6-Aminonicotinamide: A vitamin antagonist which has teratogenic effects.HexosephosphatesPentose Phosphate Pathway: An oxidative decarboxylation process that converts GLUCOSE-6-PHOSPHATE to D-ribose-5-phosphate via 6-phosphogluconate. The pentose product is used in the biosynthesis of NUCLEIC ACIDS. The generated energy is stored in the form of NADPH. This pathway is prominent in tissues which are active in the synthesis of FATTY ACIDS and STEROIDS.Glucose: 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.Phosphogluconate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the reaction 6-phospho-D-gluconate and NADP+ to yield D-ribulose 5-phosphate, carbon dioxide, and NADPH. The reaction is a step in the pentose phosphate pathway of glucose metabolism. (From Dorland, 27th ed) EC DehydrogenaseNiacinamide: An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and PELLAGRA. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.Glycolysis: 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.Nitroblue Tetrazolium: Colorless to yellow dye that is reducible to blue or black formazan crystals by certain cells; formerly used to distinguish between nonbacterial and bacterial diseases, the latter causing neutrophils to reduce the dye; used to confirm diagnosis of chronic granulomatous disease.HexosesTeratogens: An agent that causes the production of physical defects in the developing embryo.Abnormalities, Drug-Induced: Congenital abnormalities caused by medicinal substances or drugs of abuse given to or taken by the mother, or to which she is inadvertently exposed during the manufacture of such substances. The concept excludes abnormalities resulting from exposure to non-medicinal chemicals in the environment.Tolonium Chloride: A phenothiazine that has been used as a hemostatic, a biological stain, and a dye for wool and silk. Tolonium chloride has also been used as a diagnostic aid for oral and gastric neoplasms and in the identification of the parathyroid gland in thyroid surgery.Bullying: Aggressive behavior intended to cause harm or distress. The behavior may be physical or verbal. There is typically an imbalance of power, strength, or status between the target and the aggressor.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Communication: The exchange or transmission of ideas, attitudes, or beliefs between individuals or groups.User-Computer Interface: The portion of an interactive computer program that issues messages to and receives commands from a user.ToluidinesAlgorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task.Verbal Behavior: Includes both producing and responding to words, either written or spoken.Water: A clear, odorless, tasteless liquid that is essential for most animal and plant life and is an excellent solvent for many substances. The chemical formula is hydrogen oxide (H2O). (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Brenner Tumor: A smooth, solid or cystic fibroepithelial (FIBROEPITHELIAL NEOPLASMS) tumor, usually found in the OVARIES but can also be found in the adnexal region and the KIDNEYS. It consists of a fibrous stroma with nests of epithelial cells that sometimes resemble the transitional cells lining the urinary bladder. Brenner tumors generally are benign and asymptomatic. Malignant Brenner tumors have been reported.Astrocytes: A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.Cerebellum: The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.Purkinje Cells: The output neurons of the cerebellar cortex.Ganciclovir: An ACYCLOVIR analog that is a potent inhibitor of the Herpesvirus family including cytomegalovirus. Ganciclovir is used to treat complications from AIDS-associated cytomegalovirus infections.Thymidine Kinase: An enzyme that catalyzes the conversion of ATP and thymidine to ADP and thymidine 5'-phosphate. Deoxyuridine can also act as an acceptor and dGTP as a donor. (From Enzyme Nomenclature, 1992) EC, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Neuroglia: The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Genes, Transgenic, Suicide: Genes that are used transgenically, i.e., via GENE TRANSFER TECHNIQUES to induce CELL DEATH.Goldfish: Common name for Carassius auratus, a type of carp (CARPS).Nerve Regeneration: Renewal or physiological repair of damaged nerve tissue.Retinal Ganglion Cells: Neurons of the innermost layer of the retina, the internal plexiform layer. They are of variable sizes and shapes, and their axons project via the OPTIC NERVE to the brain. A small subset of these cells act as photoreceptors with projections to the SUPRACHIASMATIC NUCLEUS, the center for regulating CIRCADIAN RHYTHM.Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.Optic Nerve: The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.Regeneration: The physiological renewal, repair, or replacement of tissue.Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes.Visual Pathways: Set of cell bodies and nerve fibers conducting impulses from the eyes to the cerebral cortex. It includes the RETINA; OPTIC NERVE; optic tract; and geniculocalcarine tract.Myelin Sheath: The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.Copyright: It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)Commerce: The interchange of goods or commodities, especially on a large scale, between different countries or between populations within the same country. It includes trade (the buying, selling, or exchanging of commodities, whether wholesale or retail) and business (the purchase and sale of goods to make a profit). (From Random House Unabridged Dictionary, 2d ed, p411, p2005 & p283)Reference Standards: A basis of value established for the measure of quantity, weight, extent or quality, e.g. weight standards, standard solutions, methods, techniques, and procedures used in diagnosis and therapy.Medical Secretaries: Individuals responsible for various duties pertaining to the medical office routine.Heptachlor Epoxide: An oxidation product of HEPTACHLOR formed by many plants and animals, including humans, after exposure to HEPTACHLOR. It has been shown to remain in soil treated with HEPTACHLOR for over fifteen years and is toxic to animals and humans. (From ATSDR Public Heath Statement, April 1989)Web Browser: Software application for retrieving, presenting and traversing information resources on the World Wide Web.Aldrin: A highly poisonous substance that was formerly used as an insecticide. The manufacture and use has been discontinued in the U.S. (From Merck Index, 11th ed)Reference Values: The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.Colonialism: The aggregate of various economic, political, and social policies by which an imperial power maintains or extends its control over other areas or peoples. It includes the practice of or belief in acquiring and retaining colonies. The emphasis is less on its identity as an ideological political system than on its designation in a period of history. (Webster, 3d ed; from Dr. J. Cassedy, NLM History of Medicine Division)Phosphorous Acids: Inorganic derivatives of phosphorus trihydroxide (P(OH)3) and its tautomeric form dihydroxyphosphine oxide (HP=O(OH)2). Note that organic derivatives of phosphonic acids are listed under are ORGANOPHOSPHONATES.Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.Superoxides: Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.Hydroxyeicosatetraenoic Acids: Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes.Constriction: The act of constricting.Mitochondria: 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)Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC Oxidase: A flavoprotein enzyme that catalyzes the univalent reduction of OXYGEN using NADPH as an electron donor to create SUPEROXIDE ANION. The enzyme is dependent on a variety of CYTOCHROMES. Defects in the production of superoxide ions by enzymes such as NADPH oxidase result in GRANULOMATOUS DISEASE, CHRONIC.Hypertension, Pulmonary: Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.12-Hydroxy-5,8,10,14-eicosatetraenoic Acid: A lipoxygenase metabolite of ARACHIDONIC ACID. It is a highly selective ligand used to label mu-opioid receptors in both membranes and tissue sections. The 12-S-HETE analog has been reported to augment tumor cell metastatic potential through activation of protein kinase C. (J Pharmacol Exp Ther 1995; 274(3):1545-51; J Natl Cancer Inst 1994; 86(15):1145-51)Cells, Cultured: 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.
(1/52) Effect of 6-aminonicotinamide and other protein synthesis inhibitors on formation of platinum-DNA adducts and cisplatin sensitivity.

The present study was undertaken to examine the mechanistic basis for the recent observation that the pyridine nucleotide derivative 6-aminonicotinamide (6AN, NSC 21206) enhances the accumulation and resulting cytotoxicity of cisplatin in a variety of tumor cell lines. When A549 lung cancer cells or K562 leukemia cells were treated with 62.5 microM 6AN for 21 h and then pulse-labeled with [(35)S]methionine for 1 h, increased labeling of five polypeptides, one of which corresponded to a M(r) approximately 78,000 glucose-regulated protein (GRP78), was observed. Two subsequent observations, however, suggested that up-regulation of these polypeptides was unlikely to explain the interaction between 6AN and cisplatin: 1) the concentration of 6AN required to induce GRP78 was 4-fold higher than the dose required to sensitize cells to cisplatin; and 2) simultaneous treatment of cells with 6AN and cycloheximide prevented the increase in GRP78 but not the sensitizing effect of 6AN. On the contrary, treatment with the protein synthesis inhibitors cycloheximide, anisomycin, or puromycin as well as prolonged exposure to the RNA synthesis inhibitor actinomycin D mimicked the biochemical modulating effects of 6AN on cisplatin action. Conversely, 6AN inhibited protein synthesis, whereas 18 6AN analogs that failed to enhance Pt-DNA adducts and cisplatin cytotoxicity failed to inhibit protein synthesis. These observations are consistent with a model in which 6AN and other inhibitors of protein synthesis act as modulating agents by increasing cisplatin accumulation, thereby enhancing the formation of Pt-DNA adducts and subsequent cisplatin-induced cell death.  (+info)

(2/52) Grp78 is involved in retention of mutant low density lipoprotein receptor protein in the endoplasmic reticulum.

The low density lipoprotein (LDL) receptor is responsible for removing the majority of the LDL cholesterol from the plasma. Mutations in the LDL receptor gene cause the disease familial hypercholesterolemia (FH). Approximately 50% of the mutations in the LDL receptor gene in patients with FH lead to receptor proteins that are retained in the endoplasmic reticulum (ER). Misfolding of mutant LDL receptors is a probable cause of this ER retention, resulting in no functional LDL receptors at the cell surface. However, the specific factors and mechanisms responsible for retention of mutant LDL receptors are unknown. In the present study we show that the molecular chaperone Grp78/BiP co-immunoprecipitates with both the wild type and two different mutant (W556S and C646Y) LDL receptors in lysates obtained from human liver cells overexpressing wild type or mutant LDL receptors. A pulse-chase study shows that the interaction between the wild type LDL receptor and Grp78 is no longer detectable after 2(1/2) h, whereas it persists for more than 4 h with the mutant receptors. Furthermore, about five times more Grp78 is co-immunoprecipitated with the mutant receptors than with the wild type receptor suggesting that Grp78 is involved in retention of mutant LDL receptors in the ER. Overexpression of Grp78 causes no major alterations on the steady state level of active LDL receptors at the cell surface. However, overexpression of Grp78 decreases the processing rate of newly synthesized wild type LDL receptors. This indicates that the Grp78 interaction is a rate-limiting step in the maturation of the wild type LDL receptor and that Grp78 may be an important factor in the quality control of newly synthesized LDL receptors.  (+info)

(3/52) Inhibitors of pentose phosphate pathway cause vasodilation: involvement of voltage-gated potassium channels.

Cytosolic reducing cofactors, such as NADPH and NADH, are thought to regulate vascular smooth muscle ion channel activity and vascular tone. In this study, the effects of pentose phosphate pathway (PPP) inhibitors, 6-aminonicotinamide (6-AN), epiandrosterone (EPI), and dehydroepiandrosterone (DHEA), on vascular tone were studied in isolated perfused lungs and pulmonary artery (PA) and aortic rings from rats. In addition, effects of 6-AN on voltage-gated K(+) (K(v)) current in PA smooth muscle cells (SMCs) were also examined. Pretreatment of lungs with 6-AN and EPI reduced the pressor response to acute hypoxia and decreased tissue NADPH levels. 6-AN, EPI, and DHEA relaxed isolated PA and aortic rings precontracted with 30 mM KCl in a dose-dependent manner. The PPP inhibitor-induced PA relaxations were reduced in PA rings precontracted with 80 mM KCl but not by pretreatment with nitro-L-arginine or endothelial removal. Pretreatment of PA rings with tetraethylammonium chloride or 4-aminopyridine caused rightward shifts of concentration-relaxation curves for 6-AN, EPI, and DHEA. In contrast, glybenclamide, charybdotoxin, or apamin did not inhibit the relaxant effects of 6-AN, EPI, and DHEA. 6-AN caused an increase in K(v) current in PASMC. These results indicate that reduction of NADPH by the PPP inhibitors causes vasodilation at least partly through opening of K(v) channels.  (+info)

(4/52) Up-regulation of glucose metabolism during male pronucleus formation determines the early onset of the s phase in bovine zygotes.

After in vitro fertilization with spermatozoa from bulls with high in vitro fertility, a beneficial paternal effect is manifested during the G1 phase of the first cell cycle. This benefit determines an earlier onset of the first S phase, and then a successful morula-blastocyst transition 7 days later. We hypothesized that the origin of the paternal effect could be a shift of the metabolism of the fertilized oocyte, because in mice, sperm decondensation is responsible for a dramatic increase in glucose metabolism. In this study we investigated the interaction between both pronuclei and compared glycolysis and pentose phosphate pathway (PPP) activities in bovine oocytes fertilized with spermatozoa from bulls of high or low fertility. Here we demonstrate that male pronucleus formation is necessary for the onset of the S phase in the female pronucleus, and that the component promoting an early S phase in both pronuclei is metabolic and linked to an up-regulation of the PPP during the male pronucleus formation. This long-lasting paternal effect is more evidence of the important role of epigenetic control during early embryo development.  (+info)

(5/52) Pentose phosphate pathway coordinates multiple redox-controlled relaxing mechanisms in bovine coronary arteries.

Pentose phosphate pathway (PPP) inhibitors, 6-aminonicotinamide (6-AN) and epiandrosterone (Epi), were employed to examine whether changes in NADP(H) redox regulates contractile force in endothelium-removed bovine coronary arteries (BCAs). 6-AN (0.01-5 mM) or Epi (1-500 microM) elicited dose-dependent relaxation in BCAs contracted with 30 mM KCl, 0.1 microM U-44619, and endothelin-1 but not with phorbol 12,13-dibutyrate, a protein kinase C activator that causes Ca2+-independent contraction. Relaxation to PPP inhibition was associated with oxidation of NADPH and glutathione (GSH). Relaxation to 6-AN was not mediated by H2O2, because it was not altered by hypoxia or the peroxide scavenger ebselen (100 microM). The thiol reductant DTT (3 mM) attenuated the relaxation to 6-AN and Epi by 30-40%. Inhibition of glycolysis or mitochondrial electron transport did not elicit relaxation in BCAs contracted with 30 mM KCl, suggesting these pathways may not be involved in relaxation elicited by PPP inhibition. High doses of K+ channel blockers [e.g., TEA (10 mM) and 4-aminopyridine (10 mM)] only partially inhibited the relaxation to 6-AN. On the basis of changes in the fura-2 fluorescence ratio, 6-AN and Epi appeared to markedly reduce intracellular Ca2+. Thus PPP inhibition oxidizes NADPH and GSH and appears to activate a novel coordination of redox-controlled relaxing mechanisms in BCAs mediated primarily through decreasing intracellular Ca2+.  (+info)

(6/52) Biochemical modulation of tumor cell energy: regression of advanced spontaneous murine breast tumors with a 5-fluorouracil-containing drug combination.

This report describes a highly active chemotherapeutic drug combination, consisting of N-(phosphonacetyl)-L-aspartate plus 6-methylmercaptopurine riboside plus 6-aminonicotinamide plus 5-fluorouracil, in CD8F1 mice bearing spontaneous, autochthonous, breast tumors or first-passage advanced transplants of these spontaneous tumors. The combination and sequence of administration of these drugs were selected on the basis of known potentiating biochemical interactions. High performance liquid chromatography and nuclear magnetic resonance spectroscopy measurements of biochemical changes resulting from treatment with N-(phosphonacetyl)-L-aspartate plus 6-methylmercaptopurine riboside plus 6-aminonicotinamide indicated a severe depletion of cellular energy levels in the treated tumors. 6-Aminonicotinamide produced a severe block of the pentose shunt, and 5-fluorouracil severely inhibited both thymidylate synthase and thymidine kinase in the treated tumors. This quadruple drug combination, administered on a 10-11-day schedule, produced an impressive partial tumor regression rate of 67% of large, spontaneous, autochthonous, murine breast tumors and a tumor regression rate of 74% of first-passage transplants of the spontaneous breast tumors.  (+info)

(7/52) Insulin stimulates glucose metabolism via the pentose phosphate pathway in Drosophila Kc cells.

Drosophila melanogaster has become a prominent and convenient model for analysis of insulin action. However, to date very little is known regarding the effect of insulin on glucose uptake and metabolism in Drosophila. Here we show that, in contrast to effects seen in mammals, insulin did not alter [(3)H]2-deoxyglucose uptake and in fact decreased glycogen synthesis ( approximately 30%) in embryonic Drosophila Kc cells. Insulin significantly increased ( approximately 1.5-fold) the production of (14)CO(2) from D-[1-(14)C]glucose while the production of (14)CO(2) from D-[6-(14)C]glucose was not altered. Thus, insulin-stimulated glucose oxidation did not occur via increasing Krebs cycle activity but rather by stimulating the pentose phosphate pathway. Indeed, inhibition of the oxidative pentose phosphate pathway by 6-aminonicotinamide abolished the effect of insulin on (14)CO(2) from D-[U-(14)C]glucose. A corresponding increase in lactate production but no change in incorporation of D-[U-(14)C]glucose into total lipids was observed in response to insulin. Glucose metabolism via the pentose phosphate pathway may provide an important source of 5'-phosphate for DNA synthesis and cell replication. This novel observation correlates well with the fact that control of growth and development is the major role of insulin-like peptides in Drosophila. Thus, although intracellular signaling is well conserved, the metabolic effects of insulin are dramatically different between Drosophila and mammals.  (+info)

(8/52) Effects of small molecules on chaperone-mediated autophagy.

Autophagy, including macroautophagy (MA), chaperone-mediated autophagy (CMA), crinophagy, pexophagy and microautophagy, are processes by which cells select internal components such as proteins, secretory vesicles, organelles, or foreign bodies, and deliver them to lysosomes for degradation. MA and CMA are activated during conditions of serum withdrawal in cell culture and during short-term and prolonged starvation in organisms, respectively. Although MA and CMA are activated under similar conditions, they are regulated by different mechanisms. We used pulse/chase analysis under conditions in which most intracellular proteolysis is due to CMA to test a variety of compounds for effects on this process. We show that inhibitors of MA such as 3-methyladenine, wortmannin, and LY294002 have no effect on CMA. Protein degradation by MA is sensitive to microtubule inhibitors such as colcemide and vinblastine, but protein degradation by CMA is not. Activators of MA such as rapamycin also have no effect on CMA. We demonstrate that CMA, like MA, is inhibited by protein synthesis inhibitors anisomycin and cycloheximide. CMA is also partially inhibited when the p38 mitogen activated protein kinase is blocked. Finally we demonstrate that the glucose-6-phophate dehydrogenase inhibitor, 6-aminonicotinamide, and heat shock protein of 90 kilodaltons inhibitor, geldanamycin, have the ability to activate CMA.  (+info)

*  Tumor metabolome
1998). "6-Aminonicotinamide sensitizes human tumor cell lines to cisplatin". Clin. Cancer Res. 4 (1): 117-130. PMID 9516960. ... p53 activates hexokinase 2 (HK2) that converts glucose to glucose-6-phosphate (G6P) which enters glycolysis to produce ATP, or ... In preclinical studies, drugs such as 6-amino-nicotinamide (6-AN), which inhibits G6P dehydrogenase, the enzyme that initiates ...
*  Glucose-6-phosphate dehydrogenase
... is stimulated by its substrate G6P. The usual ratio of NADPH/NADP+ in the cytosol of tissues ... Glucose-6-phosphate dehydrogenase (G6PD or G6PDH) (EC is a cytosolic enzyme that catalyzes the chemical reaction D- ... Glucose-6-phosphate dehydrogenase deficiency is very common worldwide, and causes acute hemolytic anemia in the presence of ... Glucose-6-phosphate dehydrogenase deficiency Genetic resistance to malaria Thomas D, Cherest H, Surdin-Kerjan Y (Mar 1991). " ...
*  List of MeSH codes (D03)
... vitamin b 6 MeSH D03.383.725.676.925.500 --- pyridoxal MeSH D03.383.725.676.925.500.500 --- pyridoxal phosphate MeSH D03.383. ... 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, methyl ester MeSH D03.383.725.547.950 --- xanthinol niacinate MeSH D03.383. ... 6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- MeSH D03.438.834.775 --- sparteine MeSH D03.438.834.850 --- tetrabenazine MeSH ... 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, methyl ester MeSH D03.383.725.210 --- dimethindene MeSH D03.383.725.220 --- ...
Metabolism of glucose into glutamate via the hexose monophosphate shunt and its inhibition by 6-aminonicotinamide in rat brain...  Metabolism of glucose into glutamate via the hexose monophosphate shunt and its inhibition by 6-aminonicotinamide in rat brain...
In blood, 6-phosphogluconate increased 5-fold; glucose, 1.4-fold and glucose 6-phosphate, 1.8-fold. The metabolism of glucose ... The treatment of rats for 4 h with 6-aminonicotinamide (60 mg kg -1) resulted in an 180-fold increase in the concentration of 6 ... Metabolism of glucose into glutamate via the hexose monophosphate shunt and its inhibition by 6-aminonicotinamide in rat brain ... Metabolism of glucose into glutamate via the hexose monophosphate shunt and its inhibition by 6-aminonicotinamide in rat brain ...
more infohttp://rspb.royalsocietypublishing.org/content/231/1262/71
ChemIDplus - 329-89-5 - ZLWYEPMDOUQDBW-UHFFFAOYSA-N - 6-Aminonicotinamide - Similar structures search, synonyms, formulas,...  ChemIDplus - 329-89-5 - ZLWYEPMDOUQDBW-UHFFFAOYSA-N - 6-Aminonicotinamide - Similar structures search, synonyms, formulas,...
6-Aminonicotinamide - Similar structures search, synonyms, formulas, resource links, and other chemical information. ... Substance Name: 6-Aminonicotinamide. RN: 329-89-5. UNII: D6FNW67F2B. InChIKey: ZLWYEPMDOUQDBW-UHFFFAOYSA-N. Note. *. A vitamin ... 1S/C6H7N3O/c7-5-2-1-4(3-9-5)6(8)10/h1-3H,(H2,7,9)(H2,8,10). Download. ...
more infohttps://chem.nlm.nih.gov/chemidplus/rn/329-89-5
What does 6-aminonicotinamide mean?  What does 6-aminonicotinamide mean?
Meaning of 6-aminonicotinamide. What does 6-aminonicotinamide mean? Information and translations of 6-aminonicotinamide in the ... Definition of 6-aminonicotinamide in the Definitions.net dictionary. ... Discuss these 6-aminonicotinamide definitions with the community:. Word of the Day. Would you like us to send you a FREE new ... What does 6-aminonicotinamide mean?. Definitions for 6-aminonicotinamide. Here are all the possible meanings and translations ...
more infohttps://www.definitions.net/definition/6-aminonicotinamide
6-Aminonicotinamide and Acute Degenerative Changes in the Central Nervous System | Science  6-Aminonicotinamide and Acute Degenerative Changes in the Central Nervous System | Science
6-Aminonicotinamide and Acute Degenerative Changes in the Central Nervous System. By STEPHEN S. STERNBERG, FREDERICK S. PHILIPS ... 6-Aminonicotinamide and Acute Degenerative Changes in the Central Nervous System. By STEPHEN S. STERNBERG, FREDERICK S. PHILIPS ... 6-Aminonicotinamide and Acute Degenerative Changes in the Central Nervous System Message Subject. (Your Name) has forwarded a ...
more infohttp://science.sciencemag.org/content/127/3299/644.2
Autophagy-dependent metabolic reprogramming sensitizes TSC2-deficient cells to the antimetabolite 6-aminonicotinamide.  -...  Autophagy-dependent metabolic reprogramming sensitizes TSC2-deficient cells to the antimetabolite 6-aminonicotinamide. -...
C) Proliferation of Tsc2−/− and Tsc2+/+ MEFs treated with the autophagy inhibitor spautin-1 (5 μM), 6-AN (10 μM) or both for 4 ... A, B) Proliferation of Tsc2−/− and Tsc2+/+ MEFs treated with chloroquine (CQ, 5 μM), 6-aminonicotinamide (6-AN, 10 μM) or both ... C) Immunoblot analysis of caspase-1 (pro- and cleaved-form) in Tsc2−/− MEFs treated with chloroquine (CQ, 5 μM) and 6-AN (10 μM ... Images from this publication.See all images (6)Free text. Figure 1. Chloroquine inhibits the proliferation and tumorigenicity ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/24296756
6-Aminonicotinamide | CAS 329-89-5 | SCBT - Santa Cruz Biotechnology  6-Aminonicotinamide | CAS 329-89-5 | SCBT - Santa Cruz Biotechnology
Buy 6-Aminonicotinamide (CAS 329-89-5), a PGD inhibitor and apoptosis inducer, from Santa Cruz. Purity: ≥99%, Molecular Formula ... 6-Aminonicotinamide (CAS 329-89-5) 6-Aminonicotinamide , CAS 329-89-5 is rated 5.0 out of 5 by 1. ... Molecular Formula: C6H7N3O Supplemental Information: This is classified as a Dangerous Good for transport and may be subject to ... 6-Aminonicotinamide Product Citations See how others have used 6-Aminonicotinamide. Click on the entry to view the PubMed entry ...
more infohttps://www.scbt.com/p/6-aminonicotinamide-329-89-5/
Blocking of Pentose Phosphate Pathway in the Brain of Rats by 6-Aminonicotinamide | Springer for Research & Development  Blocking of Pentose Phosphate Pathway in the Brain of Rats by 6-Aminonicotinamide | Springer for Research & Development
The biosynthesis of derivatives of NAD and NADP containing 6-aminonicotinamide (6-AN) entails functional disorders in different ... Johnson, W.J., and J.D. McColl: Antimetabolic activity of 6-aminonicotinamide. Fed. Proc. 15, 284 (1965).Google Scholar ... Dietrich, L.S., I.M. Friedland, and L.A. Kaplan: Pyridine nucleotide metabolism: Mechanism of action of the niacin antagonist 6 ... Wolf, A., D. Cowen, and L.M. Geller: The effects of an antimetabolite, 6-aminonicotinamide, on the central nervous system. ...
more infohttps://rd.springer.com/chapter/10.1007%2F978-3-662-39718-3_165
Tumor metabolome - Wikipedia  Tumor metabolome - Wikipedia
1998). "6-Aminonicotinamide sensitizes human tumor cell lines to cisplatin". Clin. Cancer Res. 4 (1): 117-130. PMID 9516960. ... p53 activates hexokinase 2 (HK2) that converts glucose to glucose-6-phosphate (G6P) which enters glycolysis to produce ATP, or ... In preclinical studies, drugs such as 6-amino-nicotinamide (6-AN), which inhibits G6P dehydrogenase, the enzyme that initiates ...
more infohttps://en.wikipedia.org/wiki/Tumor_metabolome
7228-38-8 - 5-Chloro-1,3-benzodioxole, 98% - 3,4-Methylenedioxychlorobenzene - B22534 - Alfa Aesar  7228-38-8 - 5-Chloro-1,3-benzodioxole, 98% - 3,4-Methylenedioxychlorobenzene - B22534 - Alfa Aesar
Precautionary Statements: P210u-P261-P280a-P305+P351+P338-P405-P501a Keep away from heat/sparks/open flames/hot surfaces. - No smoking. Avoid breathing dust/fume/gas/mist/vapours/spray. Wear protective gloves and eye/face protection. IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. Store locked up. Dispose of contents/container in accordance with local/regional/national/international regulations. ...
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Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and...  Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and...
C-E: graphs depict G6PD activity (C), NADPH levels (D), and 6-phosphogluconate levels (E) in lean (n = 6) and fa/fa (n = 6) rat ... C: effects of 6-AN or gp91ds-tat O2− production in aortic rings from Zucker lean (n = 6) and fa/fa (n = 6) rats. D: ... Graphs represent G6PD activity (A) and NADPH levels (B) in aortas from Zucker lean (n = 6) and fa/fa (n = 6) rats. ... The role of glucose-6-phosphate dehydrogenase-derived NADPH.. Serpillon S1, Floyd BC, Gupte RS, George S, Kozicky M, Neito V, ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/19429815
Plus it  Plus it
N = 6/5. G-J, qRT-PCR for Nqo1, Srxn1 (G), G6pdx, Pgd, Taldo1, Tkt (H), Idh1, and Me1 (J) relative to Rps29 using RNA from ... N = 6. F and G, qRT-PCR for Nqo1 and Gsta3 (F) and Gclc, Gclm, Gss, and Gsr (G) relative to Rps29 using epidermal RNA from tg/ ... Untreated N = 4/6; 3x TPA N = 8/7. D and E, qRT-PCR for G6pdx, Pgd, Taldo1, and Tkt (D) and Me1 and Idh1 (E) relative to Rps29 ... N = 6. G, qRT-PCR for NQO1, SRXN1, and NRF2 relative to GAPDH using RNA from skin of healthy donors (N = 5 biopsies) and from ...
more infohttp://cancerres.aacrjournals.org/content/75/22/4817
Formula Browser  Formula Browser
C6H7N3O5S2 (Thiazole, 5-acetamido-2-(methylsulfonyl)-4-nitro-) ... C6H7N3O2______ (4 species). *C6H7N3O4 (Ethyl 4-nitro-1h- ... Formulas which begin with C6H7N3O. All formulas are in Hill order. ...
more infohttps://webbook.nist.gov/cgi/formula/C6H7N3O
Formula Browser  Formula Browser
C6H7N3O5S2 (Thiazole, 5-acetamido-2-(methylsulfonyl)-4-nitro-) ... C6H7N3O2______ (4 species). *C6H7N3O4 (Ethyl 4-nitro-1h- ... Formulas which begin with C6H7N3O. All formulas are in Hill order. ...
more infohttp://webbook.nist.gov/cgi/formula/C6H7N3O
Publications - Mayo Clinic  Publications - Mayo Clinic
2014 Jun; 73: (6)1137-46. View PubMed. * Deming DA, Ninan J, Bailey HH, Kolesar JM, Eickhoff J, Reid JM, Ames MM, McGovern RM, ... 2011; 6: (9)e24374. View PubMed. * George RE, Lahti JM, Adamson PC, Zhu K, Finkelstein D, Ingle AM, Reid JM, Krailo M, Neuberg ... 2002 Dec; 72(6):638-47. View PubMed. * Steinherz PG, Seibel NL, Ames MM, Avramis VI, Krailo MD, Liu-Mares W, Reid JM, Safgren ... 2016 Jun 27; 6:28699 Epub 2016 June 27 View PubMed. * Camacho-Pereira J, Tarrago MG, Chini CCS, Nin V, Escande C, Warner GM, ...
more infohttps://www.mayo.edu/research/searchpublications/publications?authid=10470859
Download Getting Acquainted In Conversation A Study Of Initial Interactions  Download Getting Acquainted In Conversation A Study Of Initial Interactions
Visitor's Guide to Hawaii credible Medicinal Chemistry, 1(6), 1143-1151. Polynomial neurons of protective download getting ... A Nitric Oxide Storage and Transport System That 6-aminonicotinamide important Sources from Endogenous Nitric Oxide ...
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Plus it  Plus it
6 a). Additionally, the astrocyte density in the double transgenics was ∼19-40% less than that in single lacZ transgenic mice ( ... Unstained sections (6 μm) were mounted on poly-l-lysine-coated slides, hybridized, and washed as described previously (Lyons et ... 3 a,e,i,m). Some transgenic animals were examined at 6 months of age after a single GCV treatment at P3. These animals were ... Either 10 μg of RNA purified by CsCl centrifugation (lanes 2,5, 6) or 20 μg of RNA purified by STAT-60 (Tel-Test "B," ...
more infohttp://www.jneurosci.org/content/16/21/6908
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99 Feedback The special steers of Genius: The new to affording Your Hidden Genius 23(6 I. Robledo Learn to counter The Best ... For QENS, 6(11 services threatening in download numerical eruption runout partnerships are reviewed destroyed. Melnichenko, ... Journal of Biological Chemistry, 6-aminonicotinamide), 17303-17318. This Latent download numerical has Even be our digital ... and book plasma in Tables 6 and S-6). download numerical mathematics: The quality of turn impacts in role bays is known in ...
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A, Untreated TSC2-deficient cells and cells incubated with 30 μmol/L Nec-1 or 3 μmol/L NSA for 6 hours were analyzed for the ... Figure 6. BSO/auranofin/Nec-1 combination synergistically inhibits growth of TSC2-deficient tumors and induces necrosis in vivo ... Cells were plated in a 6-well format (1 × 105/well), cultured overnight, and transfected with siRNA using Lipofectamine 3000 ... Autophagy-dependent metabolic reprogramming sensitizes TSC2-deficient cells to the antimetabolite 6-aminonicotinamide. Mol ...
more infohttp://cancerres.aacrjournals.org/content/76/24/7130
Regeneration in the Goldfish Visual System by Sam Nona - Webvision  Regeneration in the Goldfish Visual System by Sam Nona - Webvision
6. The fascicular pattern of the goldfish optic nerve is defined by the tissue's astrocytes. (a) and (b) show the pattern in ... 6. Axon regeneration in injured goldfish optic nerve.. The literature abounds with studies that confirm an observation made by ... 1991;6:359-370. [PubMed]. Cajal S. Ramon Y. 1928. In: Degeneration and Regeneration of the Nervous System. (Translated by May, ... Remyelination by Schwann cells of axons demyelinated by intraspinal injections of 6-aminonicotinamide. J Neurocytol. 1975;4:745 ...
more infohttps://webvision.med.utah.edu/book/part-x-repair-and-regeneration-in-the-visual-system/regeneration-in-the-goldfish-visual-system/
  • Pentose Phosphate Pathway 6-Aminonicotinamide 6-Phos-pho D -Gluconate: NADP Oxidoreductase 6-Phosphogluconate. (springer.com)
  • p53 activates hexokinase 2 (HK2) that converts glucose to glucose-6-phosphate (G6P) which enters glycolysis to produce ATP, or enters the pentose phosphate pathway (PPP). (wikipedia.org)
  • Glucose-6-phosphate dehydrogenase (G6PD or G6PDH) (EC is a cytosolic enzyme that catalyzes the chemical reaction D-glucose 6-phosphate + NADP+ ⇌ {\displaystyle \rightleftharpoons } 6-phospho-D-glucono-1,5-lactone + NADPH + H+ This enzyme participates in the pentose phosphate pathway (see image), a metabolic pathway that supplies reducing energy to cells (such as erythrocytes) by maintaining the level of the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH). (wikipedia.org)
  • Our aim was to determine whether NADPH oxidase (Nox) is a source of O(2)(-) and whether glucose-6-phosphate dehydrogenase (G6PD)-derived NADPH plays a role in augmenting O(2)(-) generation in diabetes. (nih.gov)
  • Glucose-6-phosphate dehydrogenase (G6PD) activity is elevated in type 2 diabetes. (nih.gov)
  • expression of G6PD in lean ( n = 6) and fa/fa ( n = 6) rat hearts estimated by densitometric analysis and normalized to α-tubulin levels. (nih.gov)
  • graphs depict G6PD activity ( C ), NADPH levels ( D ), and 6-phosphogluconate levels ( E ) in lean ( n = 6) and fa/fa ( n = 6) rat hearts. (nih.gov)
  • G6PD reduces NADP+ to NADPH while oxidizing glucose-6-phosphate. (wikipedia.org)
  • Recently, our laboratory also found that 20-HETE is involved in promoting prolonged hypoxia-induced pulmonary vasoconstriction and that glucose-6-phosphate dehydrogenase (G6PD), which is a major producer of NADPH in the cell, and cytochrome P -450 monooxygenase enzymes are functionally coupled in vascular smooth muscle tissue (unpublished observations). (physiology.org)
  • In addition, p53 mutation, which occurs mostly in cancer cells, plays a significant role in the resistance of cancer cells to DNA damaging agents ( 4 - 6 ). (pubmedcentralcanada.ca)
  • This is important because, in the brain, KADP is present in much lower concentrations than NAD, and because the conversion of NADP to 6-AXADP will considerably change the function of the enzymes needing NADP. (springer.com)
  • Clinical manifestation of TSC is development of tumors and neoplastic lesions in kidney, lung, brain, heart and skin, among which renal cell carcinoma (RCC), renal angiomyolipoma (AML), pulmonary lymphangioleiomyomatosis (LAM), and brain tumors constitute the most common cause of TSC-associated deaths ( 3-6 ). (aacrjournals.org)
  • Special studies on teratogenicity Mice Six groups of 25 pregnant mice were given continuously from days 6-15 of gestation 0, 6.95, 32.5, 150, or 695 mg/kg b.w./day GDL by oral intubation. (inchem.org)
  • Loss-of-function mutation in the TSC1 or TSC2 gene has been defined as the main factor driving malignancy of TSC-associated tumors ( 6, 8 ). (aacrjournals.org)