Mitochondria
Mitochondria, Liver
Mitochondria, Muscle
Mitochondrial Proteins
Mitochondrial Swelling
Oxidative Phosphorylation
Mitochondrial Membranes
Intracellular Membranes
Oxygen Consumption
Cell Respiration
DNA, Mitochondrial
Membrane Potential, Mitochondrial
Cytochromes c
Mitochondrial Membrane Transport Proteins
Uncoupling Agents
Electron Transport Complex IV
Oligomycins
Adenosine Triphosphate
Reactive Oxygen Species
Cytochrome c Group
Atractyloside
Apoptosis
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
Antimycin A
Oxidation-Reduction
Microscopy, Electron
Electron Transport
Mitochondrial ADP, ATP Translocases
Submitochondrial Particles
Cytosol
Calcium
Carbonyl Cyanide m-Chlorophenyl Hydrazone
Saccharomyces cerevisiae
Succinates
Biological Transport
Protein Transport
NAD
bcl-2-Associated X Protein
Permeability
Electron Transport Complex I
Molecular Sequence Data
Oxidative Stress
Succinic Acid
Membrane Potentials
Mitochondrial Proton-Translocating ATPases
Subcellular Fractions
Proto-Oncogene Proteins c-bcl-2
Caspases
Adenosine Diphosphate
Mersalyl
Cell Fractionation
Ruthenium Red
Amino Acid Sequence
Voltage-Dependent Anion Channels
Energy Metabolism
Mitochondrial Diseases
Cardiolipins
Membrane Proteins
Electron Transport Complex III
Ubiquinone
Carrier Proteins
NADH Dehydrogenase
Bongkrekic Acid
Ketoglutaric Acids
Succinate Dehydrogenase
Endoplasmic Reticulum
Models, Biological
Hydrogen Peroxide
Carnitine
Mitochondrial Dynamics
Rats, Wistar
Proton-Translocating ATPases
Rats, Inbred Strains
BH3 Interacting Domain Death Agonist Protein
Liver
Neurospora crassa
Saccharomyces cerevisiae Proteins
Mutation
Polarography
Organelles
Citrate (si)-Synthase
Base Sequence
Voltage-Dependent Anion Channel 1
Cells, Cultured
Valinomycin
Cell Nucleus
Apoptosis Inducing Factor
Cattle
Membranes
Cytochromes
Digitonin
Cytoplasm
Microscopy, Electron, Transmission
Pyruvic Acid
Ion Channels
Palmitoyl Coenzyme A
Oxidoreductases
Cell Death
Caspase 9
Microscopy, Fluorescence
Genes, Mitochondrial
Rhodamine 123
Microscopy, Confocal
Rats, Sprague-Dawley
Oxygen
Electron Transport Chain Complex Proteins
Caspase 3
Autophagy
Carnitine O-Palmitoyltransferase
Electron Transport Complex II
HeLa Cells
Solanum tuberosum
Protons
Adenosine Triphosphatases
Hydrogen-Ion Concentration
Myocardium
RNA Editing
Hexokinase
Citric Acid Cycle
NADP
Palmitoylcarnitine
Fatty Acids
Cyclophilins
Rhodamines
Blotting, Western
Cyclosporine
Clonazepam
Neurospora
bcl-X Protein
Superoxide Dismutase
Malate Dehydrogenase
Adipose Tissue, Brown
Pyruvate Dehydrogenase Complex
Membrane Transport Proteins
Magnesium
Cyanides
Malonyl Coenzyme A
Enzyme Activation
Signal Transduction
Fluorescent Dyes
Biological Transport, Active
Proteins
Acyl Coenzyme A
Nigericin
Glutamates
Cell Compartmentation
Cell Membrane Permeability
Plants
Protein Binding
bcl-2 Homologous Antagonist-Killer Protein
tert-Butylhydroperoxide
Brain
Cell Survival
Electrophoresis, Polyacrylamide Gel
Protein Biosynthesis
Antioxidants
Recombinant Fusion Proteins
Superoxides
Muscle, Skeletal
Chloroplasts
Aconitate Hydratase
Quinone Reductases
Green Fluorescent Proteins
Glutathione
Cytochromes c1
Ornithine Carbamoyltransferase
Adenine Nucleotide Translocator 1
Phosphate-Binding Proteins
Potassium Cyanide
Calcium Signaling
Sequence Homology, Amino Acid
NADH, NADPH Oxidoreductases
Tetramethylphenylenediamine
Fumarate Hydratase
Bcl-2 regulates amplification of caspase activation by cytochrome c. (1/26295)
Caspases, a family of specific proteases, have central roles in apoptosis [1]. Caspase activation in response to diverse apoptotic stimuli involves the relocalisation of cytochrome c from mitochondria to the cytoplasm where it stimulates the proteolytic processing of caspase precursors. Cytochrome c release is controlled by members of the Bcl-2 family of apoptosis regulators [2] [3]. The anti-apoptotic members Bcl-2 and Bcl-xL may also control caspase activation independently of cytochrome c relocalisation or may inhibit a positive feedback mechanism [4] [5] [6] [7]. Here, we investigate the role of Bcl-2 family proteins in the regulation of caspase activation using a model cell-free system. We found that Bcl-2 and Bcl-xL set a threshold in the amount of cytochrome c required to activate caspases, even in soluble extracts lacking mitochondria. Addition of dATP (which stimulates the procaspase-processing factor Apaf-1 [8] [9]) overcame inhibition of caspase activation by Bcl-2, but did not prevent the control of cytochrome c release from mitochondria by Bcl-2. Cytochrome c release was accelerated by active caspase-3 and this positive feedback was negatively regulated by Bcl-2. These results provide evidence for a mechanism to amplify caspase activation that is suppressed at several distinct steps by Bcl-2, even after cytochrome c is released from mitochondria. (+info)Hsp60 is targeted to a cryptic mitochondrion-derived organelle ("crypton") in the microaerophilic protozoan parasite Entamoeba histolytica. (2/26295)
Entamoeba histolytica is a microaerophilic protozoan parasite in which neither mitochondria nor mitochondrion-derived organelles have been previously observed. Recently, a segment of an E. histolytica gene was identified that encoded a protein similar to the mitochondrial 60-kDa heat shock protein (Hsp60 or chaperonin 60), which refolds nuclear-encoded proteins after passage through organellar membranes. The possible function and localization of the amebic Hsp60 were explored here. Like Hsp60 of mitochondria, amebic Hsp60 RNA and protein were both strongly induced by incubating parasites at 42 degreesC. 5' and 3' rapid amplifications of cDNA ends were used to obtain the entire E. histolytica hsp60 coding region, which predicted a 536-amino-acid Hsp60. The E. histolytica hsp60 gene protected from heat shock Escherichia coli groEL mutants, demonstrating the chaperonin function of the amebic Hsp60. The E. histolytica Hsp60, which lacked characteristic carboxy-terminal Gly-Met repeats, had a 21-amino-acid amino-terminal, organelle-targeting presequence that was cleaved in vivo. This presequence was necessary to target Hsp60 to one (and occasionally two or three) short, cylindrical organelle(s). In contrast, amebic alcohol dehydrogenase 1 and ferredoxin, which are bacteria-like enzymes, were diffusely distributed throughout the cytosol. We suggest that the Hsp60-associated, mitochondrion-derived organelle identified here be named "crypton," as its structure was previously hidden and its function is still cryptic. (+info)An alternative transcript of the rat renin gene can result in a truncated prorenin that is transported into adrenal mitochondria. (3/26295)
Characterization of the local renin-angiotensin system in the rat adrenal zona glomerulosa indicated a dual targeting of renin both to the secretory pathway and mitochondria. To investigate the transport of renin into mitochondria, we constructed a series of amino-terminal deletion variants of preprorenin. One of these variants, lacking the complete signal sequence for the endoplasmic reticulum and 10 amino acids of the profragment, was transported efficiently into isolated mitochondria. The transport was further shown to be dependent on mitochondrial membrane potential and ATP synthesis. Analysis of adrenal RNA revealed the existence of 2 renin transcripts. While one of the transcripts corresponds to the known full-length transcript, the other one lacks exon 1; instead, exon 2 is preceded by a domain of 80 nucleotides originating from intron 1. This domain, as well as the following region of intron 1 being excised, shows all essential sequence elements defining an additional, so-far-unknown exon. The second mRNA possibly derives from an additional transcription start in intron 1 and an alternative splicing process. Translation of this mRNA could result in a truncated prorenin representing a cytosolic form of renin, which is required for transport into mitochondria. This truncated prorenin corresponds exactly to the deletion variant being imported into mitochondria in vitro. (+info)UCP4, a novel brain-specific mitochondrial protein that reduces membrane potential in mammalian cells. (4/26295)
Uncoupling proteins (UCPs) are a family of mitochondrial transporter proteins that have been implicated in thermoregulatory heat production and maintenance of the basal metabolic rate. We have identified and partially characterized a novel member of the human uncoupling protein family, termed uncoupling protein-4 (UCP4). Protein sequence analyses showed that UCP4 is most related to UCP3 and possesses features characteristic of mitochondrial transporter proteins. Unlike other known UCPs, UCP4 transcripts are exclusively expressed in both fetal and adult brain tissues. UCP4 maps to human chromosome 6p11.2-q12. Consistent with its potential role as an uncoupling protein, UCP4 is localized to the mitochondria and its ectopic expression in mammalian cells reduces mitochondrial membrane potential. These findings suggest that UCP4 may be involved in thermoregulatory heat production and metabolism in the brain. (+info)R73A and H144Q mutants of the yeast mitochondrial cyclophilin Cpr3 exhibit a low prolyl isomerase activity in both peptide and protein-folding assays. (5/26295)
Previously we reported that the R73A and H144Q variants of the yeast cyclophilin Cpr3 were virtually inactive in a protease-coupled peptide assay, but retained activity as catalysts of a proline-limited protein folding reaction [Scholz, C. et al. (1997) FEBS Lett. 414, 69-73]. A reinvestigation revealed that in fact these two mutations strongly decrease the prolyl isomerase activity of Cpr3 in both the peptide and the protein-folding assay. The high folding activities found previously originated from a contamination of the recombinant Cpr3 proteins with the Escherichia coli protein SlyD, a prolyl isomerase that co-purifies with His-tagged proteins. SlyD is inactive in the peptide assay, but highly active in the protein-folding assay. (+info)Mitochondrial depolarization accompanies cytochrome c release during apoptosis in PC6 cells. (6/26295)
Cytochrome c is released from mitochondria into the cytosol in cells undergoing apoptosis. The temporal relationship between cytochrome c release and loss of mitochondrial membrane potential was monitored by laser-scanning confocal microscopy in single living pheochromocytoma-6 cells undergoing apoptosis induced by staurosporine. Mitochondrial membrane potential monitored by tetramethylrhodamine methyl ester decreased abruptly in individual cells from 2 to 7 h after treatment with staurosporine. Depolarization was accompanied by cytochrome c release documented by release of transfected green fluorescent protein-tagged cytochrome c in these cells. The results show that mitochondrial depolarization accompanies cytochrome c release in pheochromocytoma-6 cells undergoing apoptosis. (+info)Identification of 17-methyl-18-norandrosta-5,13(17-dien-3beta-ol, the C19 fragment formed by adrenal side chain cleavage of a 20-aryl analog of (20S)-20-hydroxycholesterol. (7/26295)
Incubation of (20R)-20-phenyl-5-pregnene-3beta,20-diol, an aromatic analog of (23S)-20-hydroxycholesterol, with an adrenal mitochondrial preparation leads to the formation of four compounds: pregnenolone, phenol, a C8 ketone, acetophenone, and a nonpolar C19 compound. This latter compound has now been identified by reverse isotope dilution analysis and by gas chromatography/mass spectrometry as 17-methyl-18-norandrosta-5,13(17)-dien-3beta-ol. From these results it is evident that enzymatic fission of the C-17,20 bond of this synthetic derivative occurs. On the other hand, when (20S)-20-hydroxy[21-14C]cholesterol was used as substrate, the analogous cleavage did not take place. Thus, substitution of an aromatic group on C-20 facilitates side chain cleavage between that carbon atom and the nucleus whereas neither of the naturally occuring precursors, cholesterol or its 20-hydroxylated counterpart, are metabolized to a C8 fragment. (+info)Role of hypoxia-induced Bax translocation and cytochrome c release in reoxygenation injury. (8/26295)
We investigated mechanisms of cell death during hypoxia/reoxygenation of cultured kidney cells. During glucose-free hypoxia, cell ATP levels declined steeply resulting in the translocation of Bax from cytosol to mitochondria. Concurrently, there was cytochrome c release and caspase activation. Cells that leaked cytochrome c underwent apoptosis after reoxygenation. ATP depletion induced by a mitochondrial uncoupler resulted in similar alterations even in the presence of oxygen. Moreover, inclusion of glucose during hypoxia prevented protein translocations and reoxygenation injury by maintaining intracellular ATP. Thus, ATP depletion, rather than hypoxia per se, was the cause of protein translocations. Overexpression of Bcl-2 prevented cytochrome c release and reoxygenation injury without ameliorating ATP depletion or Bax translocation. On the other hand, caspase inhibitors did not prevent protein translocations, but inhibited apoptosis during reoxygenation. Nevertheless, they could not confer long-term viability, since mitochondria had been damaged. Omission of glucose during reoxygenation resulted in continued failure of ATP production, and cell death with necrotic morphology. In contrast, cells expressing Bcl-2 had functional mitochondria and remained viable during reoxygenation even without glucose. Therefore, Bax translocation during hypoxia is a molecular trigger for cell death during reoxygenation. If ATP is available during reoxygenation, apoptosis develops; otherwise, death occurs by necrosis. By preserving mitochondrial integrity, BCL-2 prevents both forms of cell death and ensures cell viability. (+info)Mitochondrial diseases can affect anyone, regardless of age or gender, and they can be caused by mutations in either the mitochondrial DNA (mtDNA) or the nuclear DNA (nDNA). These mutations can be inherited from one's parents or acquired during embryonic development.
Some of the most common symptoms of mitochondrial diseases include:
1. Muscle weakness and wasting
2. Seizures
3. Cognitive impairment
4. Vision loss
5. Hearing loss
6. Heart problems
7. Neurological disorders
8. Gastrointestinal issues
9. Liver and kidney dysfunction
Some examples of mitochondrial diseases include:
1. MELAS syndrome (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes)
2. Kearns-Sayre syndrome (a rare progressive disorder that affects the nervous system and other organs)
3. Chronic progressive external ophthalmoplegia (CPEO), which is characterized by weakness of the extraocular muscles and vision loss
4. Mitochondrial DNA depletion syndrome, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
5. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
6. Leigh syndrome, which is a rare genetic disorder that affects the brain and spinal cord.
7. LHON (Leber's Hereditary Optic Neuropathy), which is a rare form of vision loss that can lead to blindness in one or both eyes.
8. Mitochondrial DNA mutation, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
9. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
10. Kearns-Sayre syndrome, which is a rare progressive disorder that affects the nervous system and other organs.
It's important to note that this is not an exhaustive list and there are many more mitochondrial diseases and disorders that can affect individuals. Additionally, while these diseases are rare, they can have a significant impact on the quality of life of those affected and their families.
Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.
Types of Starvation:
There are several types of starvation, each with different causes and effects. These include:
1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.
Effects of Starvation on the Body:
Starvation can have severe effects on the body, including:
1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.
It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.
There are several types of mitochondrial myopathies, each with different clinical features and inheritance patterns. Some of the most common forms include:
1. Kearns-Sayre syndrome: This is a rare progressive disorder that affects the nervous system, muscles, and other organs. It is characterized by weakness and paralysis, seizures, and vision loss.
2. MELAS syndrome (mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes): This condition is characterized by recurring stroke-like episodes, seizures, muscle weakness, and cognitive decline.
3. MERRF (myoclonic epilepsy with ragged red fibers): This disorder is characterized by myoclonus (muscle jerks), seizures, and progressive muscle weakness.
4. LHON (Leber's hereditary optic neuropathy): This condition affects the optic nerve and can lead to sudden vision loss.
The symptoms of mitochondrial myopathies can vary widely, depending on the specific disorder and the severity of the mutation. They may include muscle weakness, muscle cramps, muscle wasting, seizures, vision loss, and cognitive decline.
There is no cure for mitochondrial myopathies, but various treatments can help manage the symptoms. These may include physical therapy, medications to control seizures or muscle spasms, and nutritional supplements to support energy production. In some cases, a lung or heart-lung transplant may be necessary.
The diagnosis of a mitochondrial myopathy is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include blood tests to measure the levels of certain enzymes and other molecules in the body, as well as muscle biopsy to examine the muscle tissue under a microscope. Genetic testing can help identify the specific mutation responsible for the condition.
The prognosis for mitochondrial myopathies varies depending on the specific disorder and the severity of the symptoms. Some forms of the disease are slowly progressive, while others may be more rapidly debilitating. In general, the earlier the diagnosis and treatment, the better the outcome.
There is currently no cure for mitochondrial myopathies, but research is ongoing to develop new treatments and therapies. In addition, there are several organizations and support groups that provide information and resources for individuals with these conditions and their families.
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
Some common examples of neurodegenerative diseases include:
1. Alzheimer's disease: A progressive loss of cognitive function, memory, and thinking skills that is the most common form of dementia.
2. Parkinson's disease: A disorder that affects movement, balance, and coordination, causing tremors, rigidity, and difficulty with walking.
3. Huntington's disease: An inherited condition that causes progressive loss of cognitive, motor, and psychiatric functions.
4. Amyotrophic lateral sclerosis (ALS): A disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, paralysis, and eventually death.
5. Prion diseases: A group of rare and fatal disorders caused by misfolded proteins in the brain, leading to neurodegeneration and death.
6. Creutzfeldt-Jakob disease: A rare, degenerative, and fatal brain disorder caused by an abnormal form of a protein called a prion.
7. Frontotemporal dementia: A group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.
Neurodegenerative diseases can be caused by a variety of factors, including genetics, age, lifestyle, and environmental factors. They are typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment options for neurodegenerative diseases vary depending on the specific condition and its underlying causes, but may include medications, therapy, and lifestyle changes.
Preventing or slowing the progression of neurodegenerative diseases is a major focus of current research, with various potential therapeutic strategies being explored, such as:
1. Stem cell therapies: Using stem cells to replace damaged neurons and restore brain function.
2. Gene therapies: Replacing or editing genes that are linked to neurodegenerative diseases.
3. Small molecule therapies: Developing small molecules that can slow or prevent the progression of neurodegenerative diseases.
4. Immunotherapies: Harnessing the immune system to combat neurodegenerative diseases.
5. Lifestyle interventions: Promoting healthy lifestyle choices, such as regular exercise and a balanced diet, to reduce the risk of developing neurodegenerative diseases.
In conclusion, neurodegenerative diseases are a complex and diverse group of disorders that can have a profound impact on individuals and society. While there is currently no cure for these conditions, research is providing new insights into their causes and potential treatments. By continuing to invest in research and developing innovative therapeutic strategies, we can work towards improving the lives of those affected by neurodegenerative diseases and ultimately finding a cure.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
Mitochondria (song)
Mitochondria associated membranes
Horizontal transfer of mitochondria
Mitochondrion
Proto-mitochondrion
Mitochondrion (band)
Apoptosis-inducing factor, mitochondria-associated 3
Institute For Medical Research, Israel-Canada
Copurification
Intermembrane space
Mitoplast
Mitochondrial outer membrane permeabilization
Glutathione synthetase
MFN2
Mother's curse
Inner mitochondrial membrane
Citrate malate shuttle
Lynn Margulis
Lipid metabolism
Douglass Turnbull
Unicellular organism
Goulstonian Lecture
Malawimonas
Sit Kim Ping
Melatonin
Melatonin as a medication and supplement
Mitochondrial unfolded protein response
Thomas Cavalier-Smith
Archezoa
Peter G. Schultz
HD Biosciences, Luxcel Ink Marketing Deal for Mitochondria Assays | GenomeWeb
Pooled image-base screening of mitochondria with microraft isolation distinguishes pathogenic mitofusin 2 mutations |...
Mitochondria news and latest updates
mitochondria News Research Articles - Page 3 of 12
Nuclear genome-derived circular RNA circPUM1 localizes in mitochondria and regulates oxidative phosphorylation in esophageal...
Next Generation Treatments for Autism: From Mitochondria to Music - Dr Suzanne Goh | autismone.org
The Cellular Control of Mitochondria - Naturopathic Doctor News and Review
Evidence for the independent divergence of vertebrate and high C/G ratio invertebrate mitochondria from the same origin
A genome phylogeny for mitochondria among alpha-proteobacteria and a predominantly eubacterial ancestry of yeast nuclear genes
Author: Khavkin, E. E. / Subject: Mitochondria / Language: English | Search Results | Academic Commons
Mitochondria-Associated Endoplasmic Reticulum Membranes in Insulin Signaling | Diabetes | American Diabetes Association
Mitochondria Can Help Researchers Crack the Training (and Aging) Code - Women's Running
Number of mitochondria in budding cell grown - Budding yeast Saccharomyces ce - BNID 103070
Supplementation with three grams of ginseng per day increases the number of mitochondria in your cells
Metadatos: Effect of conjugated linoleic acid on non enzymatic lipid peroxidation of mitochondria obtained from different rat...
Fucoidan Extract Induces Apoptosis in MCF-7 Cells via a Mechanism Involving the ROS-Dependent JNK Activation and Mitochondria...
A Single Dose of Alcohol Can Permanently Alter the Neuronal Mitochondria
"Lysosomal Zn 2+ release triggers rapid, mitochondria-mediated, non-apoptotic cell dea . . ." by Wanlu Du, Mingxue Gu et al.
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Dissecting the distinct functions of mitochondria
Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. |...
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Evolution of RNA editing in trypanosome mitochondria<...
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MitoSciences: Mitochondria and Apoptosis
Mitochondria in hindi - Aliscience
Mitochondrial8
- Luxcel's growing portfolio of proprietary mitochondria toxicity, bioenergetics, and metabolism assays is highly complementary to our current offerings and provides early and effective identification of mitochondrial liabilities for our clients' drug-discovery programs. (genomeweb.com)
- Mitochondria have been implicated in several human diseases, including mitochondrial disorders and cardiac dysfunction, and may play a role in the aging process. (phys.org)
- Knock-down of circPUM1 would result in lower intracellular oxygen concentration, downregulated oxidative phosphorylation, decrease of mitochondrial membrane potential, increase of ROS generation and shrinking of mitochondria, respectively. (nih.gov)
- The TOM complex (translocase of the outer mitochondrial membrane) is considered the gateway to the mitochondrion, the proverbial powerhouse of the cell. (ndnr.com)
- Analyses of 55 individual and 31 concatenated protein data sets encoded in Reclinomonas americana and Marchantia polymorpha mitochondrial genomes revealed that current methods for constructing phylogenetic trees are insufficiently sensitive (or artifact-insensitive) to ascertain the sister of mitochondria among the current sample of eight alpha-proteobacterial genomes using mitochondrially-encoded proteins. (uni-muenchen.de)
- Although the number of mitochondria was different, the mitochondrial volume in ethanol-and glucose-grown cells was approximately the same (Table 1). (harvard.edu)
- In [researchers'] study, the different mitochondrial number and morphology observed in ethanol-and glucose-grown cells did not significantly affect the fraction of the cellular volume occupied by the mitochondria (6-7%, Table 1). (harvard.edu)
- We hypothesize that biological outcomes derived from these functions of mitochondria are also involved in the mechanisms mediating mitochondrial-associated diseases. (hilarispublisher.com)
Powerhouses of the cell1
- In particular, the structure of the synapses as well as the dynamics of mitochondria - the powerhouses of the cell - are influenced by alcohol. (technologynetworks.com)
Genome3
- Although most of a cell's DNA is contained in the cell nucleus, the mitochondrion has its own independent genome. (phys.org)
- However, the functions of nuclear genome-derived circRNAs localized in mitochondria of tumor cells remain largely elusive. (nih.gov)
- Here, we report that circPUM1, a circular RNA derived from back-splicing of pre-mRNAs of nuclear genome PUM1, localizes in mitochondria. (nih.gov)
Membrane4
- In cell biology, a mitochondrion (plural mitochondria ) is a membrane-enclosed organelle found in most eukaryotic cells. (phys.org)
- Researchers report a collapse of the mitochondria-associated membrane is a common halmark in two genetic forms of ALS. (neurosciencenews.com)
- Each mitochondrion is surrounded by a double limiting membrane. (bvsalud.org)
- Cadmium directly induced the opening of membrane permeability pore of mitochondria which possibly involved in cadmium-triggered apoptosis. (bvsalud.org)
Powerhouse of the cell2
- If you're lucky enough to be able to remember back to high school biology class, you may recall being introduced to the mitochondria as the powerhouse of the cell . (womensrunning.com)
- ATP, or adenosine triphosphate, is the "cellular energy currency, and this is why mitochondria is called the 'powerhouse of the cell. (womensrunning.com)
Oxidative Phosphorylation1
- Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. (bvsalud.org)
Metabolism4
- Mitochondria are considered to be the power plants of cells and are essential for human metabolism. (phys.org)
- In this way, the cell can specifically control the influx of precursor proteins for building elements of the metabolism, and it can adapt the function of the mitochondria to an altered cellular state. (ndnr.com)
- Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. (oregonstate.edu)
- It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates. (oregonstate.edu)
19761
- Researchers] used the vital stain for mitochondria methylpyridinium iodine (DASPMI), a fluorescent, non-toxic stain for mitochondria (Bereiter-Hahn 1976: Bereiter-Hahn et al. (harvard.edu)
Skeletal1
- Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. (oregonstate.edu)
Induces1
- The ARHGAP11B protein located in mitochondria induces a metabolic pathway, similar to the characteristics of cancer cells, in brain stem cells, resulting in brain development. (neurosciencenews.com)
Apoptosis1
- The involvement of mitochondria in silica -induced apoptosis of pulmonary phagocytes. (cdc.gov)
Metabolic2
Cells9
- Mitochondria are microscopic organelles found within cells, and are by far the largest producer of the molecule adenosine triphosphate (ATP), which provides energy to many processes in living cells. (phys.org)
- Energy production in nature is the responsibility of chloroplasts and mitochondria and is crucial for fabricating sustainable, synthetic cells in the lab. (phys.org)
- Many cells have only a single mitochondrion, whereas others can contain several thousand mitochondria. (phys.org)
- The most striking observation concerned the number of mitochondria, which was approximately ten-fold higher in ethanol-grown cells than in cells grown on glucose (Table 1). (harvard.edu)
- This implies that mitochondria in ethanol-grown cultures have a much larger surface area than those in glucose-grown cells. (harvard.edu)
- 2006 PMID 16464011 p.384 left column write that 'Several hundred mitochondria can be present in individual cells. (harvard.edu)
- If people use 3 grams of Korean ginseng daily, the number of mitochondria in their cells increases. (ergo-log.com)
- Supplementation with ginseng caused a sharp increase in the number of mitochondria in the cells of the test subjects. (ergo-log.com)
- Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). (bvsalud.org)
Organism1
- The number of mitochondria in a cell varies widely by organism and tissue type. (phys.org)
Depletion1
- ML-SA-caused mitochondria swelling and dysfunction lead to cellular ATP depletion. (wayne.edu)
Membranes1
- Originally described as sites for the exchange of phospholipids between organelles ( 5 ), mitochondria-associated membranes (MAMs) represent close contact sites through which endoplasmic reticulum (ER) communicates with mitochondria supporting the transfer not only of lipids but also the exchange of calcium (Ca 2+ ) ions and other species. (diabetesjournals.org)
Nucleus1
- Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA. (medlineplus.gov)
Cellular energy1
- In addition to supplying cellular energy, mitochondria are involved in a range of other processes, such as signaling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth. (phys.org)
Lung1
- The polyunsaturated fatty acid composition, chemiluminescence and peroxidizability index of mitochondria obtained from rat liver, kidney, lung and heart, were studied after oral administration of conjugated linoleic acid (CLA). (siu.edu.ar)
Molecular1
- But there's more to mitochondria than just keeping the molecular lights on. (womensrunning.com)
Genes2
- This prompted a search for methods to directly compare eukaryotic genomes to their prokaryotic counterparts to investigate the origin of the mitochondrion and its host from the standpoint of nuclear genes. (uni-muenchen.de)
- Las mitocondrias dependen de los genes del núcleo, de las células en que residen, para muchos ARN MENSAJEROS. (bvsalud.org)
Aerobic1
- Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (bvsalud.org)
Liver3
- After incubation of mitochondria in an ascorbate Fe++ system (120 min at 37°C), it was observed that the total counts per min/mg protein originated from light emission: chemiluminescence, was lower in liver and kidney mitochondria in the CLA group than in the control group. (siu.edu.ar)
- As a consequence, the peroxidizability index -a parameter based on the maximal rate of oxidation of fatty acids- showed significant changes in liver and kidney mitochondria. (siu.edu.ar)
- Aging Disrupts Circadian Rhythms in Mouse Liver Mitochondria. (bvsalud.org)
Mitocondrias1
- Aspartato aminotransferasa localizada en las MITOCONDRIAS. (bvsalud.org)
Organelles1
- Other two salient functions of mitochondria are their biosynthetic capacity and their role as signaling organelles. (hilarispublisher.com)
Protein1
- A new study reports caffeine concentration, the equivalent of four cups of coffee, can promote the movement of a regulatory protein into mitochondria. (neurosciencenews.com)
Cell2
- Mitochondria are the major site of energy production in the cell. (hilarispublisher.com)
- The phrase lives of a cell refers to the independent yet interrelated parts of a human cell including mitochondria, centrioles, and basal bodies that once led independent lives. (cdc.gov)
Damage2
- When BH3-only binds to one of the regions, BAX becomes able to damage mitochondria. (neurosciencenews.com)
- This damage results from a buildup of harmful molecules called reactive oxygen species, which are byproducts of energy production in mitochondria. (medlineplus.gov)
Characteristics1
- Several characteristics make mitochondria unique. (phys.org)
Activation1
- Researchers report amnesia caused by cannabinoids relies on the activation of the CB1 receptor in mitochondria in the hippocampus. (neurosciencenews.com)
Researchers1
- Researchers have identified how the circadian clock helps prime mitochondria to correctly use stored energy when we are not eating. (neurosciencenews.com)
Cancer2
- MAMs play important roles in several signal transduction pathways and the relevance of the ER-mitochondria interface to human diseases, including Alzheimer disease, cancer, and lysosomal storage disease ( 6 ), is slowly emerging. (diabetesjournals.org)
- During her Doctorate studies, she focused on the role of mitochondria in cancer. (hilarispublisher.com)
Functions1
- Mitochondria perform numerous functions. (womensrunning.com)
Found1
- An aspartate aminotransferase found in MITOCHONDRIA. (bvsalud.org)
Analysis1
- The techniques routinely used to study the MAMs are based on analysis of ER-mitochondria contact sites via electron microscopy, intracellular localization of MAM markers (such as FACL-4 or SigmaR1) in combination with microscopy techniques, or isolation of MAMs through subcellular fractionations followed by Western blot analysis ( 12 ). (diabetesjournals.org)
Origin1
- These findings suggest that vertebrate and high C/G ratio invertebrate mitochondria descended independently from the same origin. (scirp.org)
Close1
- However, Rhodospirillum rubrum came as close to mitochondria as any alpha-proteobacterium investigated. (uni-muenchen.de)
Study1
- A new study could be the first step to developing drugs that targets carbonic anhydrase in mitochondria to help protect against aging and neurodegeneration. (neurosciencenews.com)
Article1
- Is the Subject Area "Mitochondria" applicable to this article? (plos.org)
Method1
- An advanced imaging-based method from scientists at Scripps Research offers a new way of studying mitochondria. (phys.org)
Drug1
- NEW YORK (GenomeWeb) - Chinese contract research organization HD Biosciences (HDB) has signed an agreement to co-market and sell Luxcel Biosciences' mitochondria assays and technologies for preclinical drug safety testing, the companies announced today. (genomeweb.com)