Schlagwort: mitochondria
EU funds groundbreaking research on mitochondria in Potsdam
Fuelling nerve cell function and plasticity
How minimal genetic differences can turn healthy food into a deadly danger
Cell biology: How cellular powerhouses call for help when under stress
Unraveling the protein map of cell’s powerhouse – Study provides insight into organization of proteins in mitochondria
Mitochondria produce antioxidants to protect our cells from dying
Antioxidants are often advertised as a cure-all in nutrition and offered as dietary supplements. However, our body also produces such radical scavengers itself, one of which is coenzyme Q. Now researchers from the Max Planck Institute for Biology of Ageing have discovered how the substance, which is produced in our mitochondria, reaches the cell surface and protects our cells from dying.
Formation of pores in mitochondrial membrane elucidated
• Similarities to wine barrel structure – protein subunits Sam50 and Sam37 play central roles
• Substances are exchanged between mitochondria and the cell water through the barrel pores
How calcium ions get into the cellular power stations of plants
Scientists discover how mitochondria import antioxidants
DNA building blocks regulate inflammation
New form of symbiosis discovered
One in five brain cancers fueled by overactive mitochondria
Mitochondria and the evolutionary roots of cancer
Cancer is a group of almost 200 diseases that involve variety of changes in cell structure, morphology, and physiology. Cancer phenotype is underlying several alterations in cellular dynamics with three most critical features, which includes self-sufficiency in growth signals and insensitivity to inhibitory signals, evasion of programmed cell death and limitless replicative potential with a potential for the invasion of other organs. Cancer disease is widespread among metazoans. Some properties of cancer cells such as uncontrolled cell proliferation, lack of apoptosis, hypoxia, fermentative metabolism and free cell motility, i.e. metastasis, resemble a prokaryotic lifestyle, which leads to the assumption of a reversal like evolution from eucariotic back to proteobacterial state. This phenotype matches the phenotype of the last universal common ancestor (LUCA) that resulted from the endosymbiosis between archaebacteria and α-proteobacteria, which later became the mitochondria.
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine
Progressive increase in mtDNA 3243A>G heteroplasmy causes abrupt transcriptional reprogramming
Wallace hypothesized mitochondrial dysfunction as a central role in a wide range of age-related disorders and various forms of cancer. Steadily rising increases in mitochondrial DNA mutations cause abrupt shifts in diseases. Discrete changes in nuclear gene expression in response to small increases in DNA mutant level are analogous to the phase shifts that is well known in physics: As heat is added, the ice abruptly turns to water or with more heat abruptly to steam. Therefore, a quantitative change that is an increasing proportion of mitochondrial DNA mutation results in a qualitative change which coordinate changes in nuclear gene expression together with discrete changes in clinical symptoms.