What is mitochondrials? and the mechanism of its cells.

Researchers at UT Southwestern Medical Center have found that cells are used to detect and destroy the mechanisms of a cell called mitochondrials, which, when damaged, can lead to genetic problems such as cancer, neurodegenerative diseases, inflammatory diseases and aging.
Dr. Beth Levine, director of the UT Southwest Automation Research Center, and Dr. Beth Levine, senior author of the study, found in Cell, published today, that understanding how this process works may lead to new treatments to prevent certain diseases and even aspects of aging.
Autophagy Research Center is the only autophagy research center in the country that studies a process called autophagy, in which cells remove damaged or unnecessary parts.
mitochondrials are often referred to as "cell power chambers" because these cellular groups, like small factories within cells, convert compounds such as sugar into energy that cells can use.
mitochondrials also have a dark side: because of their high energy function, when they are damaged, they release toxic chemicals called reactive oxygen into the rest of the cell.
, a professor of internal medicine and microbiology and a researcher at the Howard Hughes Institute of Medicine, said: "The removal of damaged mitochondrials (a process called mitochondrials) through autophagy is important for cell health." "Researchers have focused on protein "labels" found on mitochondrial outer membranes -- especially the protein Parkin attached to these labels -- to explain the cell's degradation cells, called autophages, which target pathological mitochondrials," explains Dr.
Levine.
study, researchers found that a protein called prohibitin 2 (PHB2) was present in the endometrial of the mitochondrial, but was exposed when the outer membrane of a toxic mitochondrial ruptured.
LC3 protein adheres to PHB2, and autophagy carries its injected cargo into the lysosome, another cell device found in the cell, which acts like a tiny stomach and has an enzyme that breaks down cell waste.
Levine said: "This study found that PHB2 is critical to target mitochondrial autophagy degradation."
, she said, "previous studies have linked the presence of PHB2 to the prevention of cancer, aging effects, neurodegeneration and inflammation."
, given these beneficial health effects, it makes sense that the key role of PHB2 is to help rid cell-damaged mitochondrials and promote the disease process.
Levine said: "By understanding how cells remove damaged mitochondrials that contribute to cancer, neurodegenerative diseases and aging, we can develop treatments to prevent these processes."
study also found that PHB2 was necessary to routinely eliminate the parent mitochondrial DNA from a developing embryo, leaving only mitochondrial DNA from the mother.
work was carried out in ticks, but a recent study using mouse models elsewhere showed that mitochondrials were also used to remove python mitochondrials from mammalian embryos.
usually, only matrilineal mitochondrial DNA is passed on to future generations," dr. Levine said.
for unknown reasons, the continued presence of parent mitochondrial DNA indicates genetic or health problems in children.
other finding, the UTSW study showed that Parkin still needed to do so, despite scientists' increased interest in the role of parkin protein in supporting autophagy PHB2.
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