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| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| 2656- | AL, | Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics |
| - | in-vitro, | Park, | PC12 |
| 5680- | BML, | Anticancer properties of bromelain: State-of-the-art and recent trends |
| - | Review, | Var, | NA |
| 3507- | Bor, | Boron inhibits apoptosis in hyperapoptosis condition: Acts by stabilizing the mitochondrial membrane and inhibiting matrix remodeling |
| 5943- | Cela, | Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases |
| - | Review, | Arthritis, | NA | - | Review, | IBD, | NA | - | Review, | AD, | NA | - | Review, | Park, | NA |
| 2807- | CHr, | Evidence-based mechanistic role of chrysin towards protection of cardiac hypertrophy and fibrosis in rats |
| - | in-vivo, | Nor, | NA |
| 3580- | CUR, | Curcumin Acts as Post-protective Effects on Rat Hippocampal Synaptosomes in a Neuronal Model of Aluminum-Induced Toxicity |
| - | in-vivo, | AD, | NA |
| 3205- | EGCG, | The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas |
| - | Review, | Var, | NA | - | Review, | AD, | NA |
| 2904- | LT, | Luteolin from Purple Perilla mitigates ROS insult particularly in primary neurons |
| - | in-vitro, | Park, | SK-N-SH | - | in-vitro, | AD, | NA |
| 3263- | Lyco, | Lycopene protects against myocardial ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening |
| - | in-vitro, | Nor, | H9c2 | - | in-vitro, | Stroke, | NA |
| 3587- | PI, | Piperine: A review of its biological effects |
| - | Review, | Park, | NA | - | Review, | AD, | NA |
| - | in-vivo, | IBD, | NA |
| 3192- | SFN, | Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention |
| - | in-vitro, | Pca, | PC3 |
| 2448- | SFN, | Sulforaphane and bladder cancer: a potential novel antitumor compound |
| - | Review, | Bladder, | NA |
| 3313- | SIL, | Silymarin attenuates post-weaning bisphenol A-induced renal injury by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 signaling modulation in male Wistar rats |
| - | in-vivo, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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