Mitochondrial

7 products

Apoptosis is an evolutionarily conserved form of cell suicide; the central component of this process is a cascade of proteolytic enzymes called caspases. These enzymes are triggered in response to pro-apoptotic signals, causing the disassembly of the cell.

The loss of mitochondrial membrane potential is a hallmark for apoptosis. The mitochondrial permeability transition is an important step in the induction of cellular apoptosis. During this process, the electrochemical gradient across the mitochondrial membrane collapses. The collapse is thought to occur through the formation of pores in the mitochondria by dimerized Bax or activated Bid, Bak, or Bad proteins. Activation of these pro-apoptotic proteins is accompanied by the release of cytochrome C into the cytoplasm.

ICT carries several cell membrane permeant dyes with the capability of being retained within an active (polarized) mitochondrial membrane, and subsequently released upon loss of mitochondrial membrane gradient potential.

Showing 1 - 7 of 7 products

Figure 1. Jurkat cells were stimulated with Staurosporine for 3 hours (B) or DMSO (A). Mito Flow reagent was added according to the protocol, incubated for 30 minutes and analyzed by flow cytometry: Ex:488nm Em: FL2 channel.

ImmunoChemistry Technologies Mito Flow - Mitochondrial membrane potential detection kit

From $279

Figure 1. Jurkat cells were stimulated with staurosporine (B) or DMSO (A), then stained according to the kit protocol. The cells were washed twice and analyzed by flow cytometry: Ex:488nm Em: FL1 and FL2. A. Healthy cells show a strong red fluorescence (intact mitochondria) and no green fluorescence (no active caspases). B. Apoptotic cells show a loss of red fluorescence (y axis) due to loss of mitochondrial membrane potential and positive green fluorescence (x axis) indicating active caspases.

Figure 2. HeLa Cells activated with staurosporine (B) or DMSO (A), then stained according to the kit protocol. The cells were washed twice and analyzed by flow cytometry: Ex:488nm Em: FL1 and FL2. A. Healthy cells show a strong red fluorescence (intact mitochondria) and no green fluorescence (no active caspases). B. Cells becoming apoptotic show loss of red fluorescence (y axis) due to loss of mitochondrial membrane potential and positive green fluorescence (x axis) indicating active caspases.

ImmunoChemistry Technologies Dual Caspase 1 and Mitochondrial Membrane Potential Assay Kit

From $189

ImmunoChemistry Technologies Dual Caspase 3/7 and Mitochondrial Membrane Potential Assay Kit

From $189

ImmunoChemistry Technologies Dual Poly Caspase and Mitochondrial Membrane Potential Assay Kit

From $189

Figure 1. Jurkat cells were exposed to DMSO as the negative control (dark orange bars) or 50 µM CCCP depolarizing agent (light orange bars) and then incubated with TMRE or TMRM. Aliquots (100 µL) were analyzed in triplicate in a black 96-well plate using a fluorescence plate reader (550 nm excitation and 580 nm emission using a 570 nm cut-off filter). Healthy control cells had a high level of orange fluorescence compared to the CCCP-treated cells. (Ms. Tracy Hanson, ICT).

Figure 2. Jurkat cells were treated with DMSO (control) (A) or staurosporine (B), and then dually stained with TMRM and the green FLICA® poly caspase probe FAM-VAD-FMK (cat. 92) and analyzed by flow cytometer. In the staurosporine-treated cells (B), there is loss of orange fluorescence (FL-2) and a concurrent increase in cell-bound green fluorescence (FL-1) due to caspase activation. Treatment with staurosporine induced apoptosis in about 90% of cells (Ms. Tracy Hanson, ICT).

ImmunoChemistry Technologies TMRM - Orange Fluorescent Mitochondrial Membrane Depolarization Assay

$290

Figure 1. Jurkat cells were treated with DMSO (negative control) or 1 µM staurosporine to induce apoptosis, then stained with TMRE, and photographed using a photomicroscope using a green excitation filter at 510-560 nm and a 570-620 nm emission filter (left). Healthy cells, containing mitochondria with polarized inner membranes fluoresce bright orange (A) compared with apoptotic cells with depolarized mitochondria(B). The corresponding DIC images are shown (right) (Dr. Brian Lee, ICT).

Figure 2. Jurkat cells were exposed to DMSO as the negative control (dark orange bars) or 50 µM CCCP depolarizing agent (light orange bars) and then incubated with TMRE or TMRM. Aliquots (100 µL) were analyzed in triplicate in a black 96-well plate using a fluorescence plate reader (550 nm excitation and 580 nm emission using a 570 nm cut-off filter). Healthy control cells had a high level of orange fluorescence compared to the CCCP-treated cells. (Ms. Tracy Hanson, ICT).

ImmunoChemistry Technologies TMRE - Orange Fluorescent Mitochondrial Membrane Depolarization Assay

$290

Figure 1. Jurkat cells were treated with DMSO (negative control) or 1 µM staurosporine for 2 hours to induce apoptosis. Cells were then stained with JC-1 dye. Normal healthy cells (two cells, upper and lower left) concentrate JC-1 in mitochondria and fluoresce bright orange. Apoptotic cells (three cells, right), with mitochondria of various stages of permeability, exhibit a reduced orange fluorescence and increased green fluorescence, as JC-1 disperses through the cells. (Dr. Brian Lee, ICT).

Figure 2. Jurkat and HL-60 cells were exposed to DMSO (negative control) (dark orange) or 50 μM CCCP depolarizing agent (light orange) and then incubated with JC-1 for 20 minutes at 37°C, and washed. Aliquots were analyzed in triplicate in a fluorescence plate reader set at 488 nm excitation and 590 nm emission filter settings. Healthy cells exhibited a high level of orange fluorescence; the CCCP-depolarized cells had reduced orange fluorescence as the dye dispersed. (Ms. Tracy Hanson, ICT)

ImmunoChemistry Technologies JC-1 Fluorescent Mitochondrial Membrane Depolarization Assay

From $226

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Mitochondrial

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