Articles tagged with Mitochondrial Proteins
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Researchers at MD Anderson Cancer Center have found that inhibiting GFER, a mitochondrial enzyme, in combination with immune checkpoint blockade improves antitumor response in preclinical models. This two-pronged approach holds promise for patients with pancreatic cancer.
The congress brings together experts to explore mitochondria's role in cellular dynamics, metabolic control, and therapeutic targets. Key findings include the emergence of mitochondria as biological sensors and decision-makers, translating environmental signals into cellular fate.
The 17th World Congress on Targeting Mitochondria will gather world's leading experts from biotechnology, pharma and academia to discuss health, longevity and precision medicine. Over 150 academic and institutional partners and 30 industrial and investment organizations are participating.
Researchers discovered that mitochondrial dysfunction triggers a sophisticated metabolic response in brown fat cells, rewiring key enzymes to produce D-2HG. This metabolite modifies the cell nucleus, changing gene expression and nuclear structure, promoting adaptation and altering cellular identity.
An international team has uncovered a new mechanism by which mitochondria and peroxisomes work together to defend against oxidative stress, maintaining cellular health. This discovery challenges the long-standing idea that cellular defense is confined within individual compartments.
A novel mechanism linking fetal anemia to disrupted intracellular iron distribution has been identified due to impaired mitochondrial protein synthesis. Mitochondrial tRNA modification enzyme Mto1 plays a crucial role in efficient protein synthesis and maintaining proper iron homeostasis.
Scientists have discovered a novel regulator of the mitochondrial sodium-calcium exchanger (NCLX), which helps maintain calcium balance in mitochondria. The discovery of TMEM65 could lead to new therapeutic agents to combat calcium overload associated with heart failure and Alzheimer's disease.
Researchers at Johns Hopkins Medicine have discovered how a group of proteins linked to Parkinson's and ALS act as 'guardians' of mitochondria, maintaining their normal size and function. The study found that when mitochondria become too large, they leak mitochondrial DNA into the cytosol, triggering an inflammatory response.
Researchers at St. Jude Children's Research Hospital found that removing the 'signal jammer' protein VDAC2 can improve how tumors respond to immunotherapy. This breakthrough could lead to new ways to enhance immunotherapies and make them more effective in treating resistant cancers.
Researchers at Umea University discovered a way to break open protective walls of pollen grains without damaging the inside cell and its components. The study found that essential proteins for maintaining energy production were absent from mitochondria, potentially explaining why pollen grains have limited lifetimes.
Researchers found that a rare genetic syndrome causes different damage mechanisms in male and female brains, affecting neurogenesis and energy production. The study suggests that the ADNP protein plays a crucial role in brain development and aging, with distinct functions in males and females.
Researchers have discovered Mitofusin 2's unexpected function in maintaining protein quality within cells, interacting with the proteasome and chaperones to prevent toxic aggregates. This novel connection has far-reaching implications for treating CMT and other neurodegenerative diseases.
A team of scientists has uncovered the role of mitochondrial proteins in driving autophagy, a process crucial for maintaining cellular balance and energy production. By regulating this process, researchers hope to develop new strategies for treating metabolic diseases such as obesity and diabetes.
Researchers have uncovered a mitochondrial process that supports brain cells critical for learning, memory, and social recognition. The study reveals the critical role of the mitochondrial calcium uniporter in enabling neurons to strengthen connections through synaptic plasticity.
A deficiency of TLE6 protein, associated with female infertility, was also linked to abnormal sperm morphology and reduced motility in male mice. The study suggests that TLE6 plays a crucial role in energy production in sperm cells.
A new mechanism by which brown fat is converted into heat has been identified, revealing a potential target for treating obesity and related metabolic diseases. The MCJ protein plays a crucial role in this process, protecting against health problems associated with obesity such as diabetes and increased blood lipids.
Researchers from Kumamoto University identified SerpinA1 as a key regulator in combating obesity and enhancing glucose metabolism. The study found that activating brown adipose tissue could pave the way for innovative treatments for diabetes and metabolic disorders.
Researchers found that cellular RNA molecules help regulate antiviral signaling by activating the MAVS signalosome. This signaling pathway is crucial for coordinating immune responses against virus invasion. The study's findings suggest a potential role for RNA-based therapeutics in combating infections and autoimmune diseases.
Researchers identified the critical role of TIMM50 protein in mitochondrial energy production and its link to a severe and rare neurological disease. The study's findings suggest potential targets for future drug treatments and advance research on protein import into mitochondria in brain cells.
Researchers have identified a key protein that plays a crucial role in energy production in muscle cells, which can be activated by physical exercise. This discovery may lead to the development of treatments for over 200 disorders related to muscle energy production.
Researchers used machine learning to analyze data from 50 CF-LVAD patients and identified six prognostic factors that predicted post-implantation stroke. Lower levels of OxPhos proteins were associated with an increased risk of new strokes after implantation.
A new study from Karolinska Institutet found that people with type 2 diabetes have lower levels of the protein creatine kinase, leading to impaired mitochondrial function and energy production. This impairment may contribute to poorer energy metabolism in individuals with type 2 diabetes.
A recent study by FAU researchers links copper regulation to neurodegenerative disorders like Alzheimer's. The team discovered that a specific gene, swip-10, plays a crucial role in maintaining the balance of copper in cells, which can prevent mitochondrial dysfunction and oxidative stress.
A new study reveals that Meteorin-like protein saps energy from T cells, severely limiting their ability to fight cancer. By understanding this signaling pathway, researchers may be able to develop targeted treatments to restore metabolic health and enhance the immune system's power against tumors.
Targeting mitochondrial dysfunction and mtDNA mutations is a promising therapeutic strategy for HCC, with potential benefits including restored cellular metabolism and reduced cancer progression. Research has focused on pharmacological approaches to target the electron transport chain and AMPK-dependent pathways, offering novel treatme...
Pagliarini's research aims to shed light on the underlying genetic causes of mitochondrial disorders, which affect one in 5,000 people. He will use this funding to expand his work on mitochondrial proteins and their functions, with a focus on coenzyme Q.
A team of scientists from Max Planck Institute found that extremely long-lived proteins in the ovary play a crucial role in preserving fertility. These proteins, known as chaperones, help maintain cellular processes and prevent misfolded proteins from aggregating.
A multidisciplinary team developed GeneMAP to probe gene function in metabolism. They identified SLC25A48 as necessary for mitochondrial choline transport and associated it with eight human diseases.
Researchers have identified two highly soluble molecules with superior antioxidant benefits for cells, which could help prevent and manage certain degenerative diseases by maintaining lower levels of harmful free radicals. The study suggests that these molecules can transfer and accumulate in membranes, reducing the risk of cell damage.
Researchers discovered that biochemical bonds between fats and proteins in the mitochondrion play a crucial role in cellular energy production. Introducing mutations into a specific protein-lipid interaction weakened its structure and lowered its function.
Researchers at Hollings Cancer Center have identified a promising therapeutic strategy to combat pancreatic cancer. By simultaneously blocking HSP70 and autophagy, the growth of pancreatic tumors can be slowed, offering new hope for treatment.
Researchers found that boosting mitochondrial health can combat protein clumping linked to both aging and Alzheimer's. The study identifies a core insoluble proteome enriched with numerous proteins not previously considered, offering new targets for exploration.
Researchers discovered a connection between mitochondrial calcium transport and autophagy, a process where cells break down and reuse components. The study found that NCLX protein plays a crucial role in regulating this link, which has implications for understanding energy metabolism and developing disease treatments.
Researchers identify TRMT10C enzyme causing methylation of ND5 mRNA, leading to mitochondrial dysfunction and reduced energy supply to the brain. Impairment of complex I in the respiratory chain contributes to Alzheimer's disease pathology.
Researchers at U of T have mapped the movement of proteins encoded by the yeast genome throughout its cell cycle, identifying patterns of emergence and disappearance or movement to specific areas. The study provides a unique dataset that offers a genome-scale view of molecular changes during cell division.
Depletion of axonal mitochondria disrupts autophagy, leading to abnormal protein build-up in neurons. Restoring mitochondrial levels restores autophagy and recovers impaired neuron function.
Emerging from a need to understand organelle interactions, researchers have developed OrthoID, a novel strategy that refines protein identification at organelle contact sites. This method uses mutually orthogonal binding pairs to label and isolate proteins involved in cellular communication.
Researchers have discovered the first known nitrogen-fixing organelle within a eukaryotic cell, which challenges current understanding of biological nitrogen fixation. The discovery provides insight into ocean ecosystems and has potential implications for agriculture.
Researchers discovered ERMA, a cellular transport 'pump', plays a crucial role in guiding magnesium to heart cells. Targeting ERMA could lead to new treatments for heart conditions by maintaining stable calcium balances.
Researchers discovered a genetic mutation in humanin, a mitochondrial microprotein, that may help individuals with the APOE4 allele live longer and preserve cognitive function. The variant was found to reduce amyloid-beta buildup in the brains of mice engineered to express human APOE4.
In nerve cells, insulin facilitates the elimination of defective mitochondria when energy is available. However, during energy scarcity or disrupted insulin signaling, mitochondrial recycling is reduced, allowing potentially damaged power plants to continue operating. This process affects ageing processes and neurological diseases.
Researchers at St. Jude Children's Research Hospital have discovered that myeloid cell leukemia-1 (MCL-1) plays a critical role in regulating long-chain fatty acid oxidation in mitochondria, revealing new insights into its anti-apoptotic functions and potential therapeutic applications.
A team of researchers from the Medical University of South Carolina has discovered a novel protective response by which the brain naturally repairs itself after traumatic brain injury. Protein p17 plays a crucial role in this process, triggering the restorative mechanism of mitophagy to remove damaged tissue and initiate healing.
A team of researchers has discovered the role of an enzyme in recycling ribosomes at the endoplasmic reticulum. The enzyme, a special E3 ligase, joins a small protein modification called UFM1 to the large ribosomal subunit, ensuring its detachment from the ER membrane.
Researchers found that impaired mitochondrial unfolded protein response causes accelerated telomere shortening in both oocytes and somatic cells of aging mice. This study highlights the link between loss of mitochondrial protein homeostasis, infertility, and somatic aging.
Researchers develop technology that alleviates retinal pathologies by targeting mitochondrial chaperone TRAP1, which is implicated in the breakdown of blood-retinal barrier and pathological neovascularization. This treatment approach holds great promise for revolutionizing the treatment landscape for ischemic retinopathy.
A new study found that HSP10 treatment improved exploratory preferences, object contacts, and swimming time in aged mice, while also increasing proliferating cells and differentiated neuroblasts. The protein also mitigated age-related gene reductions and increased sirtuin 3 levels.
Researchers uncover the role of IGF2BP2 in responding to cardiac stress, highlighting its potential reversibility and clinical relevance. Elevated IGF2BP2 expression leads to dilated cardiomyopathy, but controlled reduction prompts recovery.
A recent study published in the Journal of Investigative Dermatology has revealed that hemoglobin is present in the epidermis, the outermost layer of our skin. This discovery adds a new facet to understanding the skin's defense mechanisms against aging and cancer.
Researchers found that mitochondrial protein CHCHD2 is associated with increased tumor growth, invasion, and resistance to chemotherapy in glioblastoma patients. CHCHD2 interacts with mutated EGFR to increase sensitivity to cytotoxic drugs, highlighting its potential as a therapeutic target.
Researchers have revealed a revolutionary new understanding of how proteins enter mitochondria, correcting long-held assumptions about the TIM complex. High-resolution cryo-electron microscopy data and advanced biochemical methods were used to re-evaluate old data and map functional organization in great detail.
Researchers at Saarland University have identified a crucial mechanism in the human OPA1 protein that enables optimal energy conversion in mitochondria. This breakthrough could lead to customized therapeutic solutions for patients with OPA1-related diseases.
The study reveals MOF's critical role in maintaining mitochondrial integrity through protein acetylation. COX17 is identified as a key target of MOF-mediated acetylation, stimulating its function and regulating oxidative phosphorylation.
Researchers at Chalmers University of Technology have shown that graphene oxide nanoflakes can reduce the accumulation of misfolded amyloid peptides in yeast cells, which are similar to human neurons affected by Alzheimer's disease. This suggests that graphene oxide may hold great potential for treating neurodegenerative diseases.
A research team has developed a technology that selectively targets and eliminates aging cells, contributing to various inflammatory conditions. This approach represents a new paradigm for treating age-related diseases with minimal toxicity concerns.
Researchers use Listeria bacteria to break open cell organelles and study their function in relation to shape. They found that function does not always follow form, with cells recognizing and increasing efforts to remove misshapen organelles.
A team of scientists at VCU Massey Cancer Center discovered a previously unknown interaction between proteins that supplies energy to tumor cells, holding significant implications for colon cancer treatments. By blocking heat shock protein 27 activity, researchers confirmed a decrease in mitochondrial function and death of cancer cells.
Researchers have found that the protein Musashi-2 plays a crucial role in regulating type 2a muscle fiber mass and metabolism. The study reveals that Msi2 knockout mice exhibit reduced muscle mass, decreased myoglobin and mitochondria levels, and impaired sugar metabolism.
Researchers have found that a genetic risk factor for schizophrenia, 3q29 deletion syndrome, impairs mitochondrial function in brain cells. This impairment contributes to the development of schizophrenia and has implications for understanding the neurobiology of the disease.
Researchers at West Virginia University are tracing the cause of diabetic heart disease using diabetic animal models to examine mitochondrial function. They hope to understand how faulty protein import affects the mitochondria and explore potential treatments to improve energy production and reduce cardiovascular risk.