MAK100
Inosine Assay Kit
sufficient for 100 fluorometric tests
Sinonimo/i:
Inosine Fluorometric Assay Kit
Autenticatiper visualizzare i prezzi riservati alla tua organizzazione & contrattuali
About This Item
Codice UNSPSC:
12161503
NACRES:
NA.84
Prodotti consigliati
impiego
sufficient for 100 fluorometric tests
Metodo di rivelazione
fluorometric
Malattie correlate
cardiovascular diseases; immunological diseases
Temperatura di conservazione
−20°C
Descrizione generale
Inosine is a purine nucleotide found at the wobble position of tRNA where it plays a role in the proper translation of mRNA at the ribosome. In addition to its role in translation, inosine also plays important roles in the immune system where is exhibits both inflammatory and anti-inflammatory effects. Inosine may be tissue protective during ischemic injury and recent reports suggest inosine may preserve cell viability during hypoxia.
Applicazioni
Inosine Assay Kit has been used for the detection of inosine in the brain tissue homogenates.
Compatibilità
Suitable for the measurement of inosine in a variety of samples including tissue and cells
Principio
The Inosine Assay Kit provides a simple and direct procedure for measuring inosine in a variety of samples. Inosine concentration is determined by a coupled enzyme reaction in which inosine is converted to hypoxanthine which reacts with the substrate mix and probe, resulting in a fluorometric product (λex = 535/λem = 587 nm), proportional to the inosine present.
Codice della classe di stoccaggio
10 - Combustible liquids
Punto d’infiammabilità (°F)
188.6 °F - closed cup
Punto d’infiammabilità (°C)
87 °C - closed cup
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Cell-subtype-specific changes in adenosine pathways in schizophrenia.
O?Donovan S M, et al.
Neuropsychopharmacology, 43, 1667?1674-1667?1674 (2018)
Sinead Marie O'Donovan et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 43(8), 1667-1674 (2018-02-28)
Prior work in animal models implicates abnormalities of adenosine metabolism in astrocytes as a possible pathophysiological mechanism underlying the symptoms of schizophrenia. In the present study, we sought to reverse-translate these findings back to the human brain in schizophrenia, focusing
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