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Search results for: Adenosine

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#35045589   2022/01/19 To Up

Characterization of sleep-related neurochemicals in the different developmental stages and insomnia models of Drosophila melanogaster.

Neurotransmitters play an important role in regulating the physiological activity of the animal, especially in emotion and sleep. While nucleotides are involved in almost all cellular processes. However, the characteristics of sleep-related neurochemicals under different life cycles and environment remain poorly understood. A rapid and sensitive analytical method was established with LC-MS/MS to determine eight endogenous neurochemicals in Drosophila melanogaster and the levels of neurochemicals in the different developmental stages of Drosophila melanogaster were evaluated. The results indicated that there were significant discrepancies among different stages, especially from pupal stage to adult. The levels of these compounds in caffeine-induced insomnia model of Drosophila melanogaster were investigated. Compared with normal group the eight endogenous metabolites did not fluctuate significantly in insomnia Drosophila melanogaster, which may be due to the mechanism of caffeine-induced insomnia through other pathways, such as adenosine. The results provide a reference for decoding of neurochemicals involved in the development of the full cycle of mammalian life and exploration of insomnia even other mental diseases induced by exogenous substances in the future.
Yu Sun, Runhua Liu, Yuelin Bi, Xin Feng, Jiaqi Wang, Tianyi Li, Hao Wu, Chenning Zhang, Yikun Sun

1248 related Products with: Characterization of sleep-related neurochemicals in the different developmental stages and insomnia models of Drosophila melanogaster.

10 ug2 Pieces/Box12 Pieces/Box1 mg

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#35044787   2022/01/19 To Up

Loss-of-function mutations in the co-chaperone protein BAG5 cause dilated cardiomyopathy requiring heart transplantation.

Dilated cardiomyopathy (DCM) is a major cause of heart failure, characterized by ventricular dilatation and systolic dysfunction. Familial DCM is reportedly caused by mutations in more than 50 genes, requiring precise disease stratification based on genetic information. However, the underlying genetic causes of 60 to 80% of familial DCM cases remain unknown. Here, we identified that homozygous truncating mutations in the gene encoding Bcl-2-associated athanogene (BAG) co-chaperone 5 () caused inherited DCM in five patients among four unrelated families with complete penetrance. BAG5 acts as a nucleotide exchange factor for heat shock cognate 71 kDa protein (HSC70), promoting adenosine diphosphate release and activating HSC70-mediated protein folding. mutant knock-in mice exhibited ventricular dilatation, arrhythmogenicity, and poor prognosis under catecholamine stimulation, recapitulating the human DCM phenotype, and administration of an adeno-associated virus 9 vector carrying the wild-type gene could fully ameliorate these DCM phenotypes. Immunocytochemical analysis revealed that BAG5 localized to junctional membrane complexes (JMCs), critical microdomains for calcium handling. -mutant mouse cardiomyocytes exhibited decreased abundance of functional JMC proteins under catecholamine stimulation, disrupted JMC structure, and calcium handling abnormalities. We also identified heterozygous truncating mutations in three patients with tachycardia-induced cardiomyopathy, a reversible DCM subtype associated with abnormal calcium homeostasis. Our study suggests that loss-of-function mutations in can cause DCM, that may be a target for genetic testing in cases of DCM, and that gene therapy may potentially be a treatment for this disease.
Hideyuki Hakui, Hidetaka Kioka, Yohei Miyashita, Shunsuke Nishimura, Ken Matsuoka, Hisakazu Kato, Osamu Tsukamoto, Yuki Kuramoto, Ayako Takuwa, Yusuke Takahashi, Shigeyoshi Saito, Kunio Ohta, Hiroshi Asanuma, Hai Ying Fu, Haruki Shinomiya, Noriaki Yamada, Tomohito Ohtani, Yoshiki Sawa, Masafumi Kitakaze, Seiji Takashima, Yasushi Sakata, Yoshihiro Asano

1104 related Products with: Loss-of-function mutations in the co-chaperone protein BAG5 cause dilated cardiomyopathy requiring heart transplantation.

1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set100ug Lyophilized1 Set100 μg1 Set

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#35044379   2022/01/19 To Up

A self-amplified ROS-responsive chemodrug-inhibitor conjugate for multi-drug resistance tumor therapy.

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Tingting Sun, Jie Xu, Tianbao Chen, Chunlai Tu, Lijuan Zhu, Deyue Yan

2296 related Products with: A self-amplified ROS-responsive chemodrug-inhibitor conjugate for multi-drug resistance tumor therapy.

100ug Lyophilized100 assays100μg100 assays100ug Lyophilized100ug Lyophilized100 assays100ug Lyophilized100ug Lyophilized100ug Lyophilized100 assays

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#35044296   2022/01/19 To Up

Comprehensive interrogation of the ADAR2 deaminase domain for engineering enhanced RNA editing activity and specificity.

Adenosine deaminases acting on RNA (ADARs) can be repurposed to enable programmable RNA editing, however their enzymatic activity on adenosines flanked by a 5' guanosine is very low, thus limiting their utility as a transcriptome engineering toolset. To address this issue, we first performed a novel deep mutational scan of the ADAR2 deaminase domain, directly measuring the impact of every amino acid substitution across 261 residues, on RNA editing. This enabled us to create a domain wide mutagenesis map while also revealing a novel hyperactive variant with improved enzymatic activity at motifs. However, exogenous delivery of ADAR enzymes, especially hyperactive variants, leads to significant transcriptome wide off-targeting. To solve this problem, we engineered a split ADAR2 deaminase which resulted in 1000-fold more specific RNA editing as compared to full-length deaminase overexpression. We anticipate that this systematic engineering of the ADAR2 deaminase domain will enable broader utility of the ADAR toolset for RNA biotechnology and therapeutic applications.
Dhruva Katrekar, Yichen Xiang, Nathan Palmer, Anushka Saha, Dario Meluzzi, Prashant Mali

2155 related Products with: Comprehensive interrogation of the ADAR2 deaminase domain for engineering enhanced RNA editing activity and specificity.

0.1 mg250 ml0.1 mg1 LITRE100μg0.2 mg100 ml100μg1 ml

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#35044153   2022/01/19 To Up

Enzyme-Free Autocatalysis-Driven Feedback DNA Circuits for Amplified Aptasensing of Living Cells.

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Yuhui Gao, Yingying Chen, Jinhua Shang, Shanshan Yu, Shizhen He, Ran Cui, Fuan Wang

2881 related Products with: Enzyme-Free Autocatalysis-Driven Feedback DNA Circuits for Amplified Aptasensing of Living Cells.

1KG500gm100gm5L50gm5 x 200ul/Unit

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#35043968   2022/01/19 To Up

2',3'-cAMP treatment mimics the stress molecular response in Arabidopsis thaliana.

The role of the RNA degradation product 2',3'-cyclic adenosine monophosphate (2',3'-cAMP) is poorly understood. Recent studies have identified 2',3'-cAMP in plant material and determined its role in stress signaling. The level of 2',3'-cAMP increases upon wounding, in the dark, and under heat, and 2',3'-cAMP binding to an RNA-binding protein, Rbp47b, promotes stress granule (SG) assembly. To gain further mechanistic insights into the function of 2',3'-cAMP, we used a multi-omics approach by combining transcriptomics, metabolomics, and proteomics to dissect the response of Arabidopsis (Arabidopsis thaliana) to 2',3'-cAMP treatment. We demonstrated that 2',3'-cAMP is metabolized into adenosine, suggesting that the well-known cyclic nucleotide-adenosine pathway of human cells might also exist in plants. Transcriptomics analysis revealed only minor overlap between 2',3'-cAMP- and adenosine-treated plants, suggesting that these molecules act through independent mechanisms. Treatment with 2',3'-cAMP changed the levels of hundreds of transcripts, proteins, and metabolites, many previously associated with plant stress responses, including protein and RNA degradation products, glucosinolates, chaperones, and SG components. Finally, we demonstrated that 2',3'-cAMP treatment influences the movement of processing bodies, confirming the role of 2',3'-cAMP in the formation and motility of membraneless organelles.
Monika Chodasiewicz, Olga Kerber, Michal Gorka, Juan C Moreno, Israel Maruri-Lopez, Romina I Minen, Arun Sampathkumar, Andrew D L Nelson, Aleksandra Skirycz

1497 related Products with: 2',3'-cAMP treatment mimics the stress molecular response in Arabidopsis thaliana.

100 UG96T96T1

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#35043676   2022/01/19 To Up

Post-ST-Segment-Elevation Myocardial Infarction Platelet Reactivity Is Associated With the Extent of Microvascular Obstruction and Infarct Size as Determined by Cardiac Magnetic Resonance Imaging.

Background Despite optimized medical management and techniques of primary percutaneous coronary intervention, a substantial proportion of patients with ST-segment-elevation myocardial infarction (STEMI) display significant microvascular damage. Thrombotic microvascular obstruction (MVO) has been implicated in the pathogenesis of microvascular and subsequent myocardial damage attributed to distal embolization and microvascular platelet plugging. However, there are only scarce data regarding the effect of platelet reactivity on MVO. Methods and Results We prospectively evaluated 105 patients in 2 distinct periods (2012-2013 and 2016-2018) who presented with first ST-segment-elevation myocardial infarction and underwent primary percutaneous coronary intervention. All patients were treated with dual antiplatelet therapy (DAPT). Blood samples were analyzed for platelet reactivity, and cardiac magnetic resonance imaging scans were evaluated for late gadolinium enhancement and MVO. DAPT suboptimal response was defined as hyporesponsiveness to either aspirin or P2Y12 receptor inhibitor agents and demonstrated in 31 patients (29.5%) of the current cohort. Suboptimal platelet response to DAPT was associated with a significantly greater extent of MVO when expressed as a percentage of the left ventricular mass, left ventricular scar, and the number of myocardial left ventricular segments showing MVO (<0.01 for each). Adjusted multivariable logistic regression model revealed that suboptimal response to DAPT is significantly associated with both greater late gadolinium enhancement (<0.01) and MVO extent (odds ratio, 3.7 [95% CI, 1.3-10.5]; =0.01). Patients with a greater extent of MVO were more likely to sustain major adverse cardiovascular events at a 1-year follow-up (37% versus 11%; <0.01). Conclusions In patients undergoing primary percutaneous coronary intervention for ST-segment-elevation myocardial infarction, platelet reactivity in response to DAPT is a key predictor of the extent of both myocardial and microvascular damage.
Eias Massalha, Daniel Oren, Orly Goitein, Yafim Brodov, Alex Fardman, Anan Younis, Anat Berkovitch, Shir Raibman-Spector, Eli Konen, Elad Maor, Paul Fefer, Amit Segev, Roy Beigel, Shlomi Matetzky

1210 related Products with: Post-ST-Segment-Elevation Myocardial Infarction Platelet Reactivity Is Associated With the Extent of Microvascular Obstruction and Infarct Size as Determined by Cardiac Magnetic Resonance Imaging.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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#35043462   2022/01/18 To Up

The serotonin reuptake transporter modulates mitochondrial copy number and mitochondrial respiratory complex gene expression in the frontal cortex and cerebellum in a sexually dimorphic manner.

Neuropsychiatric and neurodevelopmental disorders such as major depressive disorder (MDD) and autism spectrum disorder (ASD) are complex conditions attributed to both genetic and environmental factors. There is a growing body of evidence showing that serotonergic signaling and mitochondrial dysfunction contribute to the pathophysiology of these disorders and are linked as signaling through specific serotonin (5-HT) receptors drives mitochondrial biogenesis. The serotonin transporter (SERT) is important in these disorders as it regulates synaptic serotonin and therapeutically is the target of selective serotonin reuptake inhibitors which are a major class of anti-depressant drug. Human allelic variants of the serotonin transporter-linked polymorphic region (5-HTTLPR) such as the S/S variant, are associated with reduced SERT expression and increased susceptibility for developing neuropsychiatric disorders. Using a rat model that is haploinsufficient for SERT and displays reduced SERT expression similar to the human S/S variant, we demonstrate that reduced SERT expression modulates mitochondrial copy number and expression of respiratory chain electron transfer components in the brain. In the frontal cortex, genotype-related trends were opposing for males and females, such that reduced SERT expression led to increased expression of the Complex I subunit mt-Nd1 in males but reduced expression in females. Our findings suggest that SERT expression and serotonergic signaling have a role in regulating mitochondrial biogenesis and adenosine triphosphate (ATP) production in the brain. We speculate that the sexual dimorphism in mitochondrial abundance and gene expression contributes to the sex bias found in the incidence of neuropsychiatric disorders such as MDD and ASD.
Bryony N Thorne, Bart A Ellenbroek, Darren J Day

1291 related Products with: The serotonin reuptake transporter modulates mitochondrial copy number and mitochondrial respiratory complex gene expression in the frontal cortex and cerebellum in a sexually dimorphic manner.

300 units1 5 G 5 G50 ul

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#35043449   2022/01/18 To Up

TMT-based proteomics analysis to screen potential biomarkers of Achyranthis Bidentatae Radix for osteoporosis in rats.

This study aimed to explore the possible mechanism of Achyranthis Bidentatae Radix responsible for the treatment of osteoporosis using tandem mass tag-based proteomics technique combined with mass spectrometry.
Liu Yang, Ajiao Hou, Xiaojuan Zhang, Jiaxu Zhang, Song Wang, Jiaojiao Dong, Shihao Zhang, Hai Jiang, Haixue Kuang

2663 related Products with: TMT-based proteomics analysis to screen potential biomarkers of Achyranthis Bidentatae Radix for osteoporosis in rats.

1 module1 module1 module1 module1 module1 module1 module100 μg96 wells (1 kit)1 module

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