Articles tagged with Mitochondrial Proteins
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A team of scientists at Karolinska Institutet has identified a key component in mitochondria's function, which combines with another protein to control ribosome formation and energy production. The discovery sheds light on the regulation mechanisms involved in inherited and age-related diseases.
Researchers at Emory University School of Medicine found that a protein called MEF2D plays a key role inside mitochondria in brain cells, and its impairment is linked to Parkinson's disease progression. The study suggests that problems with MEF2D could represent one of the earliest steps in neurodegeneration.
Researchers have identified a link between mitochondrial fusion and a cell death pathway, with implications for treating heart disease and stroke. The study found that the proteins MFN1 and MFN2 regulate mitochondrial behavior, promoting or preventing apoptosis, depending on their combination.
Scientists at IRB Barcelona have identified a new protein crucial for mitochondrial function in the fruit fly Drosophila melanogaster. The removal of this protein leads to aberrant mitochondria and metabolic capacity loss, causing death.
A study published in Neuron reveals that the loss of Nna proteins causes mitochondrial dysfunction, leading to severe cell death in mice and fly models. Researchers believe this discovery could provide insights into human neurodegenerative disorders like Parkinson's disease.
Mutations in Parkin cause Parkinson's disease by preventing the clearance of defective mitochondria. Cells expressing mutant Parkin fail to clear damaged mitochondria through mitophagy, a specialized autophagic pathway. This leads to the accumulation of toxic protein aggregates and neurodegeneration.
Researchers at the Gladstone Institutes discovered that SIRT3 plays a crucial role in regulating fatty acid oxidation and identified it as a potential therapeutic target. Mice lacking SIRT3 exhibited impaired fat burning and increased levels of fat and triglycerides, highlighting the enzyme's importance in energy metabolism.
A University of Florida team has identified a protein that contributes to age-related hearing loss in the elderly. The findings suggest that enhancing antioxidant defenses may reduce damage and delay onset of hearing loss, offering new targets for therapy.
Scientists have developed a revolutionary technology to analyze protein mixtures, revealing a key enzyme that stabilizes proteins in mitochondria. This breakthrough has significant implications for fundamental research on proteins and their roles in cell function.
Researchers at Karolinska Institutet discovered unstable proteins cause premature ageing by impairing cell respiration. Changes in mtDNA introduce errors into mitochondrial proteins, leading to their instability and breakdown.
Researchers at Karolinska Institutet have discovered a new function for a protein essential to mitochondrial protein synthesis, which plays a key part in cell respiration. Without this protein, mitochondria cannot produce proteins and cellular respiration is impaired.
Researchers found that beta-amyloid protein generates nitric oxide, which attacks and damages mitochondria in neurons. This damage leads to synaptic injury and eventual nerve cell death, contributing to Alzheimer's disease progression.
Scientists have created a comprehensive 'parts list' to date for mitochondria, including nearly 1,100 proteins, with insights gained into the biological roles and evolutionary histories of key proteins. The researchers identified a mutation in a novel gene as the cause behind one devastating mitochondrial disease.
Researchers found that Bak protein breaks down mitochondria into vulnerable spheres, allowing Bax to poke holes and release pro-death contents. This discovery sheds light on the mechanisms of programmed cell death (apoptosis) and its potential role in diseases like stroke and cancer.
Scientists at St. Jude Children's Research Hospital have discovered that a key event during apoptosis occurs as a single, rapid event, rather than a step-by-step process. This finding sheds new light on how cells 'commit suicide' and highlights the importance of mitochondrial outer membrane permeabilization in regulating apoptosis.
A 50-amino-acid stretch of the amyloid precursor protein (APP) jams mitochondria and endoplasmic reticulum, starving cells of energy. This leads to neuronal death, a hallmark of Alzheimer's disease, according to Penn researchers.
Researchers at UT Southwestern Medical Center discovered a new protein, SMAC, which promotes apoptosis and is responsible for cell death. The study found that only seven amino acids are necessary to induce cell death, making it possible to design drugs based on these amino acids.
Researchers discovered that gatekeeper protein YidC allows essential proteins to enter bacterial membranes, while its absence leads to bacterial death. This finding suggests a new pathway for protein translocation and implies a common ancestor among bacteria, chloroplasts, and mitochondria.
A signaling protein acts as a 'messenger of death' to execute apoptosis, a process regulating cell numbers and connections. The discovery could offer targets for drugs preventing cell death related to heart attacks, strokes, or Alzheimer's disease.
The StAR protein plays a key role in the steroid-making system by partially unfolding to form a 'molten globule' conformation that enables it to work inside cells. This flexible state lowers energy required for channel opening in mitochondrial membrane, acting as an on/off switch for cholesterol transport.
Researchers at University at Buffalo and Children's Hospital have identified a critical protein involved in iron metabolism. The discovery is expected to boost understanding of iron-deficiency anemia, the most prevalent disease worldwide, and provide insights into treating hemochromatosis, an inherited iron overload disorder.
Researchers found a yeast protein similar to frataxin controls iron levels in mitochondria, leading to cell death and oxidative damage. The study suggests iron overload may be a key factor in Friedreich's ataxia, but further research is needed for treatment.