Category: imidazoles-derivatives

Bochtler, Matthias; Fernandes, Humberto published an article in 2021, the title of the article was DNA adenine methylation in eukaryotes: Enzymatic mark or a form of DNA damage.SDS of cas: 443-72-1 And the article contains the following content:

A Review. 6-Methyladenine (6mA) is fairly abundant in nuclear DNA of basal fungi, ciliates and green algae. In these organisms, 6mA is maintained near transcription start sites in ApT context by a parental-strand instruction dependent maintenance methyltransferase and is pos. associated with transcription. In animals and plants, 6mA levels are high only in organellar DNA. The 6mA levels in nuclear DNA are very low. They are attributable to nucleotide salvage and the activity of otherwise mitochondrial METTL4, and may be considered as a price that cells pay for adenine methylation in RNA and/or organellar DNA. Cells minimize this price by sanitizing dNTP pools to limit 6mA incorporation, and by converting 6mA that has been incorporated into DNA back to adenine. Hence, 6mA in nuclear DNA should be described as an epigenetic mark only in basal fungi, ciliates and green algae, but not in animals and plants. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).SDS of cas: 443-72-1

The Article related to review dna adenine methylation eukaryotes, 6ma, dna damage, dna modifications, cancer, epitranscriptome/epigenome, nucleotide salvage, transcription, Biochemical Genetics: Reviews and other aspects.SDS of cas: 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 31, 2022, Li, Xuwen; Guo, Shiyuan; Cui, Yan; Zhang, Zijian; Luo, Xinlong; Angelova, Margarita T.; Landweber, Laura F.; Wang, Yinsheng; Wu, Tao P. published an article.Synthetic Route of 443-72-1 The title of the article was NT-seq: a chemical-based sequencing method for genomic methylome profiling. And the article contained the following:

Abstract: DNA methylation plays vital roles in both prokaryotes and eukaryotes. There are three forms of DNA methylation in prokaryotes: N6-methyladenine (6mA), N4-methylcytosine (4mC), and 5-methylcytosine (5mC). Although many sequencing methods have been developed to sequence specific types of methylation, few technologies can be used for efficiently mapping multiple types of methylation. Here, we present NT-seq for mapping all three types of methylation simultaneously. NT-seq reliably detects all known methylation motifs in two bacterial genomes and can be used for identifying de novo methylation motifs. NT-seq provides a simple and efficient solution for detecting multiple types of DNA methylation. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Synthetic Route of 443-72-1

The Article related to escherichia helicobacter nt seq genome methylome dna methylation, dna methylation, next-generation sequencing, whole-genome epigenetic profiling, Biochemical Genetics: Methods and other aspects.Synthetic Route of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 1, 1979, Slaughter, Robert S.; Barnes, Eugene M. Jr. published an article.Recommanded Product: Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Hypoxanthine transport by Chinese hamster lung fibroblasts: kinetics and inhibition by nucleosides. And the article contained the following:

The transport of 3H-labeled hypoxanthine (I) was studied in monolayer cultures of mutant Chinese hamster lung fibroblasts lacking guanine phosphoribosyltransferase. Initial rates of transport were determined by rapid uptake experiments (8-20 s); a Michaelis constant of 0.68 mM for I was derived from linear, monophasic plots of v/S against v. Nucleosides are competitive inhibitors of this process; adenosine and thymidine give resp. Ki values of 86 and 300 μM. The corresponding bases give much higher inhibition constants with adenine and thymine yielding values of 3100 and 1700 μM, resp. A similar pattern was observed for competitive inhibition of I transport by inosine, adenine arabinoside, uridine, cytidine, and 2 ribofuranosylimidazo derivatives of pyrimidin-4-one; in every case the nucleoside exhibited a lower Ki value than the corresponding homologous base. The inhibition constants observed for nucleosides are remarkably similar to their Km values for nucleoside transport by cultured cells recently reported. I transport was also blocked by the 6-(2-hydroxy-5-nitrobenzylthio) derivatives of inosine and guanosine and by dipyridamole; these agents are also inhibitors of nucleoside transport. These results indicate a closer relation between base and nucleoside transport than previously recognized and suggest that these 2 transport processes may involve identical or very similar transport proteins. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Recommanded Product: Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to hypoxanthine fibroblast transport determination, biol transport hypoxanthine isotope determination, nucleoside inhibition hypoxanthine transport, Biochemical Methods: Isotopic and other aspects.Recommanded Product: Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Lowe, Paige; Olinski, Ryszard; Ruzov, Alexey published an article in 2021, the title of the article was Evidence for Noncytosine Epigenetic DNA Modifications in Multicellular Eukaryotes: An Overview.Name: N-Methyl-7H-purin-6-amine And the article contains the following content:

A review. Cytosine DNA methylation (5-methylcytsone, 5mC) is the major DNA modification found in the genomes of animals and plants. Although the roles of 5mC and its oxidized derivatives in the regulation of gene expression are relatively well attested and extensively explored, a number of recent studies imply that noncytosine DNA modifications may also convey specific biol. functions and act as “epigenetic” marks in multicellular organisms. Here we review exptl. evidence for the presence of noncytosine epigenetic modifications in metazoans and plants focusing on two “unusual” DNA bases, 5-hydroxymethyluracil (5hmU) and N6-methyladenine (6mA), and suggest potential explanations for inconsistencies in the currently available data on abundance and potential biol. roles of these DNA modifications in mammals. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Name: N-Methyl-7H-purin-6-amine

The Article related to review multicellular eukaryote noncytosine epigenetic dna modification, 5-hydroxymethyluracil, dna modifications, epigenetics, n6-methyladenine, Biochemical Genetics: Reviews and other aspects.Name: N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 2021, Lv, Hao; Dao, Fu-Ying; Zhang, Dan; Yang, Hui; Lin, Hao published an article.Application In Synthesis of N-Methyl-7H-purin-6-amine The title of the article was Advances in mapping the epigenetic modifications of 5-methylcytosine (5mC), N6-methyladenine (6mA), and N4-methylcytosine (4mC). And the article contained the following:

A review. DNA modification plays a pivotal role in regulating gene expression in cell development. As prevalent markers on DNA, 5-methylcytosine (5mC), N6-methyladenine (6mA), and N4-methylcytosine (4mC) can be recognized by specific methyltransferases, facilitating cellular defense and the versatile regulation of gene expression in eukaryotes and prokaryotes. Recent advances in DNA sequencing technol. have permitted the positions of different modifications to be resolved at the genome-wide scale, which has led to the discovery of several novel insights into the complexity and functions of multiple methylations. In this review, we summarize differences in the various mapping approaches and discuss their pros and cons with respect to their relative read depths, speeds, and costs. We also discuss the development of future sequencing technologies and strategies for improving the detection resolution of current sequencing technologies. Lastly, we speculate on the potentially instrumental role that these sequencing technologies might play in future research. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Application In Synthesis of N-Methyl-7H-purin-6-amine

The Article related to review methylcytosine methyladenine epigenetic modification, 5-methylcytosine, dna sequencing technologies, n4-methylcytosine, n6-methyladenine, Biochemical Genetics: Reviews and other aspects.Application In Synthesis of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On July 23, 2020, Li, Zheng; Zhao, Shuai; Nelakanti, Raman V.; Lin, Kaixuan; Wu, Tao P.; Alderman, Myles H. III; Guo, Cheng; Wang, Pengcheng; Zhang, Min; Min, Wang; Jiang, Zongliang; Wang, Yinsheng; Li, Haitao; Xiao, Andrew Z. published an article.COA of Formula: C6H7N5 The title of the article was N6-methyladenine in DNA antagonizes SATB1 in early development. And the article contained the following:

Abstract: The recent discovery of N6-methyladenine (N6-mA) in mammalian genomes suggests that it may serve as an epigenetic regulatory mechanism1. However, the biol. role of N6-mA and the mol. pathways that exert its function remain unclear. Here we show that N6-mA has a key role in changing the epigenetic landscape during cell fate transitions in early development. We found that N6-mA is upregulated during the development of mouse trophoblast stem cells, specifically at regions of stress-induced DNA double helix destabilization (SIDD)2-4. Regions of SIDD are conducive to topol. stress-induced unpairing of the double helix and have critical roles in organizing large-scale chromatin structures3,5,6. We show that the presence of N6-mA reduces the in vitro interactions by more than 500-fold between SIDD and SATB1, a crucial chromatin organizer that interacts with SIDD regions. Deposition of N6-mA also antagonizes SATB1 function in vivo by preventing its binding to chromatin. Concordantly, N6-mA functions at the boundaries between euchromatin and heterochromatin to restrict the spread of euchromatin. Repression of SIDD-SATB1 interactions mediated by N6-mA is essential for gene regulation during trophoblast development in cell culture models and in vivo. Overall, our findings demonstrate an unexpected mol. mechanism for N6-mA function via SATB1, and reveal connections between DNA modification, DNA secondary structures and large chromatin domains in early embryonic development. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).COA of Formula: C6H7N5

The Article related to methyladenine dna methylation satb1 embryogenesis mouse trophoblast, Biochemical Genetics: Genomic Processes and other aspects.COA of Formula: C6H7N5

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On August 31, 1999, Al Mamun, Abu Amar M.; Rahman, M. Sayeedur; Humayun, M. Zafri published an article.Application In Synthesis of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Escherichia coli cells bearing mutA, a mutant glyV tRNA gene, express a recA-dependent error-prone DNA replication activity. And the article contained the following:

A base substitution mutation (mutA) in the Escherichia coli glyV tRNA gene potentiates asp → gly mistranslation and confers a strong mutator phenotype that is SOS independent, but requires recA, recB and recC genes. Here, we demonstrate that mutA cells express an error-prone DNA polymerase by using an in vitro exptl. system based on the conversion of phage M13 single-stranded viral DNA bearing a model mutagenic lesion to the double-stranded replicative form. Amplification of the newly synthesized strand followed by multiplex DNA sequence anal. revealed that mutation fixation at 3,N4-ethenocytosine (εC) was ≈3% when the DNA was replicated by normal cell extracts, ≈48% when replicated by mutA cell extracts and ≈3% when replicated by mutA recA double mutant cell extracts, in complete agreement with previous in vivo results. Mutagenesis at undamaged DNA sites was significantly elevated by mutA cell-free extracts in the M13 lacZ(α) forward mutagenesis system. Neither polA (DNA polymerase I) nor polB (DNA polymerase II) genes are required for the mutA phenotype, suggesting that the phenotype is mediated through a modification of DNA polymerase III or the activation of a previously unidentified DNA polymerase. These findings define the major features of a novel mutagenic pathway and imply the existence of previously unrecognized links between translation, recombination and replication. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Application In Synthesis of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to trna mutation reca dependent dna replication error escherichia, Biochemical Genetics: Genomic Processes and other aspects.Application In Synthesis of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Barrio, Jorge R.; Sattsangi, Prem D.; Gruber, Bruce A.; Dammann, Laurence G.; Leonard, Nelson J. published an article in 1976, the title of the article was Species responsible for the fluorescence of 3,N4-ethenocytidine.Recommanded Product: 55662-66-3 And the article contains the following content:

The fluorescence properties of 3,N4-ethenocytidine (ε-cytidine) (I), substituted derivatives, and closely related 2-ring heterocycles were examined The chloroacetaldehyde-modified cytidine is fluorescent only in its protonated form. The fluorescence emission maximum is 340 nm and the pKa* is 4.0, very close to the value for the ground state. N-1-alkylation of I at the same position as protonation makes reversion to the nonfluorescent type of structure impossible, on changing the pH, and accordingly the fluorescence emission characteristics are preserved over a wide range of pH. The presence of the n→π* transition of the carbonyl group in I is responsible for the lack of fluorescence in neutral solution Even I.HCl has a low fluorescence quantum yield (Φ < 0.01) and a short fluorescence lifetime (τ = 30 psec). Ring substitution produces a red shift of the π → π* transition, due to inductive or mesomeric effects and a clear improvement in the fluorescence emission characteristics; e.g., 2-acetylamino-5,6-dihydro-5-oxo-6-β-D-ribofuranosylimidazo[1,2-c]pyrimidine, in its protonated form, shows Φ = 0.85 and τ = 4 ns. Imidazo[1,2-a]pyridine, a close model for I lacking the carbonyl group and accordingly the n → π* transition, has a high fluorescence quantum yield and long lifetime in either neutral solution or organic solvents. Both N-1-protonated and -alkylated imidazo[1,2-a]pyridines have emission maxima similar to those observed for I.HCl but higher quantum yields. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Recommanded Product: 55662-66-3

The Article related to fluorescence etherocytidine, cytidine etheno fluorescence, Carbohydrates: Nucleosides, Nucleotides and other aspects.Recommanded Product: 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 2, 2004, Jurado, Juan; Maciejewska, Agnieszka; Krwawicz, Joanna; Laval, Jacques; Saparbaev, Murat K. published an article.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Role of mismatch-specific uracil-DNA glycosylase in repair of 3,N4-ethenocytosine in vivo. And the article contained the following:

The 3,N4-ethenocytosine (εC) residue might have biol. role in vivo since it is recognized and efficiently excised in vitro by the E. coli mismatch-specific uracil-DNA glycosylase (MUG) and the human thymine-DNA glycosylase (hTDG). In the present work we have generated mug defective mutant of E. coli by insertion of a kanamycin cassette to assess the role of MUG in vivo. We show that human TDG complements the enzymic activity of MUG when expressed in a mug mutant. The εC-DNA glycosylase defective strain did not exhibit spontaneous mutator phenotype and did not show unusual sensitivity to any of the following DNA damaging treatments: methylmethanesulfonate, N-methyl-N’-nitro-N-nitrosoguanidine, UV light, H2O2, paraquat. However, plasmid DNA damaged by 2-chloroacetaldehyde treatment in vitro was inactivated at a greater rate in a mug mutant than in wild-type host, suggesting that MUG is required for the in vivo processing of the ethenobases. In addition, 2-chloroacetaldehyde treatment induces preferentially G·C → C·G and A·T → T·A transversions in mug mutant. Comparison of the mutation frequencies induced by the site-specifically incorporated εC residue in E. coli wild-type vs. mug indicates that MUG repairs more than 80% of εC residues in vivo. Furthermore, the results show that nucleotide excision repair and recombination are not involved in the processing of εC in E. coli. Based on the mutagenesis data we suggest that εC may be less toxic and less mutagenic than expected. The increased spontaneous mutation rate for G·C → A·T transition in the ung mug double mutant as compared to the single ung mutant suggest that MUG may be a back-up repair enzyme to the classic uracil-DNA glycosylase. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to uracil dna glycosylase repair ethenocytosine escherichia, Biochemical Genetics: Genomic Processes and other aspects.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On March 31, 1999, Rahman, M. Sayeedur; Humayun, M. Zafri published an article.Formula: C6H5N3O The title of the article was SOS and UVM pathways have lesion-specific additive and competing effects on mutation fixation at replication-blocking DNA lesions. And the article contained the following:

Escherichia coli cells have multiple mutagenic pathways that are induced in response to environmental and physiol. stimuli. Unlike the well-investigated classical SOS response, little is known about newly recognized pathways such as the UVM (UV modulation of mutagenesis) response. In this study, we compared the contributions of the SOS and UVM pathways on mutation fixation at two representative noninstructive DNA lesions: 3,N4-ethenocytosine (εC) and abasic (AP) sites. Because both SOS and UVM responses are induced by DNA damage, and defined UVM-defective E. coli strains are not yet available, we first constructed strains in which expression of the SOS mutagenesis proteins UmuD’ and UmuC (and also RecA in some cases) is uncoupled from DNA damage by being placed under the control of a heterologous lac-derived promoter. M13 single-stranded viral DNA bearing site-specific lesions was transfected into cells induced for the SOS or UVM pathway. Survival effects were determined from transfection efficiency, and mutation fixation at the lesion was analyzed by a quant. multiplex sequence anal. procedure. Our results suggest that induction of the SOS pathway can independently elevate mutagenesis at both lesions, whereas the UVM pathway significantly elevates mutagenesis at εC in an SOS-independent fashion and at AP sites in an SOS-dependent fashion. Although mutagenesis at εC appears to be elevated by the induction of either the SOS or the UVM pathway, the mutational specificity profiles for εC under SOS and UVM pathways are distinct. Interestingly, when both pathways are active, the UVM effect appears to predominate over the SOS effect on mutagenesis at εC, but the total mutation frequency is significantly increased over that observed when each pathway is individually induced. These observations suggest that the UVM response affects mutagenesis not only at class 2 noninstructive lesions (εC) but also at classical SOS-dependent (class 1) lesions such as AP sites. Our results add new layers of complexity to inducible mutagenic phenomena: DNA damage activates multiple pathways that have lesion-specific additive as well as suppressive effects on mutation fixation, and some of these pathways are not directly regulated by the SOS genetic network. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Formula: C6H5N3O

The Article related to sos uvm response dna repair mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem