... produces nigericin. ed.-in-chief, George M. Garrity (2012). Bergey's manual of systematic bacteriology ...
... such as nigericin or monensin or by inhibiting the V-ATPase that generates the H+ gradient with compounds such as bafilomycin ... nigericin or monensin). In platelets it has been suggested that SERCA3 inhibition with tBHQ can also abrogate NAADP-dependent ...
Prize for his master thesis "Formation of oligomers of ion transporters by Nigericin". 1993 - Award: cover of the journal ...
The antibiotics geldanamycin, hygromycin B, nigericin, validamycin, and cyclothiazomycin are found in S. hygroscopicus. ...
... nigericin, tunicamycin and colchicine". Biochimica et Biophysica Acta. 883 (2): 326-34. doi:10.1016/0304-4165(86)90325-9. PMID ...
... nigericin and maitotoxin, liposomes, urban particulate matter, and most notably, crystallized endogenous molecules. Cholesterol ...
... nigericin, monensin, A23187 and lasalocid A". Biochimica et Biophysica Acta. 938 (2): 125-30. doi:10.1016/0005-2736(88)90151-4 ... Nigericin (K+, H+, Pb2+) Nonactin (ammonium ionophore I) Salinomycin (K+) Tetronasin Valinomycin (potassium ionophore I) ...
Bulychev, A. A.; Vredenberg, W. J. (1976). "Effect of ionophores A-23187 and nigericin on the light induced redistribution of ...
It has also been noted that glycine transport is inhibited by a protonophore, FCCP, or valinomycin plus nigericin, indicating ...
... nigericin MeSH D03.383.312.649 --- nitrofurans MeSH D03.383.312.649.200 --- 5-amino-3-((5-nitro-2-furyl)vinyl)-1,2,4-oxadiazole ... nigericin MeSH D03.383.663.705 --- pyran copolymer MeSH D03.383.663.718 --- pyrones MeSH D03.383.679.149 --- amiloride MeSH ...
Shinkai employs this devices in actual ion transport mimicking the biochemical action of monensin and nigericin: in a biphasic ...
Family 2.B.1 The Valinomycin Carrier Family 2.B.2 The Monensin Family 2.B.3 The Nigericin Family 2.B.4 The Macrotetrolide ...
... such as The Nigericin (Nigericin) Family The Ionomycin (Ionomycin) Family 2.C: Ion-gradient-driven energizers 3.A: P-P-bond- ...
... but is thought to be due to its action as a potassium ionophore due to the detection of nigericin in the same compound screen. ...
... acts as an H+, K+, Pb2+ ionophore. Most commonly it is an antiporter of H+ and K+. In the past nigericin was used as ... Nigericin is an antibiotic derived from Streptomyces hygroscopicus. Its isolation was described in the 1950s, and in 1968 the ... The structure and properties of nigericin are similar to the antibiotic monensin. Commercially it is obtained as a byproduct, ... Steinrauf LK, Pinkerton M, Chamberlin JW (1968). "The structure of nigericin". Biochem. Biophys. Res. Commun. 33 (1): 29-31. ...
In 2001, the German Federal Institute for Risk Assessment (Bundesinstitut für Risikobewertung, BfR) objected to the addition of isolated theanine to beverages.[39][40] The institute stated the amount of theanine consumed by regular drinkers of tea or coffee is virtually impossible to determine. While it was estimated the quantity of green tea consumed by the average Japanese tea drinker per day contains about 20 mg of the substance, there are no studies measuring the amount of theanine being extracted by typical preparation methods, or the percentage lost by discarding the first infusion. Therefore, with the Japanese being exposed to possibly much less than 20 mg per day, and Europeans presumably even less, it was the opinion of the BfR that pharmacological reactions to drinks typically containing 50 mg of theanine per 500 milliliters could not be excluded-reactions such as impairment of psychomotor skills and amplification of the sedating effects of alcohol and hypnotics.[41] In 2006, a study ...
GAD67 and GAD65 are also regulated differently post-translationally. Both GAD65 and GAD67 are regulated via phosphorylation of a dynamic catalytic loop,[10][11] but the regulation of these isoforms differs; GAD65 is activated by phosphorylation while GAD67 is inhibited by phosphorylation. GAD67 is predominantly found activated (~92%), whereas GAD65 is predominantly found inactivated (~72%).[12] GAD67 is phosphorylated at threonine 91 by protein kinase A (PKA), while GAD65 is phosphorylated, and therefore regulated by, protein kinase C (PKC). Both GAD67 and GAD65 are also regulated post-translationally by Pyridoxal 5'-phosphate (PLP); GAD is activated when bound to PLP and inactive when not bound to PLP.[12] Majority of GAD67 is bound to PLP at any given time, whereas GAD65 binds PLP when GABA is needed for neurotransmission.[12] This reflects the functional properties of the two isoforms; GAD67 must be active at all times for normal cellular functioning, and is therefore constantly activated by ...
... (marketed as Depamide by Sanofi-Aventis) is a carboxamide derivative of valproic acid used in the treatment of epilepsy and some affective disorders. It is rapidly metabolised (80%) to valproic acid (another anticonvulsant) but has anticonvulsant properties itself. It may produce more stable plasma levels than valproic acid or sodium valproate and may be more effective at preventing febrile seizures. However, it is over one hundred times more potent as an inhibitor of liver microsomal epoxide hydrolase. This makes it incompatible with carbamazepine and can affect the ability of the body to remove other toxins. Valpromide is no safer during pregnancy than valproic acid. Valpromide is formed through the reaction of valproic acid and ammonia via an intermediate acid chloride. In pure form, valpromide is a white crystalline powder and has melting point 125-126 °C. It is practically insoluble in water but soluble in hot water. It is available on the market in some European countries. ...
... is an azo dye that is used as a dye-stuff. It is a direct dye for cotton textiles.[3] In biosciences, it is used as vital stain to selectively colour dead tissues or cells blue. Live cells or tissues with intact cell membranes are not coloured. Since cells are very selective in the compounds that pass through the membrane, in a viable cell trypan blue is not absorbed; however, it traverses the membrane in a dead cell. Hence, dead cells appear as a distinctive blue colour under a microscope. Since live cells are excluded from staining, this staining method is also described as a dye exclusion method. This dye may be a cause of certain birth defects, such as encephalocele.[citation needed] ...
Glutamate is the most abundant excitatory neurotransmitter in the vertebrate nervous system.[21] At chemical synapses, glutamate is stored in vesicles. Nerve impulses trigger release of glutamate from the presynaptic cell. Glutamate acts on ionotropic and metabotropic (G-protein coupled) receptors.[21] In the opposing postsynaptic cell, glutamate receptors, such as the NMDA receptor or the AMPA receptor, bind glutamate and are activated. Because of its role in synaptic plasticity, glutamate is involved in cognitive functions such as learning and memory in the brain.[22] The form of plasticity known as long-term potentiation takes place at glutamatergic synapses in the hippocampus, neocortex, and other parts of the brain. Glutamate works not only as a point-to-point transmitter, but also through spill-over synaptic crosstalk between synapses in which summation of glutamate released from a neighboring synapse creates extrasynaptic signaling/volume transmission.[23] In addition, glutamate plays ...
The existence of a specific GHB receptor was predicted by observing the action of GHB and related compounds that primarily act on the GABAB receptor, but also exhibit a range of effects which were found not to be produced by GABAB activity, and so were suspected of being produced by a novel and at the time unidentified receptor target. Following the discovery of the "orphan" G-protein coupled receptor GPR172A, it was subsequently found to be the GHB receptor whose existence had been previously predicted.[1] The rat GHB receptor was first cloned and characterised in 2003[2] followed by the human receptor in 2007.[3] ...
Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the adult vertebrate. Medium spiny cells are a typical example of inhibitory central nervous system GABAergic cells. In contrast, GABA exhibits both excitatory and inhibitory actions in insects, mediating muscle activation at synapses between nerves and muscle cells, and also the stimulation of certain glands.[4] In mammals, some GABAergic neurons, such as chandelier cells, are also able to excite their glutamatergic counterparts.[5] GABAA receptors are ligand-activated chloride channels: when activated by GABA, they allow the flow of chloride ions across the membrane of the cell. Whether this chloride flow is depolarizing (makes the voltage across the cell's membrane less negative), shunting (has no effect on the cell's membrane potential), or inhibitory/hyperpolarizing (makes the cell's membrane more negative) depends on the direction of the flow of chloride. When net ...
Penemuan penislin selalu dikaitkan dengan ilmuwan Skotlandia, Alexander Fleming pada 1929, walaupun sebenarnya banyak ilmuwan lain yang telah mencatat efek antibakteri sebelum Fleming.[2]. Fleming, dalam laboratoriumnya di Rumah Sakit Santa Maria (kini merupakan salah satu rumah sakit pendidikan di London), mencatat adanya lingkaran hambatan (zona bening) pada pertumbuhan bakteri di piringan kultur Staphylococcus. Fleming menyimpulkan bahwa hambatan itu dikarenakan sebuah subtansi penghambat pertumbuhan dan menghancurkan bakteri. Ia kemudian menumbuhkan sebuah kultur murni dan menemukan Penicillium yang kemudian dikenal sebagai Penicillium chrysogenum. Fleming memberikan istilah "penisilin" untuk menggambarkan hasil filtrasi dari kultur mikrobiologis Penicillium.[2]. Walaupun di tahapan awal ini, penisilin ditemukan efektif melawan bakteri Gram positif dan tidak efektif pada Gram negatif dan jamur. Fleming optimis bahwa penisilin akan menjadi disinfektan yang sangat berguna, berpotensi tinggi ...