for the allele. We allowed up to 10% of embryos for a given phenotype to not be homozygous, to account for errors in egg collection. Such alleles were outcrossed for further genotyping with F4 embryos at a later date. Where possible, alleles were also submitted to complementation tests.
Adult
Air Sacs
Alleles
Animals
Blood Circulation
Body Shape
Brain
Brain Death
Cardiac Arrest
Cell Death
Cells
Cranium
Digestive System
Eggs
Embryo
Epistropheus
Fishes
Genetic Complementation Test
Genotype
Heart
Heterozygote
Homozygote
Hyperostosis, Diffuse Idiopathic Skeletal
Intestines
Liver
Melanocyte
Methanol
Movement
Muscle Tissue
Mutagenesis
Mutation
Notochord
Pancreas
Phenotype
Pigmentation
Somites
Touch
Zebrafish
Electron microscopy, annexin V labeling, and DAPI staining were performed as described previously (Madeo et al., 1997 (link)). For the TdT-mediated dUTP nick end labeling (TUNEL) test, cells were prepared as described (Madeo et al., 1997 (link)), and the DNA ends were labeled using the In Situ Cell Death Detection Kit, POD (Boehringer Mannheim ). Yeast cells were fixed with 3.7% formaldehyde, digested with lyticase, and applied to a polylysine-coated slide as described for immunofluorescence (Adams and Pringle, 1984 (link)). The slides were rinsed with PBS and incubated with 0.3% H2O2 in methanol for 30 min at room temperature to block endogenous peroxidases. The slides were rinsed with PBS, incubated in permeabilization solution (0.1% Triton X-100 and 0.1% sodium citrate) for 2 min on ice, rinsed twice with PBS, incubated with 10 μl TUNEL reaction mixture (terminal deoxynucleotidyl transferase 200 U/ml, FITC-labeled dUTP 10 mM, 25 mM Tris-HCl, 200 mM sodium cacodylate, 5 mM cobalt chloride; Boehringer Mannheim ) for 60 min at 37°C, and then rinsed 3× with PBS. For the detection of peroxidase, cells were incubated with 10 μl Converter-POD (anti-FITC antibody, Fab fragment from sheep, conjugated with horseradish peroxidase) for 30 min at 37°C, rinsed 3× with PBS, and then stained with DAB-substrate solution (Boehringer Mannheim ) for 10 min at room temperature. A coverslip was mounted with a drop of Kaiser's glycerol gelatin (Merck). As staining intensity varies, only samples from the same slide were compared.
Free intracellular radicals were detected with dihydrorhodamine 123, dichlorodihydrofluorescein diacetate (dichlorofluorescin diacetate), or dihydroethidium (hydroethidine;Sigma Chemical Co. ). Dihydrorhodamine 123 was added ad-5 μg per ml of cell culture from a 2.5-mg/ml stock solution in ethanol and cells were viewed without further processing through a rhodamine optical filter after a 2-h incubation. Dichlorodihydrofluorescein diacetate was added ad-10 μg per ml of cell culture from a 2.5 mg/ml stock solution in ethanol and cells were viewed through a fluorescein optical filter after a 2-h incubation. Dihydroethidium was added ad-5 μg per ml of cell culture from a 5 mg/ml aqueous stock solution and cells were viewed through a rhodamine optical filter after a 10-min incubation. For flow cytometric analysis, cells were incubated with dihydrorhodamine 123 for 2 h and analyzed using a FACS® Calibur (Becton Dickinson ) at low flow rate with excitation and emission settings of 488 and 525–550 nm (filter FL1), respectively.
Free spin trap reagents N-tert-butyl-α−phenylnitrone (PBN;Sigma -Aldrich) and 3,3,5,5,-tetramethyl-pyrroline N-oxide (TMPO; Sigma -Aldrich) were added directly to the cell cultures as 10-mg/ml aqueous stock solutions. Viability was determined as the portion of cell growing to visible colonies within 3 d.
To determine frequencies of morphological phenotypes (TUNEL, Annexin V, DAPI, dihydrorhodamine 123), at least 300 cells of three independent experiments were evaluated.
Free intracellular radicals were detected with dihydrorhodamine 123, dichlorodihydrofluorescein diacetate (dichlorofluorescin diacetate), or dihydroethidium (hydroethidine;
Free spin trap reagents N-tert-butyl-α−phenylnitrone (PBN;
To determine frequencies of morphological phenotypes (TUNEL, Annexin V, DAPI, dihydrorhodamine 123), at least 300 cells of three independent experiments were evaluated.
3,3,5,5-tetramethyl-1-pyrroline N-oxide
Annexin A5
Antibodies, Anti-Idiotypic
Cacodylate
Cardiac Arrest
Cell Culture Techniques
Cell Death
Cells
cobaltous chloride
DAPI
deoxyuridine triphosphate
dichlorofluorescin
dihydroethidium
dihydrorhodamine 123
DNA Nucleotidylexotransferase
Domestic Sheep
Electron Microscopy
Ethanol
Flow Cytometry
Fluorescein
Fluorescein-5-isothiocyanate
Formaldehyde
Free Radicals
Gelatins
Glycerin
Horseradish Peroxidase
hydroethidine
Immunofluorescence
Immunoglobulins, Fab
In Situ Nick-End Labeling
lyticase
Methanol
Oxides
Peroxidase
Peroxidases
Peroxide, Hydrogen
Phenotype
Polylysine
Protoplasm
pyrroline
Rhodamine
Sodium
Sodium Citrate
TERT protein, human
Triton X-100
Tromethamine
Yeast, Dried
Annexin A5
Antibodies, Anti-Idiotypic
Biological Assay
Cell Death
Cells
Flow Cytometry
Gel Chromatography
Immunoprecipitation
Internal Ribosome Entry Sites
Liposomes
Mitochondria
Molar
Retroviridae
Sodium Acetate
Staurosporine
SAHBs were synthesized using our established method46 (link),47 (link) and recombinant BAX for NMR and biochemical analyses was generated as previously described33 (link),35 (link). Samples for HSQC and PRE NMR contained uniformly 15N-labeled BAX at 0.2 mM prepared in 10 mM sodium acetate solution at pH 6.0 with up to a 1:1 molar ratio of SAHB. NMR spectra were acquired at 32°C on Bruker 600 and 800 MHz spectrometers, and then processed and analyzed as described in the Full Methods. To evaluate BIM SAHB-induced BAX activation, four in vitro assays were performed. The oligomerization assay employed freshly purified monomeric BAX in combination with BIM SAHB at the indicated ratios and incubation durations followed by size-exclusion chromatography to quantify monomeric vs. oligomeric BAX. The BAX conformational change assay also employed the indicated BIM SAHB:BAX mixtures, which were exposed to the conformation-specific 6A7 anti-BAX antibody, followed by immunoprecipitation and BAX Western analysis to monitor the proportion of activated conformer of BAX upon BIM SAHB exposure. To determine if the BIM SAHB-induced BAX conformational change reflected functional activation of its release activity, we conducted liposomal and mitochondrial release assays as previously described33 (link),48 (link) and using the indicated doses and constructs of BIM SAHB and BAX. For cellular studies, DKO MEFs were reconstituted with BAX by retroviral transduction of BAX-IRES-GFP as previously reported7 (link),13 (link) and as described in the Full Methods. BAX or BAXK21E-reconstituted DKO MEFs were exposed to either BIM SAHBs or staurosporine, and cell death quantified over time by annexin-V-Cy3 staining followed by flow cytometric analysis.
Annexin A5
Antibodies, Anti-Idiotypic
Biological Assay
Cell Death
Cells
Flow Cytometry
Gel Chromatography
Immunoprecipitation
Internal Ribosome Entry Sites
Liposomes
Mitochondria
Molar
Retroviridae
Sodium Acetate
Staurosporine
Most recents protocols related to «Cell Death»
Example 7
The MTT Cell Proliferation assay determines cell survival following apple stem cell extract treatment. The purpose was to evaluate the potential anti-tumor activity of apple stem cell extracts as well as to evaluate the dose-dependent cell cytotoxicity.
Principle: Treated cells are exposed to 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT). MTT enters living cells and passes into the mitochondria where it is reduced by mitochondrial succinate dehydrogenase to an insoluble, colored (dark purple) formazan product. The cells are then solubilized with DMSO and the released, solubilized formazan is measured spectrophotometrically. The MTT assay measures cell viability based on the generation of reducing equivalents. Reduction of MTT only occurs in metabolically active cells, so the level of activity is a measure of the viability of the cells. The percentage cell viability is calculated against untreated cells.
Method: A549 and NCI-H520 lung cancer cell lines and L132 lung epithelial cell line were used to determine the plant stem cell treatment tumor-specific cytotoxicity. The cell lines were maintained in Minimal Essential Media supplemented with 10% FBS, penicillin (100 U/ml) and streptomycin (100 μg/ml) in a 5% CO2 at 37 Celsius. Cells were seeded at 5×103 cells/well in 96-well plates and incubated for 48 hours. Triplicates of eight concentrations of the apple stem cell extract were added to the media and cells were incubated for 24 hours. This was followed by removal of media and subsequent washing with the phosphate saline solution. Cell proliferation was measured using the MTT Cell Proliferation Kit I (Boehringer Mannheim, Indianapolis, IN) New medium containing 50 μl of MTT solution (5 mg/ml) was added to each well and cultures were incubated a further 4 hours. Following this incubation, DMSO was added and the cell viability was determined by the absorbance at 570 nm by a microplate reader.
In order to determine the effectiveness of apple stem cell extracts as an anti-tumor biological agent, an MTT assay was carried out and IC50 values were calculated. IC50 is the half maximal inhibitory function concentration of a drug or compound required to inhibit a biological process. The measured process is cell death.
Results: ASC-Treated Human Lung Adenocarcinoma Cell Line A549.
Results: ASC-Treated Human Squamous Carcinoma Cell Line NCI-H520.
Results: ASC-treated Lung Epithelial Cell Line L132.
Summary Results: Cytotoxicity of Apple Stem Cell Extracts.
Apple stem cell extracts killed lung cancer cells lines A549 and NCI-H520 at relatively low doses: IC50s were 12.58 and 10.21 μg/ml respectively as compared to 127.46 μg/ml for the lung epithelial cell line L132. Near complete anti-tumor activity was seen at a dose of 250 μg/ml in both the lung cancer cell lines. This same dose spared more than one half of the L132 cells. See Tables 7-10. The data revealed that apple stem cell extract is cytotoxic to lung cancer cells while sparing lung epithelial cells.
Example 9
The experiment of Example 7 was repeated substituting other plant materials for ASC. Plant stem cell materials included Dandelion Root Extract (DRE), Aloe Vera Juice (AVJ), Apple Fiber Powder (AFP), Ginkgo Leaf Extract (GLE), Lingonberry Stem Cells (LSC), Orchid Stem Cells (OSC) as described in Examples 1 and 2. The concentrations of plant materials used were nominally 250, 100, 50, 25, 6.25, 3.125, 1.562, and 0.781 μg/mL. These materials were tested only for cells the human lung epithelial cell line L132 (as a proxy for normal epithelial cells) and for cells of the human lung adenocarcinoma cell line A549 (as a proxy for lung cancer cells).
A549 cells lung cancer cell line cytotoxicity results for each of the treatment materials.
DRE-Treated Lung Cancer Cell Line A549 Cells.
AVJ-Treated Lung Cancer Cell line A549 Cells.
AFP-Treated Lung Cancer Cell line A549 Cells.
GLE-treated Lung Cancer Cell line A549 Cells.
LSC-treated lung cancer cell lines A549 cells.
OSC-treated Lung Cancer Cell line A549 Cells.
L132 cells (“normal” lung epithelial cell line) cytotoxicity results for each of the treatment materials.
DRE-Treated Lung Epithelial Cell Line L132 cells.
AVJ-Treated Lung Epithelial Cell Line L132 cells.
AFP-Treated Lung Epithelial Cell Line L132 cells.
GLE-Treated Lung Epithelial Cell Line L132 cells.
LSC-Treated Lung Epithelial Cell Line L132 cells.
OSC-Treated Lung Epithelial Cell Line L132 cells.
Calculated values.
Full text: Click here
14-3-3 Proteins
43-63
61-26
A549 Cells
Action Potentials
Adenocarcinoma of Lung
Aloe
Aloe vera
Antineoplastic Agents
Biological Assay
Biological Factors
Biological Processes
Bromides
Cardiac Arrest
Cell Death
Cell Extracts
Cell Lines
Cell Proliferation
Cells
Cell Survival
Cytotoxin
diphenyl
DNA Replication
Epistropheus
Epithelial Cells
Fibrosis
Formazans
Genetic Selection
Ginkgo biloba
Ginkgo biloba extract
Homo sapiens
Lingonberry
Lung
Lung Cancer
Lung Neoplasms
Malignant Neoplasms
Mitochondria
Mitochondrial Inheritance
Neoplasms
Neoplastic Stem Cells
Oral Cavity
PEG SD-01
Penicillins
Pharmaceutical Preparations
Phosphates
Plant Cells
Plant Leaves
Plant Roots
Plants
Powder
Psychological Inhibition
Saline Solution
SD 31
SD 62
SEM-76
Squamous Cell Carcinoma
Stem, Plant
Stem Cells
Streptomycin
Succinate Dehydrogenase
Sulfoxide, Dimethyl
Taraxacum
Tetrazolium Salts
Example 2
In the following experiments, a mouse model of RVO, which induces reproducible retinal edema was used. RVO is the model that was used for testing anti-VEGF therapies for DME. Brown et al., Ophthalmology 117, 1124-1133 el 121 (2010); and Campochiaro et al., Ophthalmology 117, 1102-1112 e1101 (2010). I n this model, Rose Bengal, a photoactivatable dye, is injected into the tail veins of adult C57B16 mice and photoactivated by laser of retinal veins around the optic nerve head. A clot is formed and edema or increased retinal thickness develops rapidly. Inflammation, also seen in diabetes, also develops.
Fluorescein leakage and maximal retinal edema, measured by fluorescein angiography and optical coherence tomography (OCT), respectively, using the Phoenix Micron IV, is observed 24 h after RVO. Retinal edema is maintained over the first 3 days RVO. By day 4 the edema decreases and the retina subsequently thins out. In addition to edema formation there is evidence of cell death in the photoreceptor cell layer by day 2 after RVO.
In this example, mice were anesthetized with intra-peritoneal (IP) injection of ketamine and xylazine. One drop of 0.5% alcaine was added to the eye as topical anesthetic. The retina was imaged with the Phoenix Micron IV to choose veins for laser ablation using the Phoenix Micron IV image guided laser. One to four veins around the optic nerve head were ablated by delivering a laser pulse (power 50 mW, spot size 50 μm, duration 3 seconds) to each vein.
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Adult
Alcaine
Cell Death
Clotrimazole
Diabetes Mellitus
Edema
Fluorescein
Fluorescein Angiography
Inflammation
Injections, Intraperitoneal
Ketamine
Laser Ablation
Mus
Neoplasm Metastasis
Optic Disk
Photoreceptor Cells
Pulse Rate
Retina
Retinal Edema
Rose Bengal
Tail
Tomography, Optical Coherence
Topical Anesthetics
Vascular Endothelial Growth Factors
Veins
Veins, Central Retinal
Vision
Xylazine
Example 4
The expression of RasCQ62L in pten− cells maintained for an additional 16-28 hours resulted in cells that underwent a catastrophic fragmentation and death (
Full text: Click here
Cell Death
Cells
Dictyostelium
Mammals
PTEN protein, human
Signal Transduction
Tears
Trypan Blue
Example 5
TUNEL staining is a marker of cell death. RVO induces TUNEL staining by 24 h in the INL. Retinas were harvested at 48 h from mice treated with Penl-XBIR3 or untreated mice, then processed for immunohistochemistry. Analysis of samples showed that TUNEL positive cells were decreased by Penl-XBIR3 eyedrops and that the eyedrops maintained INL thickness (
Full text: Click here
Cell Death
Cells
Eye Drops
Immunohistochemistry
In Situ Nick-End Labeling
Mus
Retina
Example 9
The ORF encoding the micropeptide of SEQ ID NO: 3 was cloned in frame with the HA epitope tag in the pMSCV retroviral vector. Western blot and qPCR analysis demonstrated that the micropeptide of SEQ ID NO: 3 was successfully expressed after retroviral transduction, and that the protein product was stable (
Importantly, overexpression of the micropeptide of SEQ ID NO: 3 induces massive cell death in cancer cell lines (A549, human lung cancer and HCT116, human colorectal cancer) (
Full text: Click here
Cell Death
Cloning Vectors
Colorectal Carcinoma
Epitopes
Homo sapiens
Lung Cancer
Malignant Neoplasms
Proteins
Reading Frames
Retroviridae
Western Blot
Top products related to «Cell Death»
Sourced in Germany, United States, Switzerland, China, United Kingdom, France, Canada, Belgium, Japan, Italy, Spain, Hungary, Australia
The In Situ Cell Death Detection Kit is a laboratory product designed for the detection of programmed cell death, or apoptosis, in cell samples. The kit utilizes a terminal deoxynucleotidyl transferase (TdT) to label DNA strand breaks, allowing for the visualization and quantification of cell death. The core function of this product is to provide researchers with a tool to study and analyze cell death processes.
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The FACSCalibur is a flow cytometry system designed for multi-parameter analysis of cells and other particles. It features a blue (488 nm) and a red (635 nm) laser for excitation of fluorescent dyes. The instrument is capable of detecting forward scatter, side scatter, and up to four fluorescent parameters simultaneously.
Sourced in Germany, United States, Switzerland, Spain, France, Italy, United Kingdom, China
The Cell Death Detection ELISAPLUS kit is a quantitative in vitro assay used for the detection and quantification of cytoplasmic histone-associated DNA fragments, which are indicative of apoptosis. The kit provides a simple, fast, and reliable method for the measurement of cell death.
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Propidium iodide is a fluorescent dye commonly used in molecular biology and flow cytometry applications. It binds to DNA and is used to stain cell nuclei, allowing for the identification and quantification of cells in various stages of the cell cycle.
Sourced in United States, Germany, Switzerland, Spain, France
The Cell Death Detection ELISA kit is a quantitative in vitro assay for the detection and quantification of DNA fragmentation, a hallmark of apoptosis. The kit uses an enzyme-linked immunosorbent assay (ELISA) technique to detect and measure cytoplasmic histone-associated DNA fragments.
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The FACSCanto II is a flow cytometer instrument designed for multi-parameter analysis of single cells. It features a solid-state diode laser and up to four fluorescence detectors for simultaneous measurement of multiple cellular parameters.
Sourced in Germany, United States, Switzerland
The Cell Death Detection Kit is a laboratory equipment product designed to detect and quantify cell death. It provides a reliable and standardized method for the measurement of apoptosis and necrosis in cell cultures or tissue samples.
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The FACSCalibur flow cytometer is a compact and versatile instrument designed for multiparameter analysis of cells and particles. It employs laser-based technology to rapidly measure and analyze the physical and fluorescent characteristics of cells or other particles as they flow in a fluid stream. The FACSCalibur can detect and quantify a wide range of cellular properties, making it a valuable tool for various applications in biology, immunology, and clinical research.
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The Olympus Fluorescence Microscope is an optical microscope that uses fluorescence to visualize and analyze samples. It illuminates the specimen with light of a specific wavelength, causing fluorescent molecules within the sample to emit light at a different wavelength, which is then detected and displayed.
Sourced in United States, Germany
The In Situ Cell Death Detection Kit is a laboratory product designed to detect and analyze cell death in various biological samples. It provides a sensitive and reliable tool for researchers to assess apoptosis, necrosis, and other forms of programmed cell death during different experimental conditions.
More about "Cell Death"
Cell death is a fundamental biological process that plays a crucial role in development, homeostasis, and disease.
This programmed destruction of cells can take various forms, including apoptosis, necrosis, and autophagy, each with distinct mechanisms and implications.
Understanding cell death pathways is essential for research in areas such as cancer, neurodegenerative disorders, and tissue regeneration.
Optimizing cell death research is crucial, and AI-driven comparative analysis can help identify the best protocols and products.
Tools like the In Situ Cell Death Detection Kit, FACSCalibur flow cytometer, Cell Death Detection ELISAPLUS kit, and Propidium iodide can be used to detect and analyze cell death.
The Cell Death Detection ELISA kit and FACSCanto II are other valuable tools in this field.
By utilizing the power of AI-driven comparisons, researchers can explore a wide range of cell death-related protocols and products from the literature, pre-prints, and patents.
This allows them to identify the most effective and efficient approaches, advancing their knowledge and therapeutic interventions in this critical area of biology.
Synonyms and related terms for cell death include programmed cell death, apoptosis, necrosis, autophagy, cell demise, and cell destruction.
Abbreviations like PCD (programmed cell death) and PtdIns (phosphatidylinositol) are also commonly used.
Key subtopics within cell death research include the molecular mechanisms of cell death, the role of cell death in development and homeostasis, the dysregulation of cell death in disease, and the therapeutic targeting of cell death pathways.
Unlocking the full potential of cell death research through AI-driven comparative analysis is essential for advancing our understanding and developing effective therapies in fields like cancer, neurodegenerative disorders, and tissue regeneration.
Explore the capabilities of tools like the Fluorescence microscope and the Cell Death Detection Kit to take your cell death research to the next level.
This programmed destruction of cells can take various forms, including apoptosis, necrosis, and autophagy, each with distinct mechanisms and implications.
Understanding cell death pathways is essential for research in areas such as cancer, neurodegenerative disorders, and tissue regeneration.
Optimizing cell death research is crucial, and AI-driven comparative analysis can help identify the best protocols and products.
Tools like the In Situ Cell Death Detection Kit, FACSCalibur flow cytometer, Cell Death Detection ELISAPLUS kit, and Propidium iodide can be used to detect and analyze cell death.
The Cell Death Detection ELISA kit and FACSCanto II are other valuable tools in this field.
By utilizing the power of AI-driven comparisons, researchers can explore a wide range of cell death-related protocols and products from the literature, pre-prints, and patents.
This allows them to identify the most effective and efficient approaches, advancing their knowledge and therapeutic interventions in this critical area of biology.
Synonyms and related terms for cell death include programmed cell death, apoptosis, necrosis, autophagy, cell demise, and cell destruction.
Abbreviations like PCD (programmed cell death) and PtdIns (phosphatidylinositol) are also commonly used.
Key subtopics within cell death research include the molecular mechanisms of cell death, the role of cell death in development and homeostasis, the dysregulation of cell death in disease, and the therapeutic targeting of cell death pathways.
Unlocking the full potential of cell death research through AI-driven comparative analysis is essential for advancing our understanding and developing effective therapies in fields like cancer, neurodegenerative disorders, and tissue regeneration.
Explore the capabilities of tools like the Fluorescence microscope and the Cell Death Detection Kit to take your cell death research to the next level.