DePsipher Mitochondrial Potential Kit
DePsipher Mitochondrial Potential Kit Summary
• Simple addition of DePsipher Reagent to media or reaction buffer.
• Unique Stabilizer Solution improves results.
• Assay takes only 20 minutes.
• Compatible with epifluorescence, confocal microscopy, or flow cytometry analysis.
Why Use the DePsipher Mitochondrial Potential Kit?
In the intrinsic apoptosis pathway, mitochondrial permeability transition is an important event wherein the electrochemical gradient (referred to as delta-psi or delta Ψm) across the mitochondrial membrane collapses. This collapse occurs through the formation of channels or pores in the outer mitochondrial membrane, which involves Bax insertion and oligomerization, followed by the release of Cytochrome C into the cytoplasm.
The DePsipher Kit uses a unique cationic dye (5,5’6,6’-tetrachloro-1,1’,3, 3’-tetraethylbenzimidazolyl- carbocyanine iodide) to indicate the loss of delta Ψm. The dye readily enters cells and fluoresces brightly red in its multimeric form within healthy mitochondria. In apoptotic cells, the mitochondrial membrane potential collapses, and the DePsipher reagent cannot accumulate within the mitochondria. In these cells, DePsipher returns to its green fluorescent monomeric form. Apoptotic cells, showing primarily green fluorescence, are thus easily differentiated from healthy cells which show red fluorescence. The aggregate red form has absorption/emission maxima of 585/590 nm, and the green monomeric form has absorption/emission maxima of 510/527 nm. Both apoptotic and healthy cells can be visualized simultaneously by epifluorescence microscopy using a wide band-pass filter. The DePsipher reagent is easy to use. Simply resuspend the reagent in reaction buffer or culture media (with or without the stabilizer solution), add to your cells, incubate for 15 to 20 minutes, wash and analyze by flow cytometry or microscopy. Visualization by microscopy allows a rapid inspection and qualification of apoptosis. Flow cytometric analysis allows easy quantitation of cell death as evidenced by mitochondrial potential breakdown.
• 10X Reaction Buffer
• Stabilizer Solution
For research use only. Not for diagnositic use.
Citations for DePsipher Mitochondrial Potential Kit
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
Citations: Showing 1 - 10
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Cytoprotective Effects of N-Acetylcysteine on Streptozotocin- Induced Oxidative Stress and Apoptosis in RIN-5F Pancreatic ?-Cells
Authors: AMT Al-Nahdi, A John, H Raza
Cell. Physiol. Biochem., 2018;51(1):201-216. 2018
In vitro antiglioma action of indomethacin is mediated via AMP-activated protein kinase/mTOR complex 1 signalling pathway
Authors: Aleksandar Pantovic
Int. J. Biochem. Cell Biol, 2016;0(0):. 2016
Potentiation of LPS-Induced Apoptotic Cell Death in Human Hepatoma HepG2 Cells by Aspirin via ROS and Mitochondrial Dysfunction: Protection by N-Acetyl Cysteine
PLoS ONE, 2016;11(7):e0159750. 2016
Inhibition of mTOR-dependent autophagy sensitizes leukemic cells to cytarabine-induced apoptotic death.
Authors: Bosnjak M, Ristic B, Arsikin K, Mircic A, Suzin-Zivkovic V, Perovic V, Bogdanovic A, Paunovic V, Markovic I, Bumbasirevic V, Trajkovic V, Harhaji-Trajkovic L
PLoS ONE, 2014;9(4):e94374. 2014
Obesity is associated with increased seminal insulin and leptin alongside reduced fertility parameters in a controlled male cohort.
Authors: Leisegang K, Bouic P, Menkveld R, Henkel R
Reprod Biol Endocrinol, 2014;12(0):34. 2014
Idarubicin induces mTOR-dependent cytotoxic autophagy in leukemic cells.
Authors: Ristic B, Bosnjak M, Arsikin K, Mircic A, Suzin-Zivkovic V, Bogdanovic A, Perovic V, Martinovic T, Kravic-Stevovic T, Bumbasirevic V, Trajkovic V, Harhaji-Trajkovic L
Exp Cell Res, 2014;326(1):90-102. 2014
NAC attenuates LPS-induced toxicity in aspirin-sensitized mouse macrophages via suppression of oxidative stress and mitochondrial dysfunction.
Authors: Raza H, John A, Shafarin J
PLoS ONE, 2014;9(7):e103379. 2014
Estrogenic compounds are not always cardioprotective and can be lethal in males with genetic heart disease.
Authors: Haines, Christop, Harvey, Pamela A, Luczak, Elizabet, Barthel, Kristen, Konhilas, John P, Watson, Peter A, Stauffer, Brian L, Leinwand, Leslie A
Endocrinology, 2012;153(9):4470-9. 2012
Implications of altered glutathione metabolism in aspirin-induced oxidative stress and mitochondrial dysfunction in HepG2 cells.
Authors: Raza H, John A,
PLoS ONE, 2012;7(4):e36325. 2012
The dietary flavonol fisetin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells.
Authors: Szliszka E, Helewski KJ, Mizgala E, Krol W
Int. J. Oncol., 2011;39(4):771-9. 2011
Opposite effects of nanocrystalline fullerene (C(60)) on tumour cell growth in vitro and in vivo and a possible role of immunosupression in the cancer-promoting activity of C(60).
Authors: Zogovic NS, Nikolic NS, Vranjes-Djuric SD, Harhaji LM, Vucicevic LM, Janjetovic KD, Misirkic MS, Todorovic-Markovic BM, Markovic ZM, Milonjic SK, Trajkovic VS
Biomaterials, 2009;30(36):6940-6. 2009
Lysophosphatidic acid-induced nuclear localization of protein kinase C delta in bovine theca cells stimulated with luteinizing hormone.
Authors: Budnik LT, Mukhopadhyay AK
Biol. Reprod., 2002;67(3):935-44. 2002
Autophagy sustains mitochondrial glutamine metabolism and growth of BrafV600E-driven lung tumors.
Authors: Strohecker A, Guo J, Karsli-Uzunbas G, Price S, Chen G, Mathew R, McMahon M, White E
Cancer Discov, 0;3(11):1272-85. 0
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