Articles tagged with Mitochondrial Proteins
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Researchers at Scripps Research have identified a unique mitochondrial protein structure, DELE1, that plays a crucial role in activating the cell's integrated stress response. This discovery could lead to the development of new therapies for age-related diseases such as neurodegeneration and cancer.
Scientists identified a process by which enzymes help prevent heart damage in chemotherapy patients. Enzymes normally found in mitochondria move to the nucleus, keeping cells alive. This discovery suggests new methods for testing individual patient responses and potentially preventing heart damage from chemotherapy.
Researchers discovered distinct variants of the mitochondrial protein Mitofusin 2, ERMIT2 and ERMIN2, located on the endoplasmic reticulum, forming a bridge between mitochondria and this organelle. These variants play a crucial role in maintaining optimal cellular functionality and regulating lipid metabolism.
Researchers at the Lewis Katz School of Medicine found that calcium sensor MICU1 regulates mitochondrial ultrastructure, governing inner and outer mitochondrial membrane structure. This discovery provides a framework for understanding cellular energetics and cell death, with implications for diseases such as cardiovascular disease.
Researchers have identified ATAD3A as a molecular determinant that favors the development of head and neck cancer. The protein is involved in various cellular processes, including energy metabolism and apoptosis. Targeting ATAD3A could offer a novel approach to developing effective anti-cancer therapeutics.
A study published in Neurobiology of Disease suggests that targeting the sigma-1 receptor and ATAD3A protein may prevent mitochondrial dysfunction in ALS. The researchers found that this approach could lead to a novel therapeutic strategy for neurodegenerative diseases.
Researchers uncover the critical link between cellular energy levels and mitochondrial damage through protein FNIP1. The study reveals that FNIP1 enables communication between AMPK and TFEB, instructing genes to remove damaged mitochondria and create new ones.
A team of researchers from Indiana University School of Medicine has identified Pyruvate dehydrogenase kinase 4 (PDK4) as a crucial mediator of alcohol-induced liver injury. PDK4 plays a key role in the formation of calcium channels at the ER-mitochondria interface, leading to mitochondrial dysfunction and accumulation of calcium ions.
A study found that regular exercise increases mitochondrial fusion, benefiting muscle cells and maintaining physical fitness even in old age. Daily sessions of exercise throughout life delay the accumulation of dysfunctional mitochondria and decline in physical fitness.
A new study by researchers at Florida Atlantic University explored the effects of resistance training on older adults' cellular level. The study found that resistance training did not significantly affect inflammatory proteins or redox balance markers, but showed a significant reduction in a specific protein ratio. This may support the...
Researchers have discovered a possible cause of neurodegeneration in the early stages of Alzheimer's disease using fruit flies. The study found that an overabundance of the TOMM40 gene causes marked cell death in the retina, which corresponds to the level of protein produced by the gene.
Researchers at the University of Freiburg and Kyoto Sangyo University have elucidated the guidance mechanism for mitochondrial pore formation through structural and functional experiments. The study reveals that Sam50 and Sam37 proteins play critical roles in forming barrel pores, essential for cellular function.
Researchers used cryo-electron microscopy to study mitoribosome assembly in yeast and humans, revealing similarities and differences in protein involvement and RNA folding. The findings provide insights into molecular complexity and diversity, with potential implications for severe diseases such as Perrault syndrome.
Scientists have discovered how cells eliminate mutated mitochondrial DNA (mtDNA) using autophagy, a cellular waste disposal process. This mechanism prevents mitochondrial damage and preserves function.
ATAD3A is crucial for the movement of genetic material inside mitochondria, affecting energy production. The correct distribution of mtDNA nucleoids activates expression of respiratory chain complexes.
A new study has discovered that MTCH2, a protein essential in various cellular processes, acts as a 'door' for proteins to access the mitochondrial membrane. The finding opens up potential avenues for cancer treatments by harnessing apoptosis, a programmed cell death mechanism.
A preclinical study suggests that spermidine can help alleviate the pathological features of NASH, a condition associated with cardiac and kidney disease. The compound improves mitochondrial function, reduces inflammation, and prevents scar tissue formation.
Scientists have successfully delivered a common blood pressure medication directly to the inner membrane of mitochondria, targeting energy-producing parts of cells. The new method uses the body's natural transport system to deliver drugs more precisely, potentially improving therapy efficacy and reducing negative side effects.
A mutation in the SHMOOSE protein is associated with a 20-50% higher risk of Alzheimer's disease across four cohorts. The researchers suggest that targeting SHMOOSE may prove beneficial in neurodegenerative and other diseases of aging.
Scientists at Duke-NUS Medical School have discovered the critical role of small microproteins in assembling larger protein complexes inside energy-generating cell components known as mitochondria. The study highlights how microproteins regulate energy supply and mitigate mitochondrial dysfunction, a feature underlying various diseases.
A study published in Cell Stem Cell found that mitochondrial dynamics regulate the dormant state of adult muscle stem cells, which are essential for tissue stability. The researchers discovered that the protein OPA1 regulates this process and its depletion leads to severe muscle stem cell defects.
Biochemists have discovered that glutathione, an antioxidant, plays a crucial role in moving iron-sulfur cofactors across cell membranes. This finding could lead to better understanding and treatment of diseases caused by impaired iron metabolism, such as Friedreich's ataxia.
A new study reveals that exploiting mitohormesis, a biological phenomenon where mild cellular stress boosts health and viability, can induce tolerance to influenza infection. Researchers identified a novel molecule, 9-tert-butyldoxycycline, which triggers beneficial mitochondrial responses that reduce tissue damage and inflammation.
University of Cincinnati researchers have discovered a technique using light-activated proteins to normalize dysfunctional mitochondria in cells. This method has the potential to treat certain diseases, including cancer and neurodegenerative disorders.
Scientists at Karolinska Institutet and Stockholm University have visualized the machinery that mitochondria use to form their proteins. This discovery presents opportunities to design more specific antibiotics and cancer drugs.
Researchers investigated the effects of treatment with exogenous Humanin G on inflammation markers in AMD and normal retinal cells. The study found reduced levels of inflammatory proteins in AMD plasma and treated cybrids, highlighting the positive effects of Humanin G.
Researchers have identified the genetic causes of three mitochondrial diseases and proposed 20 additional possibilities for further investigation using a new approach. The study provides a platform to better understand how mitochondria's hundreds of proteins work together, which could lead to improved diagnoses and treatments.
Researchers discovered that a conserved receptor molecule called Tom70 coordinates the balance between protein production and import into mitochondria. This finding ties to increased lifespan and delayed mitochondrial dysfunction when Tom70 levels are elevated. The study provides new insights into aging and age-related diseases.
Researchers at Ludwig-Maximilians-Universität München discovered the mechanism by which DELE1 detects organelle stress and reports it to the cell. This process involves the continuous importation of DELE1 into mitochondria, processing by proteases, and degradation within the mitochondria.
Researchers used new techniques to uncover the Tetrahymena electron transport chain, revealing gaps in our knowledge of a major branch of life. The study highlights the power of structural biology and shows potential as a discovery tool for biodiversity research.
Researchers from IRB Barcelona have discovered that damaged mitochondria accumulation triggers inflammatory processes leading to muscle atrophy. Correcting mitochondrial function through increased BNIP3 levels can mitigate inflammation and muscle loss, offering potential tools for promoting healthy ageing.
A team of scientists led by Karine Le Roch has identified two proteins, RAP01 and RAP21, crucial to the malaria parasite's survival. Knocking down these proteins can interrupt protein translation in the mitochondria, leading to the parasite's death.
Scientists at the Max Planck Institute of Biochemistry have discovered a new subtype of acute myeloid leukemia (AML) characterized by high amounts of mitochondrial proteins and altered mitochondrial metabolism. This subtype, called Mito-AML, shows clinical resistance to chemotherapy and can be effectively combated with inhibitors again...
Research reveals YME1L protein balances cellular proliferation and quiescence in neural stem cells. Defects lead to premature conversion of stem cells into neurons, impairing long-term neural regeneration.
A new pathway has been discovered to explain how excessive alcohol consumption damages the liver, specifically through mitochondrial dysfunction. By targeting an enzyme called MATα1, researchers believe they can develop a new treatment for people suffering from alcohol-associated liver disease.
Researchers found that mitochondria can respire away harmful substances to protect protein folding, revealing an unexpected 'patron saint' role. This mechanism is triggered by reductive stress and protects proteins destined for export, showcasing the flexibility of plant mitochondria.
Researchers discovered that pathogens can hijack mitochondrial defense mechanisms by mimicking host proteins, effectively disarming the mitochondria. This allows the pathogen to acquire essential nutrients and evade the host's immune response.
Researchers at the University of Cologne have identified a new direct link between proteins BAX and DRP1 and apoptosis. The study reveals that DRP1 can serve as a direct cell death activator by binding to BAX, potentially leading to new cancer therapies.
Researchers at Waseda University discovered a new protein isoform called Senp5S, which helps regulate Drp1 and mitochondrial dynamics during brain development. The study suggests a novel and vital role for post-translational SUMOylation in neuronal differentiation.
Researchers discover tBID can induce programmed cell death through mitochondrial damage, revealing a new function for a previously thought signal transducer protein. This finding has implications for treating malignant cells and combating infections like Shigella.
Researchers discovered that naked mole-rats rapidly decrease uncoupling protein 1 (UCP1) in brown adipose tissue to conserve energy in hypoxia. This mechanism may hold secrets for humans to survive and thrive in low-oxygen environments, particularly in relation to diseases like stroke and chronic pulmonary disorders.
Researchers at Salk Institute discovered that long-lived mitochondrial proteins remain stable for an extended period, protecting them from damage. This stability allows these proteins to maintain mitochondrial function even when new ones are synthesized, providing protection against errors and energy-conservation benefits.
A study found that boosting a cellular response to misfolded proteins actually shortens lifespan, contradicting previous research. The discovery highlights the complexity of aging and suggests new targets for disease prevention.
Researchers reverse lung fibrosis in a mouse model using Bcl-2 inhibitor ABT-199, suggesting a novel therapeutic target to treat idiopathic pulmonary fibrosis. The study finds that monocyte-derived macrophages play a key role in fibrosis progression and that targeting the Cpt1a-Bcl-2 interaction modulates apoptosis resistance.
A new study reveals that the small protein MOTS-c prevents the destruction of insulin-producing pancreatic cells in mice with autoimmune diabetes. MOTS-c treatment supports regulatory T-cells and reduces the activation of killer T-cells, effectively preventing disease onset.
Scientists discovered a new mitochondrial recycling pathway that may help prevent Parkinson's disease. The study, published in Science Advances, reveals that genes associated with Parkinson's disease play key roles in this process and that disruptions can contribute to neurodegeneration.
Researchers have found that targeting the FK506-binding protein 51 (FKBP51) promotes autophagy and reduces toxic Huntingtin protein levels, potentially providing a new treatment option for Huntington's disease. This new mechanism avoids worrisome side effects associated with rapamycin.
Scientists used proteomics to study how exercise affects mitochondria in skeletal muscle, revealing that different proteins respond differently to exercise. The research provides unprecedented detail on mitochondrial supercomplexes and their formation in response to exercise training.
Researchers at Kumamoto University found that ketogenesis maintains mitochondrial function, preventing excessive acetylation and fatty liver development. This discovery may lead to future therapies for protecting mitochondria and organs in newborns and individuals with nutritional deficiencies.
Cells have a quality control system that ensures the health and function of mitochondria. A new study reveals that cells also transfer mitochondria out in response to stress, leading to the development of Parkinson's disease in humans.
Researchers found that the ECSIT protein regulates the behavior of proteins linked to energy activity in mitochondria, which are affected in Alzheimer's disease. The team also discovered a link between mitochondrial dysfunction, amyloid accumulation, and early disease symptoms.
Researchers at CNIC have identified mitochondrial protein ALDH4A1 as a potential marker for cardiovascular disease diagnosis and a possible therapeutic target. The study found that ALDH4A1 accumulates in plaques and its plasma concentration is elevated in patients with carotid atherosclerosis, suggesting it as a biomarker.
By expressing neuron-enriched mitochondrial proteins at an early stage, researchers achieved a four times higher conversion rate and increased the speed of reprogramming. This breakthrough may lead to developing reliable regenerative medicine therapies for brain diseases and injuries.
Researchers have reconstructed a ciliate mitoribosome using cryo-EM, identifying nine novel proteins encoded in the mitochondrial genome and challenging existing views on mitochondrial translation evolution. The discovery provides new insights into mitochondria's structural and functional complexity.
Two mitochondrial apolipoproteins, APOO/MIC26 and APOOL/MIC27, regulate mitochondrial protein complex stability and are associated with diabetic cardiomyopathy. The study reveals the importance of cardiolipin and crista junctions in maintaining cellular respiration.
Researchers identified 115 MAM-specific proteins using a new technique, Contact-ID, which facilitates calcium transport and lipid metabolism. The discovery is significant for understanding neurodegenerative diseases such as Alzheimer's and Parkinson's.
A newly-discovered small protein in mitochondria is essential for energy production, according to a study by Duke-NUS Medical School. The protein, named BRAWNIN, was found to be necessary for the assembly of a critical molecular complex involved in oxygen-based energy generation.
Researchers discovered that a Mx protein, called MxB, helps cells fight viral infections by supporting mitochondrial function and integrity. The study provides new insights into the role of MxB in cellular defense against viral infections.
Researchers have developed a new tool to study how mitochondrial protein synthesis is affected by disease, pharmaceuticals, ageing and different physiological situations. The MitoRibo-Tag mice provide a valuable tool for future studies on how mitochondrial function regulates human health.
LMU biologists have identified a general alarm signal that activates the Unfolded Protein Response (UPR) in mitochondria, ensuring protein degradation and restoring normal cell function. The signaling pathway is triggered by a decline in mitochondrial membrane potential and involves transcription factor ATFS-1.