Monascuspiloin
Based on 1 Customer Validation
Monascuspiloin (Monascinol) is an orally active compound extracted from red mold-fermented rice, with multiple biological activities including anti-androgenic, anti-inflammatory, hypolipidemic, and anti-cancer properties. Monascuspiloin attenuates the PI3K/Akt/mTOR signaling pathway, enhances AMPK phosphorylation, downregulates FASN/SREBP2, induces apoptosis, G2/M phase arrest and autophagy in prostate cancer cells, interferes with dihydrotestosterone-receptor binding, enhances radiation-induced DNA damage, stimulates endoplasmic reticulum stress, and alleviates hepatic oxidative stress. Monascuspiloin regulates hepatic metabolic pathways and modulates the expression of genes and proteins related to hepatic lipid metabolism. Monascuspiloin can be used in studies related to prostate cancer and alcoholic liver injury.
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- Pureté : 95%
- CAS No.: 1011244-19-1
- Formule: C21H28O5
- Masse moléculaire:360.44
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Stockage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Activité biologique
Description
IC50 & Target
[1]|
Caspase 3 |
In Vitro
Monascuspiloin (compound MP) (5-200 μM; 24-48 h) inhibits the viability of both human androgen-dependent LNCaP and androgen-independent PC-3 prostate cancer cells with similar potency, showing IC50 values of 44.97 μM and 46.96 μM respectively after 48 h of treatment[1].
Monascuspiloin (50 μM;6-48 h) induces sub-G0/G1 accumulation (a marker of apoptosis) in human androgen-dependent LNCaP prostate cancer cells and G2/M arrest in human androgen-independent PC-3 prostate cancer cells[1].
Monascuspiloin (50 μM; 48 h) preferentially induces apoptosis in human androgen-dependent LNCaP prostate cancer cells via caspase activation, while only weakly inducing apoptosis in human androgen-independent PC-3 prostate cancer cells[1].
Monascuspiloin (50 μM; 6-48 h) induces apoptosis in human androgen-dependent LNCaP prostate cancer cells via inactivation of the Akt/mTOR pathway, while inducing autophagic and apoptotic cell death in human androgen-independent PC-3 prostate cancer cells via activation of the AMPK pathway[1].
Monascuspiloin (50 μM; 48 h) preferentially induces autophagic cell death in human androgen-independent PC-3 prostate cancer cells, which sensitizes cells to apoptosis, while inducing only minimal autophagy in human androgen-dependent LNCaP prostate cancer cells[1].
Monascuspiloin (MP) (5-45 μM; 48 h) reduces the viability of human prostate cancer PC-3 cells in a concentration-dependent manner[2].
Monascuspiloin (15-25 μM; in combination with ionizing radiation) enhances the radiation sensitivity of human prostate cancer PC-3 cells, reducing clonogenic survival fractions compared to ionizing radiation alone[2].
Monascuspiloin (25 μM; 48 h) enhances ionizing radiation-induced DNA damage in human prostate cancer PC-3 cells, significantly increasing comet tail length compared to either treatment alone; it induces endoplasmic reticulum stress in human prostate cancer PC-3 cells; it inhibits the Akt/mTOR signaling pathway in human prostate cancer PC-3 cells; and it induces autophagy in human prostate cancer PC-3 cells. These effects are significantly enhanced when combined with ionizing radiation[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:5, 25, 50, 100, 200 μM
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Incubation Time:24 h; 48 h
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Result:Significantly decreased cell viability in both LNCaP and PC-3 cells in a concentration- and time-dependent manner.
Exhibited IC50 values of 44.97 μM for LNCaP cells and 46.96 μM for PC-3 cells after 48 h of treatment.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:50 μM
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Incubation Time:12, 24, 48 h
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Result:Raised sub-G0/G1 population and reduced G0/G1 and G2/M fractions in LNCaP cells at 24 h and 48 h.
Slightly elevated sub-G0/G1 proportion and triggered prominent G2/M cell cycle arrest in PC-3 cells across 12 h, 24 h and 48 h.
Upregulated cyclin B and phosphorylated cdc2 in PC-3 cells in a time-dependent manner with no such change in LNCaP cells.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:50 μM
20 μM Z-VAD-FMK (HY-16658B) -
Incubation Time:6, 12, 24, 48 h; 1 h (Z-VAD-FMK pretreatment)
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Result:Triggered time-dependent apoptosis in LNCaP cells verified by DNA fragmentation, elevated Annexin V positivity, activated caspase-3, upregulated pro-apoptotic Bax/Bad and downregulated anti-apoptotic Bcl-2/Bcl-xl.
Pretreatment with Z-VAD-FMK weakened this apoptosis and rescued cell viability in LNCaP cells.
Exerted only weak pro-apoptotic effect on PC-3 cells with negligible shifts in Bax, Bad and Bcl-xl; Z-VAD-FMK failed to reverse the viability decline in PC-3 cells.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:50 μM; 2.5 mM 3-Methyladenine (HY-19312)
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Incubation Time:48 h; 1 h (3-Methyladenine pretreatment)
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Result:Induced autophagy in PC-3 cells, as evidenced by the presence of autophagic vacuoles via electron microscopy, increased AVOs (35% of cells after 48 h), and increased expression of LC3-II, Atg5, and Beclin 1.
Attenuated monascuspiloin-induced autophagy and apoptosis, and reversed cell viability loss in PC-3 cells when pretreated with 3-Methyladenine.
Induced minimal autophagy in LNCaP cells, with only 15% of cells showing AVOs after 48 h of treatment.
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Cell Line:human prostate cancer PC-3 cells
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Concentration:5 μM, 15 μM, 25 μM, 35 μM, 45 μM
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Incubation Time:48 h
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Result:Reduced PC-3 cell viability in a concentration-dependent manner.
Decreased cell viability to 60% at 25 μM for 48 h.
Resulted in significantly lower cell viability at 15, 25, 35, and 45 μM.
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Cell Line:human prostate cancer PC-3 cells
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Concentration:25 μM (alone or in combination with 4 Gy ionizing radiation)
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Incubation Time:48 h
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Result:Upregulated IRE1α and phosphorylated eIF2α expression relative to untreated groups as single treatment.
Amplified the upregulation of the two proteins upon combination with 4 Gy radiation, indicating aggravated ER stress.
Suppressed phosphorylation of Akt, mTOR and p70S6K alone versus untreated controls.
Strengthened the inhibitory effect on the phosphorylation of these kinases under combined 4 Gy irradiation, with total protein expression unaltered.
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Cell Line:human prostate cancer PC-3 cells
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Concentration:25 μM (alone or in combination with 4 Gy ionizing radiation)
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Incubation Time:48 h
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Result:Raised the proportion of acridine orange-positive AVOs to roughly 22% as single agent, matching the effect of separate 4 Gy irradiation.
Boosted the percentage of AVOs to approximately 42% under combined treatment with 4 Gy radiation, far exceeding single treatment groups.
Triggered abundant autophagic vacuoles and autolysosomes in co-treated cells without apoptotic chromatin condensation.
Upregulated LC3-II, p62/SQSTM1 and Atg5-12 expression after combined 4 Gy radiation exposure versus individual treatments.
In Vivo
Monascuspiloin (MP) (1 mg/kg; three times per week; for 2 weeks) alone inhibits the growth of prostate tumors in nude mice; when combined with 6 Gy ionizing radiation, it increases the tumor growth inhibition rate and significantly prolongs the tumor growth delay time[2].
Monascuspiloin (10 mg/kg; p.o.; once daily; for 6 consecutive weeks) alleviates alcoholic liver injury in male Kunming mice by improving liver function, reducing oxidative stress, regulating lipid metabolism, restoring intestinal flora balance, modulating hepatic metabolic pathways, and regulating hepatic gene and protein expression[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/C-nu/nu nude mice (male, 5 weeks old)[1]
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Dosage:40 mg/kg; 120 mg/kg
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Administration:i.p.; 3 times weekly; 6 total injections
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Result:Inhibited tumor growth dose-dependently by 63% and 74% on day 18, lengthened tumor quadrupling and growth delay time, reduced tumor weight, suppressed proliferation marker PCNA, activated apoptosis via cleaved caspase 3, upregulated multiple autophagy proteins, and caused no weight loss or evident toxicity.
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Animal Model:BALB/cAnN.Cg-Foxn1nu/CrlNarl (male, 6-8 weeks old, subcutaneous injection of 2×106 PC-3 human prostate cancer cells)[2]
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Dosage:1 mg/kg (monotherapy); 1 mg/kg (combined with 6 Gy ionizing radiation)
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Administration:three times per week; 2 weeks
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Result:Inhibited tumor growth by 42.5% on day 10, prolonging tumor volume quadrupling time to 20.7 days and growth delay to 10.4 days.
Enhanced antitumor effect with 6 Gy radiation to 71.4% inhibition, extending quadrupling time to 62.6 days and delay to 52.3 days.
Reduced tumor weight more effectively than single treatment alone.
Elevated LC3 and p62 levels in tumor tissues versus monotherapy groups.
Caused no weight loss and exhibited no obvious systemic toxicity.
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Animal Model:Kunming mice (male, six-week-old, specific pathogen-free)[3]
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Dosage:10 mg/kg
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Administration:p.o.; daily; 6 weeks
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Result:Corrected alcohol-caused weight loss and lowered elevated liver index by 13.01%.
Lowered serum TC, TG, LDL-C, ALT and AST while raising serum HDL-C.
Decreased hepatic TC, BAs, MDA and LDH, and boosted hepatic GSH, CAT, SOD and ADH.
Alleviated hepatic steatosis and ameliorated liver pathological lesions.
Elevated multiple fecal short-chain fatty acids and repaired alcohol-triggered intestinal mucosal injury.
Regulated the relative abundance of multiple intestinal flora genera.
Remodeled 75 hepatic metabolites and interfered with several key metabolic pathways.
Modulated the transcription of lipid metabolism, detoxification, antioxidant and inflammatory-related genes.
Upregulated LDLr, CPT-1, Nrf-2, NQO1 and HO-1 protein expression and suppressed SREBP-1 protein level.
Chemical Information
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CAS No. 1011244-19-1
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Appearance Solid
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Masse moléculaire 360.44
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Formule C21H28O5
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Color Yellow to orange
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SMILES
C[C@]12[C@@](CC3=C(COC(/C=C/C)=C3)C2=O)([H])[C@H](C(O1)=O)[C@@H](O)CCCCC
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Synonyms
Monascinol
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Structure Classification
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Initial Source
Monascus pilosus BCRC 38093-FERMENTED RICE
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protocole
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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Autophagy
Autophagy is a process in which eukaryotic cells use lysosomes to degrade their own cytoplasmic proteins and damaged organelles under the regulation of autophagy related gene (Atg). Microtubule-associated proteins light chain 3 (LC3) is recognized as autophagy marker, which transfers from cytoplasmic LC3 (LC3-I) to membrane type (LC3-II). LC3-II/I ratio could be detected by Western Blot and fluorescence microscopy.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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Lysosome and acidic-vesicle live-cell staining
Lysosome and acidic-vesicle live-cell staining detects acidic intracellular compartments by using membrane-permeant acidotropic probes that accumulate in low-pH vesicles, including lysosomes, late endosomes, autolysosomes, and acidic phagosomes. LysoTracker staining is commonly used as an intensity-based readout of acidic lysosomal compartment abundance or enlargement, while acridine orange produces green fluorescence in less concentrated compartments and red fluorescence after concentration-dependent accumulation in acidic vesicular organelles. Loss or reduction of acridine-orange red signal can be used as a readout of lysosomal membrane permeabilization or reduced acidic-vesicle integrity. This protocol is designed for live cultured cells and can be adapted for fluorescence microscopy, high-content imaging, plate-reader readout, or flow cytometry when the selected literature supports the readout. Because these dyes report acidotropic accumulation rather than lysosome identity alone,
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Macroautophagy Solutions
Macroautophagy is a conserved lysosome-dependent degradation pathway in which cytoplasmic material is sequestered into double-membrane autophagosomes and delivered to lysosomes for degradation and recycling. The pathway supports cellular homeostasis during nutrient limitation, organelle stress, protein-aggregate accumulation, infection, differentiation, and tissue remodeling by coupling cargo sequestration, autophagosome maturation, lysosomal fusion, and degradation of cargo-derived macromolecules. The core molecular sequence includes initiation by nutrient- and stress-regulated autophagy machinery, autophagosome nucleation, LC3/ATG8-family conjugation to autophagosomal membranes, cargo selection through receptors such as SQSTM1/p62, autophagosome-lysosome fusion, and lysosomal degradation. LC3 was identified as a mammalian homolog of yeast Atg8 that localizes to autophagosomal membranes after processing, and p62/SQSTM1 was shown to connect ubiquitinated cargo with autophagic degradati
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Pureté et documentation
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Fiche technique (297 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
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- Italian - IT (254 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Chen RJ, et al. Monascuspiloin induces apoptosis and autophagic cell death in human prostate cancer cells via the Akt and AMPK signaling pathways. Journal of agricultural and food chemistry. 2012 Jul 25;60(29):7185-93. [Content Brief]
[2]. Chiu HW, et al. Monascuspiloin enhances the radiation sensitivity of human prostate cancer cells by stimulating endoplasmic reticulum stress and inducing autophagy. PloS one. 2012;7(7):e40462. [Content Brief]
[3]. Wu L, et al. Monascuspiloin from -Fermented Red Mold Rice Alleviates Alcoholic Liver Injury and Modulates Intestinal Microbiota. Foods (Basel, Switzerland). 2022 Sep 30;11(19):3048. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)