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Product Details of 329-89-5. The protonation of heteroatoms in aromatic heterocycles can be divided into two categories: lone pairs of electrons are in the aromatic ring conjugated system; and lone pairs of electrons do not participate. Compound: 6-Aminonicotinamide, is researched, Molecular C6H7N3O, CAS is 329-89-5, about Ex vivo and in vivo stable isotope labelling of central carbon metabolism and related pathways with analysis by LC-MS/MS. Author is Yuan, Min; Kremer, Daniel M.; Huang, He; Breitkopf, Susanne B.; Ben-Sahra, Issam; Manning, Brendan D.; Lyssiotis, Costas A.; Asara, John M..

Targeted tandem mass spectrometry (LC-MS/MS) has been extremely useful for profiling small mols. extracted from biol. sources, such as cells, bodily fluids and tissues. Here, we present a protocol for analyzing incorporation of the non-radioactive stable isotopes carbon-13 (13C) and nitrogen-15 (15N) into polar metabolites in central carbon metabolism and related pathways. Our platform utilizes selected reaction monitoring (SRM) with polarity switching and amide hydrophilic interaction liquid chromatog. (HILIC) to capture transitions for carbon and nitrogen incorporation into selected metabolites using a hybrid triple quadrupole (QQQ) mass spectrometer. This protocol represents an extension of a previously published protocol for targeted metabolomics of unlabeled species and has been used extensively in tracing the metabolism of nutrients such as 13C-labeled glucose, 13C-glutamine and 15N-glutamine in a variety of biol. settings (e.g., cell culture experiments and in vivo mouse labeling via i.p. injection). SRM signals are integrated to produce an array of peak areas for each labeling form that serve as the output for further anal. The processed data are then used to obtain the degree and distribution of labeling of the targeted mols. (termed fluxomics). Each method can be customized on the basis of known unlabeled Q1/Q3 SRM transitions and adjusted to account for the corresponding 13C or 15N incorporation. The entire procedure takes ∼6-7 h for a single sample from exptl. labeling and metabolite extraction to peak integration.

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The three-dimensional configuration of the ester heterocycle is basically the same as that of the carbocycle. Compound: 6-Aminonicotinamide(SMILESS: O=C(N)C1=CN=C(N)C=C1,cas:329-89-5) is researched.Product Details of 75732-01-3. The article 《Human monocyte-derived dendritic cells produce millimolar concentrations of ros in phagosomes per second》 in relation to this compound, is published in Frontiers in Immunology. Let’s take a look at the latest research on this compound (cas:329-89-5).

Neutrophils kill ingested pathogens by the so-called oxidative burst, where reactive oxygen species (ROS) are produced in the lumen of phagosomes at very high rates (mM/s), although these rates can only be maintained for a short period (minutes). In contrast, dendritic cells produce ROS at much lower rates, but they can sustain production for much longer after pathogen uptake (hours). It is becoming increasingly clear that this slow but prolonged ROS production is essential for antigen cross-presentation to activate cytolytic T cells, and for shaping the repertoire of antigen fragments for presentation to helper T cells. Here, we quantified ROS production in human monocyte-derived dendritic cells by measuring the oxygen consumption rate during phagocytosis. Although a large variation in oxygen consumption and phagocytic capacity was present among individuals and cells, we estimate a ROS production rate of on average ∼0.5 mM/s per phagosome. Quant. microscopy approaches showed that ROS is produced within minutes after pathogen encounter at the nascent phagocytic cup. H2DCFDA measurements revealed that ROS production is sustained for at least ∼10 h after uptake. While ROS are produced by dendritic cells at an about 10-fold lower rate than by neutrophils, the net total ROS production is approx. similar. These are the first quant. estimates of ROS production by a cell capable of antigen cross-presentation. Our findings provide a quant. insight in how ROS affect dendritic cell function.

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The chemical properties of alicyclic heterocycles are similar to those of the corresponding chain compounds. Compound: 6-Aminonicotinamide, is researched, Molecular C6H7N3O, CAS is 329-89-5, about Targeting the pentose phosphate pathway increases reactive oxygen species and induces apoptosis in thyroid cancer cells, the main research direction is pentose phosphate reactive oxygen species apoptosis thyroid cancer cell; Apoptosis; Pentose phosphate pathway; Reactive oxygen species; Thyroid cancer.COA of Formula: C6H7N3O.

The pentose phosphate pathway (PPP) plays an important role in the biosynthesis of ribonucleotide precursor and NADPH. Cancer cells frequently increase the flux of glucose into the PPP to support the anabolic demands and regulate oxidative stress. Consistently, metabolomic analyses indicate an upregulation of the PPP in thyroid cancer. In the present study, we found that the combination of glucose-6-phosphate dehydrogenase (G6PD) and transketolase inhibitors (6-aminonicotinamide and oxythiamine) exerted an additive or synergistic effect on cell growth inhibition in thyroid cancer cells. Targeting PPP significantly increased cellular reactive oxygen species (ROS) and induced endoplasmic reticulum (ER) stress and apoptosis. Suppressed cell viability could be partially rescued with treatment with the ROS scavenger or apoptosis inhibitor but not ER-stress inhibitor. Taken together, dual PPP blockade leads to pharmacol. additivity or synergism and causes ROS-mediated apoptosis in thyroid cancer cells.

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In general, if the atoms that make up the ring contain heteroatoms, such rings become heterocycles, and organic compounds containing heterocycles are called heterocyclic compounds. An article called LEADS-FRAG: A Benchmark Data Set for Assessment of Fragment Docking Performance, published in 2020-12-28, which mentions a compound: 329-89-5, Name is 6-Aminonicotinamide, Molecular C6H7N3O, Category: pyridine-derivatives.

Fragment-based drug design is a popular approach in drug discovery, which makes use of computational methods such as mol. docking. To assess fragment placement performance of mol. docking programs, we constructed LEADS-FRAG, a benchmark data set containing 93 high-quality protein-fragment complexes that were selected from the Protein Data Bank using a rational and unbiased process. The data set contains fully prepared protein and fragment structures and is publicly available. Moreover, we used LEADS-FRAG for evaluating the small-mol. docking programs AutoDock, AutoDock Vina, FlexX, and GOLD for their fragment docking performance. GOLD in combination with the scoring function ChemPLP and AutoDock Vina performed best and generated near-native conformations (root mean square deviation <1.5 Å) for more than 50% of the data set considering the top-ranked docking pose. Taking into account all docking poses, the tested programs generated near-native conformations for up to 86% of the fragments in LEADS-FRAG. By rescoring all docking poses with the GOLD scoring functions and the Protein-Ligand Informatics force field, the number of near-native conformations increased up to 40% with respect to the top-rescored poses. Our results show that conventional small-mol. docking programs achieve a satisfactory fragment docking performance when utilizing rescoring. Here is a brief introduction to this compound(329-89-5)Category: pyridine-derivatives, if you want to know about other compounds related to this compound(329-89-5), you can read my other articles.

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Epoxy compounds usually have stronger nucleophilic ability, because the alkyl group on the oxygen atom makes the bond angle smaller, which makes the lone pair of electrons react more dissimilarly with the electron-deficient system. Compound: 6-Aminonicotinamide, is researched, Molecular C6H7N3O, CAS is 329-89-5, about SGK1 signaling promotes glucose metabolism and survival in extracellular matrix detached cells.HPLC of Formula: 329-89-5.

Loss of integrin-mediated attachment to extracellular matrix (ECM) proteins can trigger a variety of cellular changes that affect cell viability. Foremost among these is the activation of anoikis, caspase-mediated cell death induced by ECM detachment. In addition, loss of ECM attachment causes profound alterations in cellular metabolism, which can lead to anoikis-independent cell death. Here, we describe a surprising role for serum and glucocorticoid kinase-1 (SGK1) in the promotion of energy production when cells are detached. Our data demonstrate that SGK1 activation is necessary and sufficient for ATP generation during ECM detachment and anchorage-independent growth. More specifically, SGK1 promotes a substantial elevation in glucose uptake because of elevated GLUT1 transcription. In addition, carbon flux into the pentose phosphate pathway (PPP) is necessary to accommodate elevated glucose uptake and PPP-mediated glyceraldehyde-3-phosphate (G3P) is necessary for ATP production Thus, our data show SGK1 as master regulator of glucose metabolism and cell survival during ECM-detached conditions.

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Jarque, Sergio; Rubio-Brotons, Maria; Ibarra, Jone; Ordonez, Victor; Dyballa, Sylvia; Minana, Rafael; Terriente, Javier published an article about the compound: 6-Aminonicotinamide( cas:329-89-5,SMILESS:O=C(N)C1=CN=C(N)C=C1 ).Formula: C6H7N3O. Aromatic heterocyclic compounds can be classified according to the number of heteroatoms or the size of the ring. The authors also want to convey more information about this compound (cas:329-89-5) through the article.

The early identification of teratogens in humans and animals is mandatory for drug discovery and development. Zebrafish has emerged as an alternative model to traditional preclin. models for predicting teratogenicity and other potential chem.-induced toxicity hazards. To prove its predictivity, we exposed zebrafish embryos from 0 to 96 h post fertilization to a battery of 31 compounds classified as teratogens or non-teratogens in mammals. The teratogenicity score was based on the measurement of 16 phenotypical parameters, namely heart edema, pigmentation, body length, eye size, yolk size, yolk sac edema, otic vesicle defects, otoliths defects, body axis defects, developmental delay, tail bending, scoliosis, lateral fins absence, hatching ratio, lower jaw malformations and tissue necrosis. Among the 31 compounds, 20 were detected as teratogens and 11 as non-teratogens, resulting in 94.44% sensitivity, 90.91% specificity and 87.10% accuracy compared to rodents. These percentages decreased slightly when referred to humans, with 87.50% sensitivity, 81.82% specificity and 74.19% accuracy, but allowed an increase in the prediction levels reported by rodents for the same compounds Pos. compounds showed a high correlation among teratogenic parameters, pointing out at general developmental delay as major cause to explain the physiol./morphol. malformations. A more detailed anal. based on deviations from main trends revealed potential specific modes of action for some compounds such as retinoic acid, DEAB, ochratoxin A, haloperidol, warfarin, valproic acid, acetaminophen, dasatinib, imatinib, dexamethasone, 6-aminonicotinamide and bisphenol A. The high degree of predictivity and the possibility of applying mechanistic approaches makes zebrafish a powerful model for screening teratogenicity.

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