| 包装 | 价格(元) |
| 100mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
Cell lines | HL-7702 cells |
Preparation Method | HL-7702 cells were treated with DMSO, gefitinib, CCCP for 24 h or starved with HBSS for 3 h. |
Reaction Conditions | 20 μM CCCP for 24 h |
Applications | Mitochondrial inducer carbonyl cyanide m-chlorophenizone (CCCP) activates mitophagy. CCCP failed to selectively reduce COX6A1 levels. |
| 产品描述 | Carbonylcyanide-3-chlorophenylhydrazone (CCCP) is a protonophore, which causes uncoupling of proton gradient in the inner mitochondrial membrane, thus inhibiting the rate of ATP synthesis. CCCP inhibits STING-mediated IFN-β production via disrupting mitochondrial membrane potential (MMP). In HL-7702 cells, Mitochondrial inducer CCCP activates mitophagy. CCCP failed to selectively reduce COX6A1 levels[1]. CCCP alone significantly increased chondrocyte apoptosis treatment with CCCP and eugenol significantly decreased chondrocyte apoptosis, suggesting that eugenol reduces CCCP-induced apoptosis. Our results showed that eugenol significantly the CCCP-induced mitochondrial membrane potential changes[4].CCCP inhibits activation of STING and its downstream signaling molecules, TBK1 and IRF3, but not STING translocation to the perinuclear region. CCCP down-modulates the STING pathway through DRP1-mediated mitochondria fragmentation[3].Cultured human osteosarcoma cells were imaged to visualize changes of mitochondrial membrane potential, morphology, and permeability transition. during treatment with a protonophore, CCCP. Cells rapidly exhibited mitochondrial permeability transition and swelling after addition of CCCP, but the swelling subsided within hours, leaving mitochondria that appeared in punctate form[5]. CCCP -induced mitochondrial fission inhibited IFN-β expression supporting the idea that mitochondrial dynamics modulated activation of STING signaling Mitochondrial dynamics regulated by MFN1 MFN2 and OPA1 mediated fusion and DRP1 and TBC1D15-mediated mitochondrial fission[8].The mitochondrial homeostasis of a carp fish Megalobrama amblycephala was investigated systematically in a time-course manner by using CCCP. CCCP treatment resulted in the imbalance of mitochondrial homeostasis in Megalobrama amblycephala by promoting mitochondrial oxidative stress, fission and mitophagy, but depressing mitochondrial fusion, biogenesis and function[9].The proton ionophore CCCP inhibited antigen-stimulated secretion and calcium influx in rat basophilic leukemia cells[6].The protonophore CCCP suppressed DMXAA-induced type I IFN production through dissipation of mitochondria membrane potential (MMP)[7].In combination with starvation and CCCP, damaged mitochondria in GC-1 cell lines overexpressing Spata33 were phagocytosed by autophagosomes, in which damaged mitochondria were degraded[2]. References: |
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