Tag: M.W=300-350

Zhu, Yiran published the artcileEffects of Cr(VI)-induced calcium-sensing receptor activation on DF-1 cell pyroptosis, Product Details of C19H21N3O, the publication is Ecotoxicology and Environmental Safety (2019), 257-264, database is CAplus and MEDLINE.

This study aims to investigate the effects of Cr(VI)-induced calcium-sensing receptor (CaSR) activation on DF-1 cell pyroptosis. Previous studies show that Cr(VI) could accumulate in the body of chickens and change Ca levels. Hence, a Ca-related pathway may be an important mechanism participating in some pathol. processes. Pyroptosis level, which is meditated by CaSR, increases under Cr(VI) accumulation. In the present study, pyroptosis was determined by flow cytometry to detect SYTOX blue and caspase-1 staining followed by morphol. observation. Interleukin (IL)-1β and IL-18 levels were detected by ELISA, while CaSR protein and [Ca²⁺]_i contents were detected by Western blot and fluorescence microplate spectrophotometry, resp. The results showed that Cr(VI) causes DF-1 cell pyroptosis in a time- and dose-dependent manner and that this effect is caspase-1 dependent. Further experiments indicated that pyroptosis could be induced by Cr(VI) and is accompanied by up-regulated [Ca²⁺]_i content. CaSR inhibition led to decreases in pyroptosis level. Some mechanisms may be involved in Cr(VI)-triggered CaSR activation and enhance DF-1 cell pyroptosis. Taken together, the results of this study support future investigations on Cr(VI)-induced pyroptosis in DF-1 cells.

Ecotoxicology and Environmental Safety published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C10H12O5, Product Details of C19H21N3O.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Sun, Ji-Fu published the artcileCaSR and calpain contribute to the ischemia reperfusion injury of spinal cord, Recommanded Product: N-(Adamantan-1-yl)quinoxaline-2-carboxamide, the publication is Neuroscience Letters (2017), 49-55, database is CAplus and MEDLINE.

Spinal cord ischemia reperfusion injury (SCIRI) can cause spinal cord dysfunction and even devastating paraplegia. Calcium-sensing receptor (CaSR) and calpain are two calcium related mols. which have been reported to be involved in the ischemia reperfusion injury of cardiomyocytes and the subsequent apoptosis. Here, we studied the expression of CaSR and calpain in spinal cord neurons and tissues, followed by the further investigation of the role of CaSR/calpain axis in the cellular apoptosis process during SCIRI. The results of in vitro and in vivo studies showed that the expression of CaSR and calpain in spinal cord neurons increased during SCIRI. Moreover, the CaSR agonist GdCl₃ and antagonist NPS-2390 enhanced or decreased the expression of CaSR and calpain resp. The expressions of CaSR and calpain were also consistent with the cellular apoptosis in spinal cord. Taken together, CaSR-calpain contributes to the SCIRI apoptosis, and CaSR antagonist might be a helpful drug for alleviating SCIRI.

Neuroscience Letters published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C6H5F4NO3S, Recommanded Product: N-(Adamantan-1-yl)quinoxaline-2-carboxamide.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Zhang, Wei-hua published the artcileCalcium sensing receptor is involved in neonate rat cardiomyocyte apoptosis induced by hypoxia/reoxygenation via regulating calcium concentration in mitochondria, Formula: C19H21N3O, the publication is Harbin Yike Daxue Xuebao (2012), 46(6), 534-538, database is CAplus.

Calcium sensing receptor (CaR) activation plays a role in the regulation of SR-mitochondrial inter-organelle Ca²⁺ signaling, causing apoptosis during ischemia/reperfusion (I/R). Neonatal rat cardiomyocytes were subjected to 3 h of hypoxia, followed by 6 h of reoxygenation. Ca²⁺ m were determined using x-rhod-1 and the mitochondrial membrane potential was detected with JC-1 during reoxygenation. The apoptotic rates detected by Hoechst33342 were lower in NPS-2390 + Ca + Ni + Cd + H-Re (±4)%, 2-APB + Ca + Ni + Cd + H-Re (18±4)% and Ru + Ca + Ni + Cd + H-Re (23±5)% groups than H-Re (33±6)%, Ca+Ni+Cd+H-Re (31±5)% and Gd+Ni+Cd+HRe (34±3)% groups. [Ca ²⁺] m was increased in the Ca + Ni + Cd + H-Re group. The mitochondria transmembrane potential was lower in Ca + Ni + Cd + H-Re group than that in 2-APB + Ca + Ni + Cd + H-Re and Ru + Ca + Ni + Cd + H-Re groups. CaR activation causes Ca²⁺ release from the SR into the mitochondria through IP3 Rs and induces cardiomyocyte apoptosis during hypoxia/reoxygenation.

Harbin Yike Daxue Xuebao published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C25H23NO4, Formula: C19H21N3O.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Maklad, Noha published the artcilePositive and negative modulation of group 1 metabotropic glutamate receptors, Name: N-(Adamantan-1-yl)quinoxaline-2-carboxamide, the publication is Chemtracts (2008), 21(5), 165-171, database is CAplus.

A review. Vanejevs et al. developed a pharmacophore hypothesis using potent and com. available metabotropic glutamate receptor 1 (mGluR1) analogs. This was done by aligning the potent and com. available mGluR1 antagonists using the flexible alignment tool included in the Mol. Operating Environment software. The developed pharmacophore model offers a new and different methodol. to discover such analogs.

Chemtracts published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C19H21N3O, Name: N-(Adamantan-1-yl)quinoxaline-2-carboxamide.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Liu, Cong published the artcileThe extracellular calcium-sensing receptor promotes porcine egg activation via calcium/calmodulin-dependent protein kinase II, Recommanded Product: N-(Adamantan-1-yl)quinoxaline-2-carboxamide, the publication is Molecular Reproduction & Development (2020), 87(5), 598-606, database is CAplus and MEDLINE.

Extracellular calcium is required for intracellular Ca²⁺ oscillations needed for egg activation, but the regulatory mechanism is still poorly understood. The present study was designed to demonstrate the function of calcium-sensing receptor (CASR), which could recognize extracellular calcium as first messenger, during porcine egg activation. CASR expression was markedly upregulated following egg activation. Functionally, the addition of CASR agonist NPS R-568 significantly enhanced pronuclear formation rate, while supplementation of CASR antagonist NPS2390 compromised egg activation. There was no change in NPS R-568 group compared with control group when the egg activation was performed without extracellular calcium addition The addition of NPS2390 precluded the activation-dependent [Ca²⁺]_i rise. When egg activation was conducted in intracellular Ca²⁺ chelator BAPTA-AM and NPS R-568 containing medium, CASR function was abolished. Meanwhile, CASR activation increased the level of the [Ca²⁺]_i effector p-CAMKII, and the presence of KN-93, an inhibitor of CAMKII, significantly reduced the CASR-mediated increasement of pronuclear formation rate. Furthermore, the increase of CASR expression following activation was reversed by inhibiting CAMKII activity, supporting a pos. feedback loop between CAMKII and CASR. Altogether, these findings provide a new pathway of egg activation about CASR, as the extracellular Ca²⁺ effector, promotes egg activation via its downstream effector and upstream regulator CAMKII.

Molecular Reproduction & Development published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C19H21N3O, Recommanded Product: N-(Adamantan-1-yl)quinoxaline-2-carboxamide.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Cao, Qi published the artcileMechanism research on CSE restraining macrophages into foam cells by calcium sensing receptor, Quality Control of 226878-01-9, the publication is Xiandai Yufang Yixue (2015), 42(19), 3555-3559, 3596, database is CAplus.

Objective To confirm calcium sensing receptor (CaR) can increase the expression of CSE and the secretion of H₂S, thereby inhibiting the transformation of macrophages into foam cells. Methods Sensitive sulfur electrodes method was used to detect the change of the H₂S content in macrophages. The relative content of pos. cells was tested by oil red O staining and the HPLC method was sued to do the determination of intracellular cholesterol content. ELISA assay detected the secretion situation of cytokine IL-10, MIF, and TNF-α. The expression of CaR, CSE, CD36 and ACAT-1 in each group cells were detected by Western blot. Results Compared with the blank control group, the relative contents of H₂S in the GdCl₃ group and the NaHS group significantly increased, while the NPS2390 group, the relative content of H₂S significantly decreased. The number of pos. cells in the GdCl₃ group and the NaHS group obviously decreased, while the number in NPS2390 group adversely increased. The levels of TNF-α and MIF in cell supernatant significantly ascended, and the IL-10 level fell in the GdCl₃ and NaHS groups. However, there was a rising trend on the levels of TNF-α and MIF in cell supernatant, and the IL-10 level dropped significantly in the NPS2390 group. The expression of CaR and CSE significantly enhanced in GdCl₃ group, while the expression of CD36 and ACAT-1 were significantly inhibited in GdCl₃ group. Meanwhile, the expressions of CaR and CSE were significantly inhibited in NPS2390 group, while the expression of CD36 and ACAT-1 were significantly enhanced in NPS2390 group. GdCl₃ group significantly increased the expression of CSE, while GdCl₃ + CSE siRNA group and CSE siRNA group significantly reduced the expression of CSE. GdCl₃ group significantly increased the relative content of H₂S, while GdCl₃ + CSE siRNA group and CSE siRNA group significantly reduced the relative content of H₂S. Conclusion CaR could enhance the expression of CSE in macrophages to increase the secretion of H₂S, thereby inhibiting the transformation of macrophages into foam cells.

Xiandai Yufang Yixue published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C19H21N3O, Quality Control of 226878-01-9.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Lavreysen, Hilde published the artcileMetabotropic glutamate 1 receptor distribution and occupancy in the rat brain: a quantitative autoradiographic study using [³H]R214127, Application of N-(Adamantan-1-yl)quinoxaline-2-carboxamide, the publication is Neuropharmacology (2004), 46(5), 609-619, database is CAplus and MEDLINE.

We used the selective metabotropic glutamate (mGlu) 1 receptor antagonist [³H]1-(3,4-dihydro-2H-pyrano[2,3-b]quinolin-7-yl)-2-phenyl-1-ethanone ([³H]R214127) to investigate the distribution of mGlu1 receptor binding sites in rat brain. We found high mGlu1 receptor binding in the cerebellum, thalamus, dentate gyrus and medial central gray, moderate binding within the CA3 of the hippocampus and hypothalamus, and low mGlu1 receptor binding in the basal ganglia and cortex. The mGlu1 receptor is also present in variable degree in the dorsal lateral septal nucleus, amygdala, interpeduncular nucleus and median raphe nucleus. Addnl., we employed [³H]R214127 autoradiog. as a means of investigating the occupancy of central mGlu1 receptors following in vivo administration of mGlu1 receptor antagonists that prevent binding of this radioligand. We found that the mGlu1 receptor antagonist (3aS,6aS)-6a-naphtalan-2-ylmethyl-5-methyliden-hexahydro-cyclopenta[c]furan-1-on (BAY 36-7620), administered s.c. at 10 mg/kg, only occupied about 30% of cerebellar and thalamic mGlu1 receptors. The mGlu1/5 receptor antagonist 2-quinoxaline-carboxamide-N-adamantan-1-yl (NPS 2390) exhibited a relatively high potency in occupying mGlu1 receptors in rat cerebellum (ED₅₀ = 0.75 mg/kg, s.c.) and thalamus (ED₅₀ = 0.63 mg/kg, s.c). In the future, this method can be employed to gain more insight into the in vivo profile and central activity of potential therapeutic agents that act upon the mGlu1 receptor.

Neuropharmacology published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C19H21N3O, Application of N-(Adamantan-1-yl)quinoxaline-2-carboxamide.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Huang, Shuaishuai published the artcileTranscription factor CREB is involved in CaSR-mediated cytoskeleton gene expression, Recommanded Product: N-(Adamantan-1-yl)quinoxaline-2-carboxamide, the publication is Anatomical Record (2015), 298(3), 501-512, database is CAplus and MEDLINE.

Our previous studies illustrated that a steady increase of intracellular calcium concentration ([Ca²⁺]i) was important for maintaining microtubules (MTs) rearrangement in apoptotic cells. However, little is known about the effect of calcium sensing receptor (CaSR)-mediated increase in [Ca²⁺]i on cytoskeleton gene expression. We examined the impact of taxol or CaSR agonist/antagonist on the regulation of [Ca²⁺]i concentration, cytoskeleton arrangement, phosphorylated CREB and cytoskeleton gene expressions in HeLa cells with dominant neg. plasmid of CREB (PM). This study demonstrated that Gdcl3 (a specific CaSR agonist) evoked a rapid increase of [Ca²⁺]i, formed a rigid bundle of MTs which surrounded the nucleus and decreased the cytoskeleton gene expressions in HeLa cells. These effects were rescued by addition of NPS2390 (a specific CaSR antagonist). Moreover, CaSR activity affected cytoskeleton gene expression through transcription factor CREB. Histoscores of pCREB immunoreactivity in tissues of cervical adenocarcinoma, renal clear cell carcinoma, and diffuse large B-cell lymphoma were markedly increased compared with non malignant tissue. These data demonstrate, for the first time, that CaSR-mediated increase in [Ca²⁺]i probably modulate cytoskeleton organization and gene expression via transcription factor CREB. Anat Rec, 298:501-512, 2015. © 2014 Wiley Periodicals, Inc.

Anatomical Record published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C19H21N3O, Recommanded Product: N-(Adamantan-1-yl)quinoxaline-2-carboxamide.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Xue, Zhaoliang published the artcileCalcium-sensing receptor antagonist NPS2390 attenuates neuronal apoptosis though intrinsic pathway following traumatic brain injury in rats, SDS of cas: 226878-01-9, the publication is Biochemical and Biophysical Research Communications (2017), 486(2), 589-594, database is CAplus and MEDLINE.

Traumatic brain injury (TBI) initiates a complex cascade of neurochem. and signaling changes that leads to neuronal apoptosis, which contributes to poor outcomes for patients with TBI. Previous study indicates that calcium-sensing receptor (CaSR) activation contributes to neuron death in focal cerebral ischemia-reperfusion mice, however, its role in neuronal apoptosis after TBI is not well-established. Using a controlled cortical impact model in rats, the present study was designed to determine the effect of CaSR inhibitor NPS2390 upon neuronal apoptosis after TBI. Rats were randomly distributed into three groups undergoing the sham surgery or TBI procedure, and NPS2390 (1.5 mg/kg) was infused s.c. at 30 min and 120 min after TBI. All rats were sacrificed at 24 h after TBI. Our data indicated that NPS2390 significantly reduced the brain edema and improved the neurol. function after TBI. In addition, NPS2390 decreased caspase-3 levels and the number of apoptotic neurons. Furthermore, NPS2390 up-regulated anti-apoptotic protein Bcl-2 expression and down-regulated pro-apoptotic protein Bax, and reduced subsequent release of cytochrome c into the cytosol. In summary, this study indicated that inhibition of CaSR by NPS2390 attenuates neuronal apoptosis after TBI, in part, through modulating intrinsic apoptotic pathway.

Biochemical and Biophysical Research Communications published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C15H14O, SDS of cas: 226878-01-9.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider

Yanamala, Naveena published the artcilePreferential binding of allosteric modulators to active and inactive conformational states of metabotropic glutamate receptors, Category: quinoxaline, the publication is BMC Bioinformatics (2008), No pp. given, database is CAplus and MEDLINE.

Metabotropic glutamate receptors (mGluRs) are G protein coupled receptors that play important roles in synaptic plasticity and other neuro-physiol. and pathol. processes. Allosteric mGluR ligands are particularly promising drug targets because of their modulatory effects – enhancing or suppressing the response of mGluRs to glutamate. The mechanism by which this modulation occurs is not known. Here, the authors propose the hypothesis that pos. and neg. modulators will differentially stabilize the active and inactive conformations of the receptors, resp. To test this hypothesis, the authors have generated computational models of the transmembrane regions of different mGluR subtypes in two different conformations. The inactive conformation was modeled using the crystal structure of the inactive, dark state of rhodopsin as template and the active conformation was created based on a recent model of the light-activated state of rhodopsin. Ligands for which the nature of their allosteric effects on mGluRs is exptl. known were docked to the modeled mGluR structures using ArgusLab and Autodock softwares. The authors find that the allosteric ligand binding pockets of mGluRs are overlapping with the retinal binding pocket of rhodopsin, and that ligands have strong preferences for the active and inactive states depending on their modulatory nature. In 8 out of 14 cases (57%), the neg. modulators bound the inactive conformations with significant preference using both docking programs, and 6 out of 9 cases (67%), the pos. modulators bound the active conformations. Considering results by the individual programs only, even higher correlations were observed: 12/14 (86%) and 8/9 (89%) for ArgusLab and 10/14 (71%) and 7/9 (78%) for AutoDock. These findings strongly support the hypothesis that mGluR allosteric modulation occurs via stabilization of different conformations analogous to those identified in rhodopsin where they are induced by photochem. isomerization of the retinal ligand – despite the extensive differences in sequences between mGluRs and rhodopsin.

BMC Bioinformatics published new progress about 226878-01-9. 226878-01-9 belongs to quinoxaline, auxiliary class Neuronal Signaling,mGluR, name is N-(Adamantan-1-yl)quinoxaline-2-carboxamide, and the molecular formula is C38H74Cl2N2O4, Category: quinoxaline.

Referemce:
https://en.wikipedia.org/wiki/Quinoxaline,
Quinoxaline | C8H6N2 | ChemSpider