Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those IONOPHORES that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.
A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.
A closely related group of toxic substances elaborated by various strains of Streptomyces. They are 26-membered macrolides with lactone moieties and double bonds and inhibit various ATPases, causing uncoupling of phosphorylation from mitochondrial respiration. Used as tools in cytochemistry. Some specific oligomycins are RUTAMYCIN, peliomycin, and botrycidin (formerly venturicidin X).
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.
The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.
Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Established cell cultures that have the potential to propagate indefinitely.
The process by which ELECTRONS are transported from a reduced substrate to molecular OXYGEN. (From Bennington, Saunders Dictionary and Encyclopedia of Laboratory Medicine and Technology, 1984, p270)
Organic compounds that contain two nitro groups attached to a phenol.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
The rate dynamics in chemical or physical systems.
A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Mitochondria of skeletal and smooth muscle. It does not include myocardial mitochondria for which MITOCHONDRIA, HEART is available.
The mitochondria of the myocardium.
Double-stranded DNA of MITOCHONDRIA. In eukaryotes, the mitochondrial GENOME is circular and codes for ribosomal RNAs, transfer RNAs, and about 10 proteins.
A flavoprotein and iron sulfur-containing oxidoreductase complex that catalyzes the conversion of UBIQUINONE to ubiquinol. In MITOCHONDRIA the complex also couples its reaction to the transport of PROTONS across the internal mitochondrial membrane. The NADH DEHYDROGENASE component of the complex can be isolated and is listed as EC
A toxic dye, chemically related to trinitrophenol (picric acid), used in biochemical studies of oxidative processes where it uncouples oxidative phosphorylation. It is also used as a metabolic stimulant. (Stedman, 26th ed)
The phosphoric acid ester of serine.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins.
A class of nucleotide translocases found abundantly in mitochondria that function as integral components of the inner mitochondrial membrane. They facilitate the exchange of ADP and ATP between the cytosol and the mitochondria, thereby linking the subcellular compartments of ATP production to those of ATP utilization.
Proton-translocating ATPases responsible for ADENOSINE TRIPHOSPHATE synthesis in the MITOCHONDRIA. They derive energy from the respiratory chain-driven reactions that develop high concentrations of protons within the intermembranous space of the mitochondria.
An antibiotic substance produced by Streptomyces species. It inhibits mitochondrial respiration and may deplete cellular levels of ATP. Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed)
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
A multisubunit enzyme complex containing CYTOCHROME A GROUP; CYTOCHROME A3; two copper atoms; and 13 different protein subunits. It is the terminal oxidase complex of the RESPIRATORY CHAIN and collects electrons that are transferred from the reduced CYTOCHROME C GROUP and donates them to molecular OXYGEN, which is then reduced to water. The redox reaction is simultaneously coupled to the transport of PROTONS across the inner mitochondrial membrane.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A glycoside of a kaurene type diterpene that is found in some plants including Atractylis gummifera (ATRACTYLIS); COFFEE; XANTHIUM, and CALLILEPIS. Toxicity is due to inhibition of ADENINE NUCLEOTIDE TRANSLOCASE.
Derivatives of SUCCINIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,4-carboxy terminated aliphatic structure.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
Inorganic salts of phosphoric acid.
A proton ionophore that is commonly used as an uncoupling agent in biochemical studies.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
A botanical insecticide that is an inhibitor of mitochondrial electron transport.
Multisubunit enzymes that reversibly synthesize ADENOSINE TRIPHOSPHATE. They are coupled to the transport of protons across a membrane.
A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A group of muscle diseases associated with abnormal mitochondria function.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
An amino acid that occurs in endogenous proteins. Tyrosine phosphorylation and dephosphorylation plays a role in cellular signal transduction and possibly in cell growth control and carcinogenesis.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
A proton ionophore. It is commonly used as an uncoupling agent and inhibitor of photosynthesis because of its effects on mitochondrial and chloroplast membranes.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
A subtype of mitochondrial ADP, ATP translocase found primarily in heart muscle (MYOCARDIUM) and skeletal muscle (MUSCLE, SKELETAL).
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A series of oxidative reactions in the breakdown of acetyl units derived from GLUCOSE; FATTY ACIDS; or AMINO ACIDS by means of tricarboxylic acid intermediates. The end products are CARBON DIOXIDE, water, and energy in the form of phosphate bonds.
An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)
Inorganic salts of HYDROGEN CYANIDE containing the -CN radical. The concept also includes isocyanides. It is distinguished from NITRILES, which denotes organic compounds containing the -CN radical.
An electrochemical technique for measuring the current that flows in solution as a function of an applied voltage. The observed polarographic wave, resulting from the electrochemical response, depends on the way voltage is applied (linear sweep or differential pulse) and the type of electrode used. Usually a mercury drop electrode is used.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
A cell line derived from cultured tumor cells.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
The phosphoric acid ester of threonine. Used as an identifier in the analysis of peptides, proteins, and enzymes.
Any of various enzymatically catalyzed post-translational modifications of PEPTIDES or PROTEINS in the cell of origin. These modifications include carboxylation; HYDROXYLATION; ACETYLATION; PHOSPHORYLATION; METHYLATION; GLYCOSYLATION; ubiquitination; oxidation; proteolysis; and crosslinking and result in changes in molecular weight and electrophoretic motility.
A group of enzymes which catalyze the hydrolysis of ATP. The hydrolysis reaction is usually coupled with another function such as transporting Ca(2+) across a membrane. These enzymes may be dependent on Ca(2+), Mg(2+), anions, H+, or DNA.
A complex of enzymes and PROTON PUMPS located on the inner membrane of the MITOCHONDRIA and in bacterial membranes. The protein complex provides energy in the form of an electrochemical gradient, which may be used by either MITOCHONDRIAL PROTON-TRANSLOCATING ATPASES or BACTERIAL PROTON-TRANSLOCATING ATPASES.
The various filaments, granules, tubules or other inclusions within mitochondria.
Transport proteins that carry specific substances in the blood or across cell membranes.
Multisubunit enzyme complexes that synthesize ADENOSINE TRIPHOSPHATE from energy sources such as ions traveling through channels.
Analysis of PEPTIDES that are generated from the digestion or fragmentation of a protein or mixture of PROTEINS, by ELECTROPHORESIS; CHROMATOGRAPHY; or MASS SPECTROMETRY. The resulting peptide fingerprints are analyzed for a variety of purposes including the identification of the proteins in a sample, GENETIC POLYMORPHISMS, patterns of gene expression, and patterns diagnostic for diseases.
A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC
A ubiquitous casein kinase that is comprised of two distinct catalytic subunits and dimeric regulatory subunit. Casein kinase II has been shown to phosphorylate a large number of substrates, many of which are proteins involved in the regulation of gene expression.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Elements of limited time intervals, contributing to particular results or situations.
A PROTEIN-TYROSINE KINASE family that was originally identified by homology to the Rous sarcoma virus ONCOGENE PROTEIN PP60(V-SRC). They interact with a variety of cell-surface receptors and participate in intracellular signal transduction pathways. Oncogenic forms of src-family kinases can occur through altered regulation or expression of the endogenous protein and by virally encoded src (v-src) genes.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
Proteins prepared by recombinant DNA technology.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Unstable isotopes of phosphorus that decay or disintegrate emitting radiation. P atoms with atomic weights 28-34 except 31 are radioactive phosphorus isotopes.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A group of enzymes removing the SERINE- or THREONINE-bound phosphate groups from a wide range of phosphoproteins, including a number of enzymes which have been phosphorylated under the action of a kinase. (Enzyme Nomenclature, 1992)
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A multisubunit enzyme complex that contains CYTOCHROME B GROUP; CYTOCHROME C1; and iron-sulfur centers. It catalyzes the oxidation of ubiquinol to UBIQUINONE, and transfers the electrons to CYTOCHROME C. In MITOCHONDRIA the redox reaction is coupled to the transport of PROTONS across the inner mitochondrial membrane.
A proline-directed serine/threonine protein kinase which mediates signal transduction from the cell surface to the nucleus. Activation of the enzyme by phosphorylation leads to its translocation into the nucleus where it acts upon specific transcription factors. p40 MAPK and p41 MAPK are isoforms.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
Used in the form of the hydrochloride as a reagent in ANALYTICAL CHEMISTRY TECHNIQUES.
Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion.
A CALMODULIN-dependent enzyme that catalyzes the phosphorylation of proteins. This enzyme is also sometimes dependent on CALCIUM. A wide range of proteins can act as acceptor, including VIMENTIN; SYNAPSINS; GLYCOGEN SYNTHASE; MYOSIN LIGHT CHAINS; and the MICROTUBULE-ASSOCIATED PROTEINS. (From Enzyme Nomenclature, 1992, p277)
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851)
A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.
A 44-kDa extracellular signal-regulated MAP kinase that may play a role the initiation and regulation of MEIOSIS; MITOSIS; and postmitotic functions in differentiated cells. It phosphorylates a number of TRANSCRIPTION FACTORS; and MICROTUBULE-ASSOCIATED PROTEINS.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
An increase in MITOCHONDRIAL VOLUME due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed)
A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)
A mitogen-activated protein kinase subfamily that is widely expressed and plays a role in regulation of MEIOSIS; MITOSIS; and post mitotic functions in differentiated cells. The extracellular signal regulated MAP kinases are regulated by a broad variety of CELL SURFACE RECEPTORS and can be activated by certain CARCINOGENS.
Serologic tests in which a positive reaction manifested by visible CHEMICAL PRECIPITATION occurs when a soluble ANTIGEN reacts with its precipitins, i.e., ANTIBODIES that can form a precipitate.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
An enzyme that catalyzes the conversion of ATP and a D-hexose to ADP and a D-hexose 6-phosphate. D-Glucose, D-mannose, D-fructose, sorbitol, and D-glucosamine can act as acceptors; ITP and dATP can act as donors. The liver isoenzyme has sometimes been called glucokinase. (From Enzyme Nomenclature, 1992) EC
A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565)
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
An intracellular signaling system involving the MAP kinase cascades (three-membered protein kinase cascades). Various upstream activators, which act in response to extracellular stimuli, trigger the cascades by activating the first member of a cascade, MAP KINASE KINASE KINASES; (MAPKKKs). Activated MAPKKKs phosphorylate MITOGEN-ACTIVATED PROTEIN KINASE KINASES which in turn phosphorylate the MITOGEN-ACTIVATED PROTEIN KINASES; (MAPKs). The MAPKs then act on various downstream targets to affect gene expression. In mammals, there are several distinct MAP kinase pathways including the ERK (extracellular signal-regulated kinase) pathway, the SAPK/JNK (stress-activated protein kinase/c-jun kinase) pathway, and the p38 kinase pathway. There is some sharing of components among the pathways depending on which stimulus originates activation of the cascade.
The aggregation of soluble ANTIGENS with ANTIBODIES, alone or with antibody binding factors such as ANTI-ANTIBODIES or STAPHYLOCOCCAL PROTEIN A, into complexes large enough to fall out of solution.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
A highly poisonous compound that is an inhibitor of many metabolic processes and is used as a test reagent for the function of chemoreceptors. It is also used in many industrial processes.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A cytochrome oxidase inhibitor which is a nitridizing agent and an inhibitor of terminal oxidation. (From Merck Index, 12th ed)
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
A broad category of carrier proteins that play a role in SIGNAL TRANSDUCTION. They generally contain several modular domains, each of which having its own binding activity, and act by forming complexes with other intracellular-signaling molecules. Signal-transducing adaptor proteins lack enzyme activity, however their activity can be modulated by other signal-transducing enzymes
Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
Organic or inorganic compounds that contain the -N3 group.
A flavoprotein containing oxidoreductase that catalyzes the dehydrogenation of SUCCINATE to fumarate. In most eukaryotic organisms this enzyme is a component of mitochondrial electron transport complex II.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
A flavoprotein oxidase complex that contains iron-sulfur centers. It catalyzes the oxidation of SUCCINATE to fumarate and couples the reaction to the reduction of UBIQUINONE to ubiquinol.
Electrophoresis in which a second perpendicular electrophoretic transport is performed on the separate components resulting from the first electrophoresis. This technique is usually performed on polyacrylamide gels.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Intracellular signaling protein kinases that play a signaling role in the regulation of cellular energy metabolism. Their activity largely depends upon the concentration of cellular AMP which is increased under conditions of low energy or metabolic stress. AMP-activated protein kinases modify enzymes involved in LIPID METABOLISM, which in turn provide substrates needed to convert AMP into ATP.
The smaller subunits of MYOSINS that bind near the head groups of MYOSIN HEAVY CHAINS. The myosin light chains have a molecular weight of about 20 KDa and there are usually one essential and one regulatory pair of light chains associated with each heavy chain. Many myosin light chains that bind calcium are considered "calmodulin-like" proteins.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
An enzyme that catalyzes the phosphorylation of AMP to ADP in the presence of ATP or inorganic triphosphate. EC
Systems of enzymes which function sequentially by catalyzing consecutive reactions linked by common metabolic intermediates. They may involve simply a transfer of water molecules or hydrogen atoms and may be associated with large supramolecular structures such as MITOCHONDRIA or RIBOSOMES.
A specific inhibitor of phosphoserine/threonine protein phosphatase 1 and 2a. It is also a potent tumor promoter. (Thromb Res 1992;67(4):345-54 & Cancer Res 1993;53(2):239-41)
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
Phosphoprotein with protein kinase activity that functions in the G2/M phase transition of the CELL CYCLE. It is the catalytic subunit of the MATURATION-PROMOTING FACTOR and complexes with both CYCLIN A and CYCLIN B in mammalian cells. The maximal activity of cyclin-dependent kinase 1 is achieved when it is fully dephosphorylated.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Inorganic or organic salts and esters of arsenic acid.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
A carbodiimide that is used as a chemical intermediate and coupling agent in peptide synthesis. (From Hawley's Condensed Chemical Dictionary, 12th ed)
A cyclododecadepsipeptide ionophore antibiotic produced by Streptomyces fulvissimus and related to the enniatins. It is composed of 3 moles each of L-valine, D-alpha-hydroxyisovaleric acid, D-valine, and L-lactic acid linked alternately to form a 36-membered ring. (From Merck Index, 11th ed) Valinomycin is a potassium selective ionophore and is commonly used as a tool in biochemical studies.
The naturally occurring or experimentally induced replacement of one or more AMINO ACIDS in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish, enhance, or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties.
Agents that inhibit PROTEIN KINASES.
A highly poisonous compound that is an inhibitor of many metabolic processes, but has been shown to be an especially potent inhibitor of heme enzymes and hemeproteins. It is used in many industrial processes.
Antibodies directed against immunogen-coupled phosphorylated PEPTIDES corresponding to amino acids surrounding the PHOSPHORYLATION site. They are used to study proteins involved in SIGNAL TRANSDUCTION pathways. (From Methods Mol Biol 2000; 99:177-89)
An enzyme group that specifically dephosphorylates phosphotyrosyl residues in selected proteins. Together with PROTEIN-TYROSINE KINASE, it regulates tyrosine phosphorylation and dephosphorylation in cellular signal transduction and may play a role in cell growth control and carcinogenesis.
A family of non-receptor, PROLINE-rich protein-tyrosine kinases.
A family of ribosomal protein S6 kinases that are structurally distinguished from RIBOSOMAL PROTEIN S6 KINASES, 70-KDA by their apparent molecular size and the fact they contain two functional kinase domains. Although considered RIBOSOMAL PROTEIN S6 KINASES, members of this family are activated via the MAP KINASE SIGNALING SYSTEM and have been shown to act on a diverse array of substrates that are involved in cellular regulation such as RIBOSOMAL PROTEIN S6 and CAMP RESPONSE ELEMENT-BINDING PROTEIN.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
A large family of signal-transducing adaptor proteins present in wide variety of eukaryotes. They are PHOSPHOSERINE and PHOSPHOTHREONINE binding proteins involved in important cellular processes including SIGNAL TRANSDUCTION; CELL CYCLE control; APOPTOSIS; and cellular stress responses. 14-3-3 proteins function by interacting with other signal-transducing proteins and effecting changes in their enzymatic activity and subcellular localization. The name 14-3-3 derives from numerical designations used in the original fractionation patterns of the proteins.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.
The biosynthesis of PEPTIDES and PROTEINS on RIBOSOMES, directed by MESSENGER RNA, via TRANSFER RNA that is charged with standard proteinogenic AMINO ACIDS.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Integral membrane proteins that transport protons across a membrane. This transport can be linked to the hydrolysis of ADENOSINE TRIPHOSPHATE. What is referred to as proton pump inhibitors frequently is about POTASSIUM HYDROGEN ATPASE.
Paxillin is a signal transducing adaptor protein that localizes to FOCAL ADHESIONS via its four LIM domains. It undergoes PHOSPHORYLATION in response to integrin-mediated CELL ADHESION, and interacts with a variety of proteins including VINCULIN; FOCAL ADHESION KINASE; PROTO-ONCOGENE PROTEIN PP60(C-SRC); and PROTO-ONCOGENE PROTEIN C-CRK.
Oxyvanadium ions in various states of oxidation. They act primarily as ion transport inhibitors due to their inhibition of Na(+)-, K(+)-, and Ca(+)-ATPase transport systems. They also have insulin-like action, positive inotropic action on cardiac ventricular muscle, and other metabolic effects.
A phosphoprotein phosphatase subtype that is comprised of a catalytic subunit and two different regulatory subunits. At least two genes encode isoforms of the protein phosphatase catalytic subunit, while several isoforms of regulatory subunits exist due to the presence of multiple genes and the alternative splicing of their mRNAs. Protein phosphatase 2 acts on a broad variety of cellular proteins and may play a role as a regulator of intracellular signaling processes.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.

Cyanide poisoning: pathophysiology and treatment recommendations. (1/2221)

This paper aims to assess and compare currently available antidotes for cyanide poisoning. Such evaluation, however, is difficult. Thus, extrapolation from the results of animal studies has potential pitfalls, as significant inter-species differences in response may exist, and these experiments often involve administration of toxin and antidote almost simultaneously, rather than incorporating a more realistic time delay before initiation of treatment. Direct inference from human case reports is also problematic; either because of uncertainties over the exposure levels involved (and hence the likely outcome without treatment), or because of difficulties in identifying the specific contribution of a particular antidote within the overall treatment regimen. Certainly an effort to compare the relative efficacy of cyanide antidotes produces equivocal findings, with no single regimen clearly standing out. Indeed, factors such as the risks of antidote toxicity to various individuals and other practical issues, may be more important considerations. There is therefore no single treatment regimen which is best for all situations. Besides individual risk factors for antidote toxicity, the nature of the exposure and hence its likely severity, the evolving clinical features and the number of persons involved and their proximity to hospital facilities, all need to be considered. Clinically mild poisoning may be treated by rest, oxygen and amyl nitrite. Intravenous antidotes are indicated for moderate poisoning. Where the diagnosis is uncertain, sodium thiosulphate may be the first choice. With severe poisoning, an additional agent is required. Given the various risks with methaemoglobin formers or with unselective use of kelocyanor, hydroxocobalamin may be preferred from a purely risk-benefit perspective. However the former alternatives will likely remain important.  (+info)

Nitric oxide inhibits cardiac energy production via inhibition of mitochondrial creatine kinase. (2/2221)

Nitric oxide biosynthesis in cardiac muscle leads to a decreased oxygen consumption and lower ATP synthesis. It is suggested that this effect of nitric oxide is mainly due to the inhibition of the mitochondrial respiratory chain enzyme, cytochrome c oxidase. However, this work demonstrates that nitric oxide is able to inhibit soluble mitochondrial creatine kinase (CK), mitochondrial CK bound in purified mitochondria, CK in situ in skinned fibres as well as the functional activity of mitochondrial CK in situ in skinned fibres. Since mitochondrial isoenzyme is functionally coupled to oxidative phosphorylation, its inhibition also leads to decreased sensitivity of mitochondrial respiration to ADP and thus decreases ATP synthesis and oxygen consumption under physiological ADP concentrations.  (+info)

Bcl-xL prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange. (3/2221)

Growth factor withdrawal is associated with a metabolic arrest that can result in apoptosis. Cell death is preceded by loss of outer mitochondrial membrane integrity and cytochrome c release. These mitochondrial events appear to follow a relative increase in mitochondrial membrane potential. This change in membrane potential results from the failure of the adenine nucleotide translocator (ANT)/voltage-dependent anion channel (VDAC) complex to maintain ATP/ADP exchange. Bcl-xL expression allows growth factor-deprived cells to maintain sufficient mitochondrial ATP/ADP exchange to sustain coupled respiration. These data demonstrate that mitochondrial adenylate transport is under active regulation. Efficient exchange of ADP for ATP is promoted by Bcl-xL expression permitting oxidative phosphorylation to be regulated by cellular ATP/ADP levels and allowing mitochondria to adapt to changes in metabolic demand.  (+info)

Nitric-oxide-induced apoptosis in human leukemic lines requires mitochondrial lipid degradation and cytochrome C release. (4/2221)

We have previously shown that nitric oxide (NO) stimulates apoptosis in different human neoplastic lymphoid cell lines through activation of caspases not only via CD95/CD95L interaction, but also independently of such death receptors. Here we investigated mitochondria-dependent mechanisms of NO-induced apoptosis in Jurkat leukemic cells. NO donor glycerol trinitrate (at the concentration, which induces apoptotic cell death) caused (1) a significant decrease in the concentration of cardiolipin, a major mitochondrial lipid; (2) a downregulation in respiratory chain complex activities; (3) a release of the mitochondrial protein cytochrome c into the cytosol; and (4) an activation of caspase-9 and caspase-3. These changes were accompanied by an increase in the number of cells with low mitochondrial transmembrane potential and with a high level of reactive oxygen species production. Higher resistance of the CD95-resistant Jurkat subclone (APO-R) cells to NO-mediated apoptosis correlated with the absence of cytochrome c release and with less alterations in other mitochondrial parameters. An inhibitor of lipid peroxidation, trolox, significantly suppressed NO-mediated apoptosis in APO-S Jurkat cells, whereas bongkrekic acid (BA), which blocks mitochondrial permeability transition, provided only a moderate antiapoptotic effect. Transfection of Jurkat cells with bcl-2 led to a complete block of apoptosis due to the prevention of changes in mitochondrial functions. We suggest that the mitochondrial damage (in particular, cardiolipin degradation and cytochrome c release) induced by NO in human leukemia cells plays a crucial role in the subsequent activation of caspase and apoptosis.  (+info)

Changes in mitochondrial phosphorylative activity and adenylate energy charge of regenerating rabbit liver. (5/2221)

The changes in the cellular concentrations of ATP, ADP, and AMP and in oxidative phosphorylation of mitochondria were investigated in the remaining liver of partially hepatectomized rabbits. The energy charge (defined as half of the average number of anhydride-bonded phosphate groups per adenosine moiety) of the liver remnant decreased from 0.866 to 0.767 (p less than 0.01) within 24 hr after hepatectomy, and then increased to a substantially higher level than normal within 7 days. On the other hand, the mitochondrial phosphyorylative activity increased rapidly to 170 per cent of the control within 12 hr and then retruned to normal within 7 days. The mitochondrial phosphorylative activity was inversely correlated with energy charge of the liver remnant (r = -0.75, p less less than 0.01). The maximal enhancement of mitochondrial phosphorylative activity was found in mitochondria obtained from the liver remnant with the lowest level of energy charge, suggesting a response of mitochondria in vivo involving enhanced biosynthetic ATP-utilizing reactions at an early stage of the regenerating process. The enhancement of phosphorylative activity was accompanied by a rise in the respiratory control ratio, P/O ratio and state 3 respiration. The adenylate kinase [EC] activity in the liver remnant increased to more than 160% of the control within 2 days after partial hepatectomy, while the pyruvate kinase [EC] activity decreased remarkably. However, the changes in the two enzyme activities did not correlate with those of mitochondrial phosphorylative activity or the energy charge of the liver remnant.  (+info)

Efficiency of oxidative phosphorylation and energy dissipation by H+ ion recycling in rat-liver mitochondrial metabolizing pyruvate. (6/2221)

A method was developed for the calculation of metabolic fluxes through individual enzymatic reactions of pyruvate metabolism including the citric acid cycle in rat liver mitochondrial incubated at metabolic states between state 4 and state 3. This method is based on the measurement of the specific radioactivities of the products formed from [2-14C]pyruvate. With this procedure the energy balance of mitochondria incubated in the presence of [2-14C]pyruvate, ATP, bicarbonate and phosphate at different ATP/ADP ratios in the medium was calculated. The ATP/ADP ratios were maintained at a steady state with creatine kinase plus creatine as a phosphoryl acceptor. The calculations revealed that by adding increasing concentrations of creatine up to 20 mM the energy dissipated by the mitochondria decreased but showed a local maximum at 13mM creatine. Omission of bicarbonate from the medium led to a shift of this maximum. When energy dissipation was minimal the overall P/O ratio was maximal. The amount of energy dissipated was paralleled by the magnitude of the pH gradient across the inner membrane. From these results it was concluded that the recycling of H+ ions which consists of a passive leakage of H+ ions into the matrix and an active extrusion of these ions out of this compartment, is an important energy dissipating process. The H+ ion recycling is thus one of the processes which give rise to the state 4 respiration in mitochondria.  (+info)

Influence of bioenergetic stress on heat shock protein gene expression in nucleated red blood cells of fish. (7/2221)

The physiological and biochemical signals that induce stress protein (HSP) synthesis remain conjectural. In this study, we used the nucleated red blood cells from rainbow trout, Oncorhynchus mykiss, to address the interaction between energy status and HSP gene expression. Heat shock (25 degrees C) did not significantly affect ATP levels but resulted in an increase in HSP70 mRNA. Hypoxia alone did not induce HSP transcription in these cells despite a significant depression in ATP. Inhibition of oxidative phosphorylation with azide, in the absence of thermal stress, decreased ATP by 56% and increased lactate production by 62% but did not induce HSP gene transcription. Inhibition of oxidative phosphorylation and glycolysis with azide and iodoacetic acid respectively, decreased ATP by 79% and prevented lactate production, but did not induce either HSP70 or HSP30 gene transcription in these cells. This study demonstrates that a reduction in the cellular energy status will not induce stress protein gene transcription in rainbow trout red blood cells and may, in fact, limit induction during extreme metabolic inhibition.  (+info)

Uncouplers of oxidative phosphorylation can enhance a Fas death signal. (8/2221)

Recent work suggests a participation of mitochondria in apoptotic cell death. This role includes the release of apoptogenic molecules into the cytosol preceding or after a loss of mitochondrial membrane potential DeltaPsim. The two uncouplers of oxidative phosphorylation carbonyl cyanide m-chlorophenylhydrazone (CCCP) and 2, 4-dinitrophenol (DNP) reduce DeltaPsim by direct attack of the proton gradient across the inner mitochondrial membrane. Here we show that both compounds enhance the apoptosis-inducing capacity of Fas/APO-1/CD95 signaling in Jurkat and CEM cells without causing apoptotic changes on their own account. This amplification occurred upstream or at the level of caspases and was not inhibited by Bcl-2. The effect could be blocked by the cowpox protein CrmA and is thus likely to require caspase 8 activity. Apoptosis induction by staurosporine in Jurkat cells as well as by Fas in SKW6 cells was unaffected by CCCP and DNP. The role of cytochrome c during Fas-DNP signaling was investigated. No early cytochrome c release from mitochondria was detected by Western blotting. Functional assays with cytoplasmic preparations from Fas-DNP-treated cells also indicated that there was no major contribution by cytochrome c or caspase 9 to the activation of effector caspases. Furthermore, an increase of rhodamine-123 uptake into intact cells, which has been explained by mitochondrial swelling, occurred considerably later than the caspase activation and was blocked by Z-VAD-fmk. These data show that uncouplers of oxidative phosphorylation can presensitize some but not all cells for a Fas death signal and provide information about the existence of separate pathways in the induction of apoptosis.  (+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.

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.

Mitochondrial encephalomyopathies can be classified into several types based on the specific symptoms and the location of the mutations in the mitochondrial DNA. Some of the most common forms of these disorders include:

1. MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes): This is a rare condition that affects the brain, muscles, and other organs. It is characterized by recurrent stroke-like episodes, seizures, and muscle weakness.
2. Kearns-Sayre syndrome: This is a rare genetic disorder that affects the nervous system and the muscles. It is characterized by progressive weakness and paralysis of the muscles, as well as vision loss and cognitive impairment.
3. Chronic progressive external ophthalmoplegia (CPEO): This is a rare disorder that affects the muscles of the eyes and the extraocular system. It is characterized by progressive weakness of the eye muscles, which can lead to droopy eyelids, double vision, and other vision problems.
4. Mitochondrial DNA depletion syndrome: This is a group of disorders that are caused by a decrease in the amount of mitochondrial DNA. These disorders can affect various parts of the body, including the brain, muscles, and other organs. They can cause a wide range of symptoms, including muscle weakness, seizures, and vision loss.
5. Myoclonic dystonia: This is a rare genetic disorder that affects the muscles and the nervous system. It is characterized by muscle stiffness, spasms, and myoclonus (involuntary jerky movements).
6. Neuronal ceroid lipofuscinoses (NCL): These are a group of rare genetic disorders that affect the brain and the nervous system. They can cause progressive loss of cognitive and motor functions, as well as vision loss and seizures.
7. Spinocerebellar ataxia: This is a group of rare genetic disorders that affect the cerebellum and the spinal cord. They can cause progressive weakness, coordination problems, and other movement disorders.
8. Friedreich's ataxia: This is a rare genetic disorder that affects the nervous system and the muscles. It is characterized by progressive loss of coordination and balance, as well as muscle weakness and wasting.
9. Charcot-Marie-Tooth disease: This is a group of rare genetic disorders that affect the peripheral nerves. They can cause muscle weakness, numbness or tingling in the hands and feet, and other problems with movement and sensation.
10. Progressive supranuclear palsy: This is a rare genetic disorder that affects the brain and the nervous system. It is characterized by progressive loss of movement control, as well as dementia and behavioral changes.

It is important to note that this list is not exhaustive and there may be other rare movement disorders that are not included here. If you suspect that you or a loved one may have a rare movement disorder, it is important to consult with a healthcare professional for proper diagnosis and treatment.

The symptoms of Leigh disease usually become apparent during infancy or early childhood and may include:

* Delayed development
* Loss of motor skills
* Muscle weakness
* Seizures
* Vision loss
* Hearing loss
* Poor feeding and growth

Leigh disease is often diagnosed through a combination of clinical evaluations, laboratory tests, and imaging studies such as MRI or CT scans. There is no cure for Leigh disease, but treatment may include supportive care, such as physical therapy, occupational therapy, and speech therapy, as well as medications to manage seizures and other symptoms. In some cases, a liver transplant may be necessary.

The progression of Leigh disease can vary widely, and the age of onset and rate of progression can vary depending on the specific type of mutation causing the disorder. Some forms of Leigh disease are more severe and progress rapidly, while others may be milder and progress more slowly. In general, however, the disease tends to progress over time, with worsening symptoms and declining function.

Leigh disease is a rare disorder, and there is no specific data on its prevalence. However, it is estimated that mitochondrial disorders, of which Leigh disease is one type, affect approximately 1 in 4,000 people in the United States.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.

Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.

In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.

It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.

See also: Cancer, Tumor

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The symptoms of optic atrophy, autosomal dominant typically begin in adulthood and may include:

* Gradual loss of vision in one or both eyes
* Blurred vision
* Difficulty with peripheral vision
* Sensitivity to light
* Eye pain
* Abnormal eye movements

The condition is caused by mutations in several genes that are responsible for the structure and function of the optic nerve. The exact cause of the condition can be determined through genetic testing.

There is no cure for optic atrophy, autosomal dominant, but treatment may include:

* Glasses or contact lenses to correct refractive errors
* Prism glasses to improve vision
* Low vision aids such as telescopes or magnifying glasses
* Counseling and support to help cope with the visual loss.

The progression of the condition can vary widely, and some people may experience a rapid decline in vision while others may remain stable for many years. Regular monitoring by an eye care professional is important to monitor for any changes in vision and to adjust treatment as needed.

Examples of inborn errors of metabolism include:

1. Phenylketonuria (PKU): A disorder that affects the body's ability to break down the amino acid phenylalanine, leading to a buildup of this substance in the blood and brain.
2. Hypothyroidism: A condition in which the thyroid gland does not produce enough thyroid hormones, leading to developmental delays, intellectual disability, and other health problems.
3. Maple syrup urine disease (MSUD): A disorder that affects the body's ability to break down certain amino acids, leading to a buildup of these substances in the blood and urine.
4. Glycogen storage diseases: A group of disorders that affect the body's ability to store and use glycogen, a form of carbohydrate energy.
5. Mucopolysaccharidoses (MPS): A group of disorders that affect the body's ability to produce and break down certain sugars, leading to a buildup of these substances in the body.
6. Citrullinemia: A disorder that affects the body's ability to break down the amino acid citrulline, leading to a buildup of this substance in the blood and urine.
7. Homocystinuria: A disorder that affects the body's ability to break down certain amino acids, leading to a buildup of these substances in the blood and urine.
8. Tyrosinemia: A disorder that affects the body's ability to break down the amino acid tyrosine, leading to a buildup of this substance in the blood and liver.

Inborn errors of metabolism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood and urine tests. Treatment for these disorders varies depending on the specific condition and may include dietary changes, medication, and other therapies. Early detection and treatment can help manage symptoms and prevent complications.

COX deficiency can present in various forms, including:

1. Leigh syndrome: A severe form of COX deficiency that typically becomes apparent during infancy or early childhood and is characterized by progressive loss of motor function, intellectual disability, seizures, and death in the first few years of life.
2. Late-onset COX deficiency: A milder form of the condition that may not become apparent until adulthood and can present with a range of symptoms such as muscle weakness, ataxia, and neuropathy.
3. COX deficiency with cognitive impairment: A rare form of the condition that is characterized by cognitive impairment, seizures, and other neurological symptoms.

Symptoms of COX deficiency can vary in severity and may include:

1. Muscle weakness
2. Muscle wasting
3. Ataxia (loss of coordination)
4. Neuropathy (nerve damage)
5. Seizures
6. Intellectual disability
7. Developmental delays
8. Vision and hearing loss
9. Optic atrophy (degeneration of the optic nerve)
10. Retinal degeneration

The diagnosis of COX deficiency is based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment for the condition typically involves managing symptoms and addressing any underlying complications. This may include:

1. Medications to control seizures and other neurological symptoms
2. Physical therapy to improve muscle strength and coordination
3. Occupational therapy to assist with daily activities
4. Speech therapy to address communication and swallowing difficulties
5. Vision and hearing aids as needed
6. Dietary supplements to manage any nutritional deficiencies
7. Other supportive measures as needed, such as respiratory support or feeding tubes.

It is important for individuals with COX deficiency to receive early and ongoing medical care from a team of healthcare professionals, including specialists in neurology, ophthalmology, and genetics. With appropriate management, many individuals with COX deficiency can lead active and fulfilling lives despite the challenges posed by the condition.

The term "lipodystrophy" refers to a group of conditions in which there is a loss or abnormal distribution of fat cells. Congenital generalized lipodystrophy is the most severe form of lipodystrophy and is usually diagnosed at birth or soon after.

The symptoms of CGL can vary depending on the severity of the condition, but may include:

1. Poor muscle tone (hypotonia)
2. Delayed development of motor skills
3. Fatigue and weakness
4. Poor appetite and growth delay
5. Abnormal fat distribution in the body
6. Metabolic problems, such as high blood sugar and insulin resistance
7. Increased risk of infections and other complications.

CGL is caused by mutations in genes that are important for adipose tissue development and function. There is currently no cure for CGL, but treatment may involve a combination of medication, nutritional support, and lifestyle modifications to manage the associated symptoms and complications.

The prognosis for individuals with CGL can vary depending on the severity of the condition and the presence of any additional health problems. However, with appropriate medical care and support, many individuals with CGL are able to lead active and fulfilling lives.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

... (UK /ɒkˈsɪd.ə.tɪv/, US /ˈɑːk.sɪˌdeɪ.tɪv/ ) or electron transport-linked phosphorylation or terminal ... The field of oxidative phosphorylation began with the report in 1906 by Arthur Harden of a vital role for phosphate in cellular ... Oxidative phosphorylation uses these molecules and O2 to produce ATP, which is used throughout the cell whenever energy is ... The term oxidative phosphorylation was coined by Volodymyr Belitser [uk] in 1939. For another twenty years, the mechanism by ...
Stryer L (1995). "Oxidative phosphorylation.". Biochemistry (Fourth ed.). New York: W.H. Freeman and Company. pp. 537-549. ISBN ... But the speed at which ATP is produced in this manner is about 100 times that of oxidative phosphorylation. The pH in the ... H+ oxidized in a process called oxidative phosphorylation. The pyruvate produced by glycolysis is an important intermediary in ... Furthermore, the second phosphorylation event is necessary to allow the formation of two charged groups (rather than only one) ...
Berg, Jeremy M.; Tymoczko, J. L.; Stryer, L. (2006). "Oxidative phosphorylation". Biochemistry (5 ed.). pp. 491-526. ISBN 978- ...
Whittam's research was on electrolyte and water in relation to metabolism; oxidative phosphorylation; the relationship between ...
The biosynthesis of ATP is achieved throughout processes such as substrate-level phosphorylation, oxidative phosphorylation, ... "Oxidative phosphorylation". W H Freeman, 2002. Retrieved 4 April 2013. Medh, J. D. "Electron Transport Chain (Overview)" (PDF ... It is this energy coupling and phosphorylation of ADP to ATP that gives the electron transport chain the name oxidative ... Oxidative phosphorylation produces 26 of the 30 equivalents of ATP generated in cellular respiration by transferring electrons ...
Utilizing one full oxygen in oxidative phosphorylation requires the transfer of four electrons. The oxygen will then consume ... "Oxidative phosphorylation revisited". Biotechnology and Bioengineering. 112 (3): 429-437. doi:10.1002/bit.25492. ISSN 1097-0290 ... 464 An electrochemical gradient is essential to mitochondrial oxidative phosphorylation. The final step of cellular respiration ... bacteriorhodopsin and noncyclic photophosphorylation and oxidative phosphorylation. The way bacteriorhodopsin generates a ...
The dissertation was entitled "The influence of thyroidhormones in vivo on oxidative phosphorylation and enzyme activities in ... 1800, 205-212 (2010). B. Kadenbach (ed.): Mitochondrial Oxidative Phosphorylation. Nuclear-Encodes Genes, Enzyme Regulation, ... New extension of the Mitchell Theory for oxidative phosphorylation in mitochondria of living organisms, Biochim. Biophys. Acta ... A hypothesis on the cause of oxidative stress, aging and disease was published by Kadenbach in 2013. Member of the Gesellschaft ...
Uncouplers of oxidative phosphorylation are specifically acting toxicants. Oxidative phosphorylation is a coupling reaction in ... Uncouplers of oxidative phosphorylation disrupt the production of ATP. They do so by binding to the protons in the inner ... Uncouplers of oxidative phosphorylation*AChE inhibitors Irritants CNS seizure agents Respiratory blockers*Dioxins A toxicant ... Terada H (July 1990). "Uncouplers of oxidative phosphorylation". Environ. Health Perspect. 87: 213-8. doi:10.1289/ehp.9087213. ...
The electron transport chain and enzymes in the matrix play a large role in the citric acid cycle and oxidative phosphorylation ... The citric acid cycle produces NADH and FADH2 through oxidation that will be reduced in oxidative phosphorylation to produce ... The inner membrane is a phospholipid bilayer that contains the complexes of oxidative phosphorylation. which contains the ... ISBN 978-0-7167-4684-3. Mitchell, Peter; Moyle, Jennifer (1967-01-14). "Chemiosmotic Hypothesis of Oxidative Phosphorylation". ...
A variety of disorders can be caused by nuclear mutations of oxidative phosphorylation enzymes, such as coenzyme Q10 deficiency ... The majority of ATP in tumor cells is generated via the oxidative phosphorylation pathway (OxPhos). Interference with OxPhos ... Eugene Kennedy and Albert Lehninger discovered in 1948 that mitochondria are the site of oxidative phosphorylation in ... Mitchell P, Moyle J (January 1967). "Chemiosmotic hypothesis of oxidative phosphorylation". Nature. 213 (5072): 137-139. ...
These mutations impair oxidative phosphorylation. As a result, muscle cells cannot produce enough energy, leading to the muscle ... The tRNAGlu molecule is localized to the mitochondria, and is involved in the assembly of oxidative phosphorylation proteins. ...
This is called oxidative phosphorylation. This generates much more ATP than glycolysis alone. For this reason, fermentation is ...
Moyle conducted a lot of research regarding cellular respiration, oxidative phosphorylation, and properties of purified ... The chemiosmotic theory explained the mechanism for oxidative phosphorylation, stating that ATP synthesis requires chemiosmosis ... Jennifer Moyle; Mitchell, Peter (January 1967). "Chemiosmotic Hypothesis of Oxidative Phosphorylation". Nature. 213 (5072): 137 ...
Salts of tetraphenylborate uncouple oxidative phosphorylation. Sodium tetraphenylborate Potassium tetraphenylborate ...
Kalckar referred to this process as "aerobic phosphorylation" (now called oxidative phosphorylation, a biochemical process ... The Coris had unsuccessfully attempted to reproduce Kalckar's oxidative phosphorylation work, and Kalckar was able to point out ... Kalckar HM (1974). "Origins of the concept oxidative phosphorylation". Mol. Cell. Biochem. 5 (1-2): 55-63. doi:10.1007/ ... "oxidative phosphorylation". During this period, Lundsgaard was preoccupied as physiology department chair, consequently Fritz ...
MLYCD Combined oxidative phosphorylation deficiency 1; 609060; GFM1 Combined oxidative phosphorylation deficiency 2; 610498; ... MRPS16 Combined oxidative phosphorylation deficiency 3; 610505; TSFM Combined oxidative phosphorylation deficiency 4; 610678; ... TUFM Combined oxidative phosphorylation deficiency 5; 611719; MRPS22 Combined oxidative phosphorylation deficiency 6; 300816; ...
Casiday R, Herman C, Frey R (5 September 2008). "Energy for the Body: Oxidative Phosphorylation". www.chemistry.wustl.edu. ...
This enzyme participates in oxidative phosphorylation. It has four cofactors: cytochrome c1, cytochrome b-562, cytochrome b-566 ... oxidative phosphorylation). Complex III is a multisubunit transmembrane protein encoded by both the mitochondrial (cytochrome b ... Muller, F. L.; Lustgarten, M. S.; Jang, Y.; Richardson, A. & Van Remmen, H. (2007). "Trends in oxidative aging theories". Free ...
This is important in driving oxidative phosphorylation. ATP is dephosphorylated to ADP and inorganic phosphate. On the cellular ... Casiday R, Herman C, Frey R (5 September 2008). "Energy for the Body: Oxidative Phosphorylation". Department of Chemistry, ... Phosphatase Phosphorylation Ardito F, Giuliani M, Perrone D, Troiano G, Lo Muzio L (August 2017). "The crucial role of protein ... Phosphorylation of a protein produces many biochemical effects, such as changing its conformation to alter its binding to a ...
"KEGG DISEASE: Combined oxidative phosphorylation deficiency". www.genome.jp. Atkinson, Gemma C; Hauryliuk, Vasili; Tenson, ...
... oxidative phosphorylation and ATP synthesis. Inhibitor and Uncouplers of oxidative phosphorylation". Retrieved 2020-02-02. ... In the process of oxidative phosphorylation, a globular cytochrome cc protein is involved in the electron transfer from the ...
This enzyme participates in oxidative phosphorylation. It has four cofactors: cytochrome c1, cytochrome b-562, cytochrome b-566 ...
Roles of photophosphorylation and oxidative phosphorylation". Planta. 161 (2): 129-136. doi:10.1007/bf00395472. ISSN 0032-0935 ...
Kalckar HM (November 1974). "Origins of the concept oxidative phosphorylation". Molecular and Cellular Biochemistry. 5 (1-2): ... Søballe B, Poole RK (August 1999). "Microbial ubiquinones: multiple roles in respiration, gene regulation and oxidative stress ... These alterations are distinct from other post-translation protein modifications, such as phosphorylation, methylation, or ...
NADH can be used by the electron transport chain to create further ATP as part of oxidative phosphorylation. To fully oxidize ... from Krebs cycle Oxidative phosphorylation 2 NADH+H+ from glycolysis: 2 × 1.5 ATP (if glycerol phosphate shuttle transfers ... oxidative phosphorylation occurs in the mitochondrial cristae. It comprises the electron transport chain that establishes a ... Most of the ATP produced by aerobic cellular respiration is made by oxidative phosphorylation. The energy released is used to ...
This structure traps one proton, which is quite helpful for oxidative phosphorylation. As the head group forms such compact ... Complex V of the oxidative phosphorylation machinery also displays high binding affinity for CL, binding four molecules of CL ... Thomas H. Haines; Norbert A. Dencher (2002). "Cardiolipin: a proton trap for oxidative phosphorylation". FEBS Lett. 528 (1-3): ... During the oxidative phosphorylation process catalyzed by Complex IV, large quantities of protons are transferred from one side ...
This process is part of oxidative phosphorylation. A stepwise model for the emergence of chemiosmosis, a key element in the ... This process is called oxidative phosphorylation because it uses energy released by the oxidation of NADH and FADH2 to ... Cellular respiration Citric acid cycle Electrochemical gradient Glycolysis Oxidative phosphorylation Mitchell P (July 1961). " ... "Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism". Nature. 191 (4784): 144- ...
... is an uncoupler of oxidative phosphorylation. It is a weak acid that can pass through lipid membranes when it's in the ... Dinoseb interferes with the oxidative phosphorylation by acting as an uncoupler, which is the production of ATP in the ...
Elamipretide, an agent which protects CL from oxidative damage to maintain mitochondrial cristae and oxidative phosphorylation ... Further, CL plays important roles in oxidative phosphorylation by stabilizing the chain complexes with its linkages between ... Haines TH, Dencher NA (September 2002). "Cardiolipin: a proton trap for oxidative phosphorylation". FEBS Letters. 528 (1-3): 35 ... and remodeling by tafazzin aids in removing and replacing acyl chains damaged by oxidative stress. During apoptosis and similar ...
At the time, the biochemical mechanism of ATP synthesis by oxidative phosphorylation was unknown. Mitchell realised that the ... Mitchell's chemiosmotic hypothesis was the basis for understanding the actual process of oxidative phosphorylation. ... Mitchell, P. (1966). "Chemiosmotic Coupling in Oxidative and Photosynthetic Phosphorylation". Biological Reviews. 41 (3): 445- ... Mitchell, P. (1961). "Coupling of Phosphorylation to Electron and Hydrogen Transfer by a Chemi-Osmotic type of Mechanism" (PDF ...
It was shown that Daxx associates with Pml only when exposed to high oxidative stress or UV-irradiation. Another study showed ... This transport mechanism is phosphorylation dependent. Nevertheless, it is not known whether the Fas-receptor stimuli or the ... phosphorylation and polyubiquitination. Daxx is uniformly expressed throughout the body, except in the testes and thymus, which ...
A related problem for aerobic organisms is oxidative stress. Here, processes including oxidative phosphorylation and the ... In many organisms, the capture of solar energy is similar in principle to oxidative phosphorylation, as it involves the storage ... In oxidative phosphorylation, the electrons removed from organic molecules in areas such as the citric acid cycle are ... It also serves as a carrier of phosphate groups in phosphorylation reactions. A vitamin is an organic compound needed in small ...
Cao C, Leng Y, Kufe D (August 2003). "Catalase activity is regulated by c-Abl and Arg in the oxidative stress response". J. ... Miyoshi-Akiyama T, Aleman LM, Smith JM, Adler CE, Mayer BJ (July 2001). "Regulation of Cbl phosphorylation by the Abl tyrosine ... Mayer BJ, Hirai H, Sakai R (March 1995). "Evidence that SH2 domains promote processive phosphorylation by protein-tyrosine ... The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, ...
Phosphorylation of the transcription factor may activate it and that activated transcription factor may then activate the ... Liefke R, Windhof-Jaidhauser IM, Gaedcke J, Salinas-Riester G, Wu F, Ghadimi M, Dango S (June 2015). "The oxidative demethylase ... Li QJ, Yang SH, Maeda Y, Sladek FM, Sharrocks AD, Martins-Green M (January 2003). "MAP kinase phosphorylation-dependent ... enhancer to which it is bound (see small red star representing phosphorylation of transcription factor bound to enhancer in the ...
Wen JJ, Garg N (2005). "Oxidative modification of mitochondrial respiratory complexes in response to the stress of Trypanosoma ... 2006). "Global, in vivo, and site-specific phosphorylation dynamics in signaling networks". Cell. 127 (3): 635-48. doi:10.1016/ ...
The heavy strand is rich in guanine and encodes 12 subunits of the oxidative phosphorylation system, two ribosomal RNAs (12S ... Some of which are increasingly recognized as an important cause of human pathology such as oxidative phosphorylation (OXPHOS) ... all of which are involved in the oxidative phosphorylation process. The complete sequence of the human mitochondrial DNA in ... higher levels of reactive oxygen species and increased oxidative stress. Mutant huntingtin protein promotes oxidative damage to ...
Enzymes of this family in anaerobic oxidative phosphorylation and inorganic-donor-based lithotrophic respiration. These enzymes ...
More recently, S-nitrosothiols have been implicated as primary mediators of protein S-nitrosylation, the oxidative modification ... bioactivity and to regulate protein function through enzymatic mechanisms analogous to phosphorylation and ubiquitinylation: ...
Oxidative phosphorylation Electron transport chain Metabolism PDB: 1SUW​; Liu J, Lou Y, Yokota H, Adams PD, Kim R, Kim SH (Nov ... Thus, NADK can modulate responses to oxidative stress by controlling NADP synthesis. Bacterial NADK is shown to be inhibited ... "Evidence that feedback inhibition of NAD kinase controls responses to oxidative stress". Proceedings of the National Academy of ... and the yeast mitochondrial isoform accepts both NAD+ and NADH as substrates for phosphorylation. ATP + NAD+ ⇌ {\displaystyle \ ...
... utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. ATP synthase is ...
... enzymes needed for the biosynthesis of lipids and carotenoids and the processes of photosynthesis and oxidative phosphorylation ... Breen ME, Soellner MB (January 2015). "Small molecule substrate phosphorylation site inhibitors of protein kinases: approaches ...
... and oxidative stress response kinase 1 (OXSR1). Phosphorylation of SPAK's T loop located in its catalytic domain will activate ... Further, phosphorylation at another site (Ser378) increases WNK1 activity. An autoinhibitory domain is located within the C- ... ACH phosphorylation by WNK1 promotes the translocation of ROMK1 to clathrin coated pits triggering endocytosis. WNK1 may ... The increased WNK1 leads to activation of SPAK/OSR1 that activate NKCC1/2 via subsequent phosphorylation. NKCC1/2 will promote ...
... is a chemical inhibitor of oxidative phosphorylation. It is a nitrile, hydrazone and protonophore. In general, CCCP causes the ...
Proteolytic activity can further complicate the reduction in energy metabolism and an increase in oxidative damage as a result ... mechanism for regulation of the human mitochondrial branched-chain alpha-ketoacid dehydrogenase complex by phosphorylation". ...
... oxidative decarboxylation - oxidative phosphorylation - oxygen - oxytocin - oxytocin receptor P42 MAP kinase -p53 - pancreatic ... phosphorylation - phosphoserine - phosphothreonine - phosphotyrosine - photobiology - photolysis - photophosphorylation - ...
... phosphorylation (NetPhos 2.0), sumoylation (SUMOplot Analysis Program) and O-ß-GlcNAc attachment(YinOYang WWW). The CXorf49 ... Oxidative Medicine and Cellular Longevity. 2015: 296146. doi:10.1155/2015/296146. PMC 4452872. PMID 26078803. Protein BLAST ( ...
Unlike oxidative phosphorylation, oxidation and phosphorylation are not coupled in the process of substrate-level ... Most ATP is generated by oxidative phosphorylation in aerobic or anaerobic respiration while substrate-level phosphorylation ... 2 molecules of NADH are also produced and can be used in oxidative phosphorylation to generate more ATP. ATP can be generated ... An alternative method used to create ATP is through oxidative phosphorylation, which takes place during cellular respiration. ...
... and tachypnea is experienced until energy is produced via oxidative phosphorylation, primarily from Free Fatty Acids. Oxidative ... leaving oxygen and blood borne fuels unable to be delivered to muscle cells adequately for oxidative phosphorylation). The ... phosphorylation is only achievable for light-moderate aerobic activity, as high-intensity (fast-paced) aerobic activity relies ...
In addition, mutations in ELAC2 are known to cause combined oxidative phosphorylation deficiency 17 (COXPD17), a rare autosomal ...
This was uncovered using the spectroscopy of lipoxidation signals, which are byproducts of oxidative phosphorylation and ...
Srivastava S, Barrett JN, Moraes CT (2007). "PGC-1α/β upregulation is associated with improved oxidative phosphorylation in ...
... stem cells often use oxidative phosphorylation or glutamine as a primary energy source. Several studies have indicated ... Zheng J (2012). "Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review)". Oncology Letters. 4 (6): ... But a minority of cancer types rely on oxidative phosphorylation as the primary energy source, including lymphoma, leukemia, ... but promotes cancers that depend upon oxidative phosphorylation. A low-carbohydrate diet (ketogenic diet) has sometimes been ...
... as it is an extremely potent uncoupler of oxidative phosphorylation with an IC50 of about 1 micromolar (≈500 nanograms per ... a structurally novel uncoupler of oxidative phosphorylation". Biochim. Biophys. Acta. 1016 (3): 344-8. doi:10.1016/0005-2728(90 ...
Oligomerization and trans-phosphorylation of Ire1p (Ern1p) are required for kinase activation". The Journal of Biological ... as well as to induce a switch of skeletal fibers to slow oxidative muscle fibers, as these are fatigue-resistant. Therefore, ... A downstream effect of the ER stress is a significant decrease in insulin-stimulated phosphorylation of tyrosine residues of ...
After the phosphorylation, the first degrading enzyme, beta-amylase (BAM) can attack the glucose chain at its non-reducing end ... Sucrose can then be used in the oxidative pentose phosphate pathway in the mitochondria, to generate ATP at night. While ...
DBT protein causes phosphorylation and turnover of monomeric PER proteins. TIM is also phosphorylated by shaggy until sunset. ... "including oxidative stress, cell metabolism, immune and inflammatory responses, epigenetic modification, hypoxia/hyperoxia ... PER undergoes progressive phosphorylation and ultimately degradation. Absence of PER and TIM allows activation of clk and cyc ... February 2001). "An hPer2 phosphorylation site mutation in familial advanced sleep phase syndrome". Science. 291 (5506): 1040-3 ...
BCS1L is a protein that adds Rieske Fe/S to complex III during oxidative phosphorylation of cellular respiration. Mutations of ... The protein product of this gene is BCS1L, which plays an important role in oxidative phosphorylation. Mutated BCS1L increases ... which reduces oxidative phosphorylation and increases the production of reactive oxygen species. Two missense mutations linked ...
... and site-specific phosphorylation dynamics in signaling networks". Cell. 127 (3): 635-48. doi:10.1016/j.cell.2006.09.026. PMID ... "Enhanced exercise and regenerative capacity in a mouse model that violates size constraints of oxidative muscle fibres , eLife ...
... particularly the electron transport chain and oxidative phosphorylation. Green was born in Brooklyn, New York, the son of ... making vital contributions to studies on oxidative phosphorylation, the electron transport chain and beta oxidation. He was ...
Finally, phosphorylation by M cyclins (e.g., Clb1, 2, 3 and 4) in complex with Cdk1 leads to spindle assembly and sister ... oxidative metabolism, and cellular transport". Exp. Cell Res. 289 (2): 211-221. doi:10.1016/S0014-4827(03)00261-1. PMID ... Multisite phosphorylation, by Cdk1-Cln1/2, of Sic1 is thought to time Sic1 ubiquitination and destruction, and by extension, ... Cdk1 phosphorylation also leads to the activation of the ubiquitin-protein ligase APCCdc20, an activation which allows for ...
Combined oxidative phosphorylation deficiency 1 is a severe condition that primarily impairs neurological and liver function. ... medlineplus.gov/genetics/condition/combined-oxidative-phosphorylation-deficiency-1/ Combined oxidative phosphorylation ... fewer mitochondrial proteins involved in oxidative phosphorylation are produced. (The process of oxidative phosphorylation ... Combined oxidative phosphorylation deficiency 1 is caused by mutations in the GFM1 gene. This gene provides instructions for ...
Nuclear genome-derived circular RNA circPUM1 localizes in mitochondria and regulates oxidative phosphorylation in esophageal ... Knock-down of circPUM1 would result in lower intracellular oxygen concentration, downregulated oxidative phosphorylation, ... circPUM1 plays a critical role in maintaining the stability of mitochondrial complex III to enhance oxidative phosphorylation ...
Oxidative Phosphorylation These data illustrate essential roles for course I PI3Ks in mediating the consequences of RANKL on ... Oxidative Phosphorylation As the delivery decides the effective concentration from the probes designed for cell targeting, ...
2 of the Biochemistry questions and answers section on Oxidative Phosphorylation Section 1. Discussion Page 1 of 1, sorted by ...
... : This post include the list of inhibitors and uncouplers involved in the ... This antibiotic also inhibits both ETC and oxidative phosphorylation.. 3. Atractylate. *It backs oxidative phosphorylation by ... Inhibitors of Oxidative Phosphorylation. The given below is the list of inhibitors in Oxidative Phosphorylation. ... Uncouplers of Oxidative Phosphorylation. Uncouplers can be defined as A substance that uncouples phosphorylation of ADP from ...
Metabolism - Oxidative Phosphorylation PubMed MeSh Term *Overview. Overview. subject area of * Cationic gold nanoparticles ... Interleukin 37 reverses the metabolic cost of inflammation, increases oxidative respiration, and improves exercise tolerance ...
OXA1L mutations cause mitochondrial encephalopathy and a combined oxidative phosphorylation defect. Lookup NU author(s): Dr ...
Oxidative-phosphorylation; Cytopathology; Cell-alteration; Alveolar-cells; Cellular-respiration; Humans; Nucleotides; Cell- ...
Dysfunctional oxidative phosphorylation shunts branched‐chain amino acid catabolism onto lipogenesis in skeletal muscle. 0 ... "Dysfunctional Oxidative Phosphorylation Shunts Branched‐Chain Amino Acid Catabolism onto Lipogenesis in Skeletal Muscle." The ... dependent inhibition of mitochondrial respiratory complex II enhancing oxidative phosphorylation dysfunction which results in ...
Interests: cell culture; western blot analysis; apoptosis; reactive oxygen species; mitochondria; oxidative phosphorylation; ... Interests: mitochondria; respiratory complexes; Coenzyme Q; electron tansfer; oxidative phosphorylation; reactive oxygen ... Special Issue in Biomolecules: Involvement of Oxidative Stress Signalling Pathways in Cell Death. ... Interests: molecular physiology/pharmacology; oxidative stress; cell death pathways; aldehyde dehydrogenases; cancer stem cells ...
High expression of oxidative phosphorylation genes predicts improved survival in squamous cell carcinomas of the head and neck ... Lin, C.-S., Wang, L.-S., Tsai, C.-M. & Wei, Y.-H. Low copy number and low oxidative damage of mitochondrial DNA are associated ... They switch to glycolysis to evade damage that could result from the high levels of ROS inevitably produced during oxidative ... Indeed, prior studies have shown that oxidative stress and several pathological conditions, including cancer, alter mtDNA ...
We suggest that cancer cells can decouple the TCA cycle from oxidative phosphorylation on an "on demand" basis. This decoupling ... glyclolysis and mitochondrial oxidative phosphorylation. These methods measure oxygen consumption rate (OCR) and extracellular ... human glioblastoma cells partially decouple the TCA cycle from oxidative phosphorylation associated with rapid cell ... human glioblastoma cells partially decouple the TCA cycle from oxidative phosphorylation associated with rapid cell ...
In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to glucose.
reduced oxidative phosphorylation.. *Another mechanism involves substitution of As (V) for phosphorus in many biochemical ... These include modes that are predominately genotoxic (i.e., chromosomal abnormalities, oxidative stress, and gene amplification ...
Oxidative-phosphorylation; Protein-biochemistry; Animal-studies; Molecular-biology; Oxidative-processes; Radiation-effects; ... These results demonstrate that H2O2 generation is required for UV-induced phosphorylation of Akt and p70(S6k), and involved in ... p38 kinase and led to increases in phosphorylation of Akt and p70(S6k) in mouse epidermal JB6 cells. The scavenging of UV- ... Genes; Free-radicals; Author Keywords: oxidative stress; antioxidants; oxyradical scavengers; MAP kinases ...
This process is called oxidative phosphorylation. . Although most DNA is packaged in chromosomes within the nucleus (nuclear ... These deletions impair oxidative phosphorylation and decrease the energy available to cells. ... in Pearson syndrome result in the loss of genes that provide instructions for proteins involved in oxidative phosphorylation. ...
2003) Neuroprotection and neuronal dysfunction upon repetitive inhibition of oxidative phosphorylation. Exp Neurol 183:346-354. ... 1995) Nerve growth factor triggers microfilament assembly and paxillin phosphorylation in human B lymphocytes. J Exp Med 181: ... 1998) Actin depolymerizing factor and cofilin phosphorylation dynamics: response to signals that regulate neurite extension. ...
... young RPE prefers an oxidative metabolic state and uses the generated lactate as a substrate for oxidative phosphorylation and ... However, under stress, a shift from oxidative phosphorylation to aerobic glycolysis induces the M1 microglia phenotype through ... The resting metabolic state of M0 homeostatic microglia is oxidative phosphorylation. ... As the delicate mutualism between oxidative and glycolytic tissue processes fails, cones begin to die from malnutrition (5). ...
Oxidative phosphorylation:,/b> able to synthesize ATP by oxidative phosphorulation. structural genoes for cytochrome bd quinol ...
AIF deficiency compromises oxidative phosphorylation. EMBO J. 2004;23:4679-4689. doi: 10.1038/sj.emboj.7600461.. 30. Stambolsky ... A healthy cell produces 89% of its energy using oxygen, and 11% through non-oxidative metabolism (non-oxidative metabolism is ... Oxidative energy production is far more efficient than fermentation. Almost 20 times more energy is released when glucose is ... Oxidative energy production takes place in a cellular organelle called the mitochondria. The mitochondria are commonly referred ...
The most overrepresented pathways included ribosomal protein, translation, oxidative phosphorylation and cytochrome-C oxidase ...
Blood agents include cyanide, which works by blocking oxidative phosphorylation in the body.. Toxic industrial chemicals such ...
... occurs through oxidative phosphorylation. Uncoupling oxidative phosphorylation at the mitochondrial level leads to profound ... but this and other chlorinated phenols are known to uncouple oxidative phosphorylation (6). Most production of adenosine ...
Little is known about the proteins function; it is thought to contribute to oxidative phosphorylation (Martherus et al., 2010 ...
... and so it contributes to protection from oxidative damages. ... during oxidative phosphorylation takes place mainly in the ... Inflammation and increased oxidative stress are also common features in chronic kidney disease patients [130, 141]. Oxidative ... of the ATP produced in aerobic cells is a result of mitochondrial oxidative phosphorylation [59]. The ETC which is coupled to ... decrease in oxidative stress, and increase in immune system activity [130, 131]. Oxidative stress has complex and different ...
... oxidative phosphorylation, and glycolysis. It contributes to the structural development of bone and is required for the ...
Oxidative phosphorylation. 1.18. map00130. Ubiquinone biosynthesis. 1.18. map04320. Dorso-ventral axis formation. ...
  • Combined oxidative phosphorylation deficiency 1 is a severe condition that primarily impairs neurological and liver function. (medlineplus.gov)
  • Liver disease is common in people with combined oxidative phosphorylation deficiency 1, with individuals quickly developing liver failure. (medlineplus.gov)
  • Individuals with combined oxidative phosphorylation deficiency 1 usually do not survive past early childhood, although some people live longer. (medlineplus.gov)
  • Combined oxidative phosphorylation deficiency 1 is likely a rare disorder, although its prevalence is unknown. (medlineplus.gov)
  • Combined oxidative phosphorylation deficiency 1 is caused by mutations in the GFM1 gene. (medlineplus.gov)
  • The condition is called combined oxidative phosphorylation deficiency 1 because it impairs the function of more than one of these complexes. (medlineplus.gov)
  • A shortage of energy in these tissues leads to cell death, causing the neurological and liver problems in people with combined oxidative phosphorylation deficiency 1. (medlineplus.gov)
  • 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 reducing equivalents mainly generated in the mitochondria by the final common oxidative pathway, the citric acid cycle. (biochemden.com)
  • Oxidative phosphorylation is a metabolic pathway in which the energy produced by the oxidation of nutrients is stored in the mitochondria in the form of ATP. (assignmentexpert.com)
  • As a result, fewer mitochondrial proteins involved in oxidative phosphorylation are produced. (medlineplus.gov)
  • The molecular basis for tissue specificity of the oxidative phosphorylation deficiencies in patients with mutations in the mitochondrial translation factor EFG1. (medlineplus.gov)
  • Therefore, we conclude that circPUM1 plays a critical role in maintaining the stability of mitochondrial complex III to enhance oxidative phosphorylation for ATP production of ESCC cells and moreover propose that ESCC cells exploit circPUM1 during cell adaptation. (nih.gov)
  • It backs oxidative phosphorylation by compelling with ATP & ADP for a site on the ADP-ATP antiport of the mitochondrial membranes. (biochemden.com)
  • In turn, muscle accumulation of acetyl‐CoA leads to acetylation‐dependent inhibition of mitochondrial respiratory complex II enhancing oxidative phosphorylation dysfunction which results in augmented ROS production. (bioinfor.com)
  • Genes on mtDNA provide instructions for proteins that are primarily involved in the process of converting the energy from food into a form cells can use ( oxidative phosphorylation ). (medlineplus.gov)
  • The process of oxidative phosphorylation involves five groups of proteins, or complexes. (medlineplus.gov)
  • The mtDNA deletions involved in Pearson syndrome result in the loss of genes that provide instructions for proteins involved in oxidative phosphorylation. (medlineplus.gov)
  • The most overrepresented pathways included ribosomal protein, translation, oxidative phosphorylation and cytochrome-C oxidase activity. (usda.gov)
  • Are you looking for the details of Inhibitors and UnCouplers of Oxidative Phosphorylation? (biochemden.com)
  • The given below is the list of inhibitors in Oxidative Phosphorylation. (biochemden.com)
  • One of the inhibitors list which blocks the oxidative phosphorylation. (biochemden.com)
  • Magnesium is required for energy production, oxidative phosphorylation, and glycolysis. (nih.gov)
  • What is the significance of oxidative phosphorylation?Illustrate your answer with an example for each. (assignmentexpert.com)
  • Oxidative phosphorylation is associated with the transfer of electrons from donor compounds to acceptor compounds during redox reactions. (assignmentexpert.com)
  • These deletions impair oxidative phosphorylation and decrease the energy available to cells. (medlineplus.gov)
  • Remarkably, most of oxylipins linked to inflammation and oxidative stress derived from arachidonic acid (AA), like prostaglandins and mono-hydroxides, were increased in ALS 120d rats. (bvsalud.org)
  • The oxidative phosphorylation is a crucial metabolic process that results in the formation of ATP. (assignmentexpert.com)
  • Consequently, melatonin has beneficial effects including stimulation of antioxidant enzymes, inhibition of lipid peroxidation, and so it contributes to protection from oxidative damages. (intechopen.com)
  • Treatment of cells with UV radiation or H2O2 also markedly activated Erks, JNKs, p38 kinase and led to increases in phosphorylation of Akt and p70(S6k) in mouse epidermal JB6 cells. (cdc.gov)
  • The oxidative phosphorylation also results in the release of heat in adipocytes involved in the thermoregulatory processes. (assignmentexpert.com)
  • The following compounds inhibit both electron transport and oxidative phosphorylation. (biochemden.com)
  • They inhibit the transfer of high-energy phosphate to ADP and also inhibit electron transfers coupled to phosphorylation. (biochemden.com)
  • There are several well-known biologically active substances and toxins that inhibit oxidative phosphorylation and lead to death. (assignmentexpert.com)
  • The process results in the accumulation of the potential energy composed of a proton gradient and an electric potential that are used by ATP synthase to synthesize ATP from ADP during the phosphorylation reaction. (assignmentexpert.com)
  • Organs that have high energy demands, such as the brain and liver, are particularly affected by the resulting impairment of oxidative phosphorylation. (medlineplus.gov)
  • It transports a proton down the gradient and uses the energy to complete the phosphorylation of ADP to ATP. (moviecultists.com)
  • These include modes that are predominately genotoxic (i.e., chromosomal abnormalities, oxidative stress, and gene amplification) vs. more nongenotoxic (i.e., altered growth factors, enhanced cell proliferation and promotion of carcinogenesis, and altered DNA repair). (cdc.gov)
  • Blood agents include cyanide, which works by blocking oxidative phosphorylation in the body. (scienceblog.com)
  • MCQ on ELECTRON TRANSPORT SYSTEM AND OXIDATIVE PHOSPHORYLATION class 11 Biology with answers were prepared based on the latest pattern.We have provided class 11 Biology MCQs question with Answers to help students understand the concept very well. (biologysir.com)