Necrostatin, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
Average 94 stars, based on 7 article reviews
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1) Product Images from "Modulation of P2X 4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death"
Article Title: Modulation of P2X 4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death
Journal: Scientific Reports
Figure Legend Snippet: Ivermectin kills breast cancer cells through a mixed apoptotic and necrotic mechanism. ( A ) Mouse (4T1.2) and human (MDA-MB-231) TNBC cells manifest similar sensitivity to Ivermectin. Viability of cells treated with various doses of Ivermectin for 24 h. ( B ) Extended exposure time reduces IC50 values to as low as 2 μM. 4T1.2 cells were seeded at 100 cells/well and individual colonies were counted after a week. Cancer cells were exposed to Ivermectin during the initial 24 h or during the entire duration of the assay. ( C ) MDA-MB-231 breast cancer cells manifest higher sensitivity to Ivermectin compared to normal non-transformed human foreskin fibroblasts (HFFs). ( D ) Flow cytometry analysis showing that cell death proceeds through two distinct pathways: a directly necrotic 7AAD-single positive or Annexin V/PS-single positive apoptotic pathway. ( E ) Kinetics of necrotic versus apoptotic killing of 4T1.2 breast cancer cells. ( F ) Ivermectin-induced cell death can be reversed by inhibition of various controlled cell death pathways. 4T1.2 cells were treated for 4 h with 32 μM Ivermectin in the presence of μM concentrations of Z-vad-fmk, Necrostatin-1, Digoxin, or VX-765, as indicated. ( G ) Activation of Caspase-1, Caspase-3 and cleavage of PARP in 4T1.2 and MDA-MB-231 cells treated with 32 μM for 4h. Asterisk (*) indicates p
Techniques Used: Multiple Displacement Amplification, Transformation Assay, Flow Cytometry, Cytometry, Inhibition, Activation Assay
2) Product Images from "Persistent Mitochondrial Hyperfusion Promotes G2/M Accumulation and Caspase-Dependent Cell Death"
Article Title: Persistent Mitochondrial Hyperfusion Promotes G2/M Accumulation and Caspase-Dependent Cell Death
Journal: PLoS ONE
Figure Legend Snippet: Mitochondrial Hyperfusion Promotes Caspase 8 Dependent Cell Death. (A-C) U2OS cells were transfected with control (black), Drp1 (green), or Mff (red) siRNA for 96 hours. Cells were collected and stained for (A) cleaved caspase 3 or (B) cleaved caspase 8. Positivity of cleaved caspase 3 or 8 is indicated by an increase in fluorescence on the FACS histogram compared to control. (C) U2OS cells transfected with control, Drp1, or Mff siRNAs were treated with pan caspase inhibitor, zVAD (20 μM; dark gray bars), or the necroptosis inhibitor, necrostatin (10 μM; light gray bars), or vehicle (DMSO; black bars) every 24 hours for 96 hours following transfection. Cells were stained with propidium iodide (PI) and percent PI positivity was used as a marker of cell death. Error bars represent standard deviation from two replicate experiments where at least 10,000 events were collected for each treatment.
Techniques Used: Transfection, Staining, Fluorescence, FACS, Marker, Standard Deviation
3) Product Images from "Altered Mitochondria Morphology and Cell Metabolism in Apaf1-Deficient Cells"
Article Title: Altered Mitochondria Morphology and Cell Metabolism in Apaf1-Deficient Cells
Journal: PLoS ONE
Figure Legend Snippet: Caspase-independent cell death in SV40IM Apaf1 KO cells. (A) Cell survival was measured by the trypan blue exclusion assay in SV40IM and SIM MEFS, WT and Apaf1-depleted cells in the presence of etoposide (5 µM) for 24 h. (B) Caspase-3-like activity was measured under the same etoposide treatment conditions (+; 5 µM) described above. In all cases, bars represent the mean of three experiments ± s.d. (C) Cell survival was measured in the SV40IM cell lines treated with etoposide (5 µM) in the presence or the absence of z-VAD (5 µM), necrostatin (Nec; 100 µM) or SVT016426 (10 µM). (mean ± s.d, n = 3, * p ≤0.05). (D) DAPI staining to analyse the apoptotic features between WT and Apaf1 KO cells in the presence of etoposide (5 µM). In all, 500 nuclei were counted and classified according to apoptotic nuclear bodies (white arrows). Quantification is shown in the right panel. (E) Cell survival was measured by the trypan blue exclusion assay in the HeLa cells transfected with random siRNA (Rsi) or Apaf1 siRNA (Asi) for 24 h and treated with etoposide (+; 5 µM) for another 24-hour period. (F) Caspase-3-like activity was measured under the same conditions described above. Bars represent the mean of three experiments ± s.d. The immunoblotting of the Apaf1 silencer is shown in the right panel.
Techniques Used: Trypan Blue Exclusion Assay, Activity Assay, Staining, Transfection