Tag: 100-200

Kang, Xiaoxu; Wang, Yushu; Chen, Zhigang; Wu, Yixin; Chen, Hao; Yang, Xi; Yu, Changyuan published an article in 2020, the title of the article was Imidazole modified Pt(IV) prodrug-loaded multi-stage pH responsive nanoparticles to overcome cisplatin resistance.Quality Control of N-(3-Aminopropyl)-imidazole And the article contains the following content:

An imidazole modified Pt(IV) prodrug with a long lipid tail can assemble into multi-stage pH responsive nanoparticles via electrostatic complexation with a neg. charged hydrophilic polymer. This strategy could overcome cisplatin resistance significantly. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Quality Control of N-(3-Aminopropyl)-imidazole

The Article related to imidazole platinum prodrug ph responsive nanoparticle antitumor resistance, Pharmaceuticals: Formulation and Compounding and other aspects.Quality Control of N-(3-Aminopropyl)-imidazole

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Singer, B.; Spengler, S. J. published an article in 1986, the title of the article was Replication and transcription of polynucleotides containing ethenocytosine, ethenoadenine and their hydrated intermediates.Product Details of 55662-66-3 And the article contains the following content:

A review with 27 references on replication and transcription using ribo- or deoxyribonucleotides containing 1,N6-ethenoadenine  [13875-63-3] or 3,N4-ethinocytosine  [55662-66-3] and the resulting misincorporations. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Product Details of 55662-66-3

The Article related to review polynucleotide transcription replication, Toxicology: Reviews and other aspects.Product Details of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Ludlum, D. B. published an article in 1986, the title of the article was Formation of cyclic adducts in nucleic acids by the haloethylnitrosoureas.Formula: C6H5N3O And the article contains the following content:

A review with 13 references on the isolation and characterization of cyclic nucleosides of adenine and cytosine and discusses the mutagenic, carcinogenic and cytotoxic activities of haloethylnitroseureas. 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 haloethylnitrosourea nucleic acid adduct review, Toxicology: Reviews and other aspects.Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 29, 2003, Gros, Laurent; Ishchenko, Alexander A.; Saparbaev, Murat published an article.Electric Literature of 55662-66-3 The title of the article was Enzymology of repair of etheno-adducts. And the article contained the following:

A review. Etheno(ε)-adducts such as 1,N6-ethenoadenine (εA), 3,N4-ethenocytosine (εC), N2,3-ethenoguanine (N2,3-εG), and 1,N2-ethenoguanine (1,N2-εG) are produced in cellular DNA by two independent pathways: (i) by reaction with oxidized metabolites of vinyl chloride, 2-chloroacetaldehyde and 2-chloroethylene oxide; (ii) by endogenous processes through the interaction of lipid peroxidation (LPO)-derived aldehydes and hydroxyalkenals. They have been found in DNA isolated from human and rodent tissues. However, the levels of adducts were significantly increased by cancer risk factors contributing to lipid peroxidation and oxidative stress. The highly mutagenic and genotoxic properties of ε-adducts have been established in vitro by analyzing steady-state kinetics of primer extension assays and in vivo by site-specific mutagenesis in mammalian cells. Therefore, the repair processes eliminating exocyclic adducts from DNA should play a crucial role in maintaining the stability of genetic information. The ε-adducts are eliminated by the base excision repair (BER) pathway, with DNA glycosylases being the key enzymes of this pathway. They remove ε-adducts from DNA by hydrolyzing the N-glycosidic bond between the damaged base and deoxyribose, leaving an abasic site in DNA. The ethenobase-DNA glycosylases have been identified and their enzymic properties described. They are specific for a given ε-base although they can also excise different types of modified bases, such as alkylated purines, hypoxanthine and uracil. The fact that ethenoadducts are recognized and excised with high efficiency by various DNA glycosylases in vitro suggests that these enzymes may be responsible for repair of these mutagenic lesions in vivo, and thus constitute important contributors to genetic stability. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Electric Literature of 55662-66-3

The Article related to review dna glycosylase repair etheno adduct, Toxicology: Reviews and other aspects.Electric Literature of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 31, 2005, Delaney, James C.; Smeester, Lisa; Wong, Cintyu; Frick, Lauren E.; Taghizadeh, Koli; Wishnok, John S.; Drennan, Catherine L.; Samson, Leona D.; Essigmann, John M. published an article.Synthetic Route of 55662-66-3 The title of the article was AlkB reverses etheno DNA lesions caused by lipid oxidation in vitro and in vivo. And the article contained the following:

Oxidative stress converts lipids into DNA-damaging agents. The genomic lesions formed include 1,N6-ethenoadenine (εA) and 3,N4-ethenocytosine (εC), in which two carbons of the lipid alkyl chain form an exocyclic adduct with a DNA base. Here we show that the newly characterized enzyme AlkB repairs εA and εC. The potent toxicity and mutagenicity of εA in Escherichia coli lacking AlkB was reversed in AlkB+ cells; AlkB also mitigated the effects of εC. In vitro, AlkB cleaved the lipid-derived alkyl chain from DNA, causing εA and εC to revert to adenine and cytosine, resp. Biochem., εA is epoxidized at the etheno bond. The epoxide is putatively hydrolyzed to a glycol, and the glycol moiety is released as glyoxal. These reactions show a previously unrecognized chem. versatility of AlkB. In mammals, the corresponding AlkB homologs may defend against aging, cancer and oxidative stress. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Synthetic Route of 55662-66-3

The Article related to alkb escherichia ethenoadenine ethenocytosine dna repair lipid oxidation, Enzymes: Other and other aspects.Synthetic Route of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 31, 2020, Zhang, Shuming; Li, Bianbian; Du, Ke; Liang, Tingting; Dai, Mengyuan; Huang, Wenxin; Zhang, Huizhi; Ling, Yihui; Zhang, Huidong published an article.Application of 443-72-1 The title of the article was Epigenetically modified N6-methyladenine inhibits DNA replication by human DNA polymerase iota. And the article contained the following:

Among human four Y-family DNA polymerases, hPol ι is exceptionally error-prone in DNA synthesis. 6 mA plays significant roles in epigenetic regulation of numerous biol. processes. Nonetheless, its effects on DNA replication by hPol ι is still unclear. In this work, we found that 6 mA and Hyp, the intermediate of 6 mA, inhibited the replication of DNA by hPol ι. 6 mA lost priority in extension beyond 6 mA:T pair, partially reducing dTTP incorporation efficiency and inhibiting next-base extension. Hyp was prone to dCTP incorporation and extension beyond Hyp:C instead of Hyp:T pair. Statistically, 6 mA primarily reduced the burst incorporation rate (kpol) and slightly increased the dissociation constant (Kd,dTTP). However, Hyp mainly increased the Kd,dCTP yet did not affect the kpol, both reducing the burst incorporation efficiency (kpol/Kd,dCTP). 6 mA together with Hyp weakened the binding affinity of hPol ι to DNA in binary or ternary complex. The misincorporation opposite 6 mA or Hyp further weakened this binding affinity. The Me group in 6 mA doesn′t almost affect the H-bond formation with dTTP, therefore mildly inhibiting dTTP incorporation. As an analog of G, Hyp can form only two H-bonds with dCTP, thus reducing dCTP incorporation. This work provides a new insight in how the epigenetically modified 6 mA and its intermediate Hyp affect replication of DNA by human DNA polymerase ι. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Application of 443-72-1

The Article related to dna polymerase, dna replication, human dna polymerase ι, hypoxanthine (hyp), n(6)-methyladenine (6 ma), steady-state and pre-steady-state kinetics, and other aspects.Application of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Shan, Li; Lu, Ye; Song, Yihua; Zhu, Xiaoli; Xiang, Cheng-Cheng; Zuo, Er-Dong; Cheng, Xu published an article in 2022, the title of the article was Identification of nine M6A-related long noncoding RNAs as prognostic signatures associated with oxidative stress in oral cancer based on data from the cancer genome atlas.Synthetic Route of 443-72-1 And the article contains the following content:

Objective. Although the expression of long noncoding RNAs (lncRNAs) and N6-methyladenosine (M6A) is correlated with different tumors, it remains unclear how M6A-related lncRNA functioning affects the initiation and progression of oral squamous cell carcinoma (OSCC). Materials and Methods. Gene expression and clin. data were retrieved from The Cancer Genome Atlas. The prognostic value of M6A-related lncRNAs was determined using univariate Cox regression analyses. Gene set enrichment anal. of OSCC patient clusters revealed the pathways that elucidate the mechanism. Furthermore, a risk-based model was established. The difference in the overall survival (OS) between groups, including low-/high-risk groups, was determined by Kaplan-Meier anal. Relationships among immune cells, clusters, clinicopathol. characteristics, and risk scores were explored. Results. Among 1,080 M6A-related lncRNAs, 36 were prognosis-related. Patients with OSCC were divided into two clusters. T stage and the pathol. grade were noticeably lower in cluster 2 than in cluster 1. Epithelial-mesenchymal transition showed greater enrichment in cluster 1. Nine hub M6A-related lncRNAs were identified for the model of risk score for predicting OSCC prognosis. The OS was longer in patients with a low-risk score than in patients with a high-risk score. The risk score was an independent prognostic factor of OSCC and was associated with the infiltration of different immune cells. T stages and the American Joint Committee on Cancer (AJCC) stages were more advanced in the high-risk score group than in the low-risk score group. Finally, expression correlation anal. showed that the risk score is associated with the expression of oxidative stress markers. Conclusion. M6A-related lncRNAs play an important role in OSCC progression. Immune cell infiltration was related to the risk score model in OSCC and could accurately predict OSCC prognosis. 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 adenine: analogs & derivatives, biomarkers, tumor: genetics, biomarkers, tumor: metabolism, carcinoma, squamous cell: diagnosis, carcinoma, squamous cell: genetics, carcinoma, squamous cell: pathology, gene expression regulation, neoplastic, head and neck neoplasms: diagnosis, head and neck neoplasms: genetics, humans and other aspects.Synthetic Route of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Guo, Ye; Pei, Yuqing; Li, Kexin; Cui, Wei; Zhang, Donghong published an article in 2020, the title of the article was DNA N6-methyladenine modification in hypertension.Synthetic Route of 443-72-1 And the article contains the following content:

DNA methylation has a role in the pathogenesis of essential hypertension. DNA N6-methyladenine (6mA) modification as a novel adenine methylation exists in human tissues, but whether it plays a role in hypertension development remains unclear. Here, we reported that the global 6mA DNA level in leukocytes was significantly reduced in patients with hypertension and was reversed with successful treatment. Age, systolic blood pressure, and serum total cholesterol and high-d. lipoprotein levels were associated with decreased leukocyte 6mA DNA level. Elevated ALKBH1 (AlkB homolog 1), a demethylase of 6mA, level mediated this dynamic change in 6mA level in leukocytes and vascular smooth muscle cells in hypertension mouse and rat models. Knockdown of ALKBH1 suppressed angiotensin II-induced vascular smooth muscle phenotype transformation, proliferation and migration. ALKBH1-6mA directly and neg. regulated hypoxia inducible factor 1 α (HIF1α), which responded to angiotensin II-induced vascular remodeling. Collectively, our results demonstrate a potential epigenetic role for ALKBH1-6mA regulation in hypertension development, diagnosis and treatment. 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 adenine: analogs & derivatives, adenine: metabolism, alkb homolog 1, histone h2a dioxygenase: genetics, angiotensin ii: metabolism, animals, dna methylation, dna repair enzymes, epigenesis, genetic, hypertension: blood, hypertension: metabolism, hypertension: therapy, leukocytes: metabolism, mice, muscle, smooth and other aspects.Synthetic Route of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Chen, Luyang; Zhang, Meiying; Guo, Mingzhou published an article in 2020, the title of the article was DNA N6-methyladenine increased in human esophageal squamous cell carcinoma..Product Details of 443-72-1 And the article contains the following content:

Esophageal cancer is one of the most common malignancies worldwide. DNA N6-methyladenine (6mA) has been well-studied in prokaryotes, while the distribution and biological functions of DNA 6mA in eukaryotic cells remain to be elucidated. Recently, DNA 6mA epigenetic modification was found in human gastric and liver cancers. To explore the status of DNA 6mA epigenetic modification in esophageal cancer, 101 cases of human esophageal squamous cell carcinoma (ESCC) and matched adjacent normal tissue samples were analyzed by dot blot assay. The levels of genomic DNA 6mA were significantly higher in ESCC tissue samples than in matched adjacent normal tissue samples (P<0.001). Increased DNA 6mA was associated with poor tumor differentiation (P<0.05), while no association was found between 6mA modification and gender, age, tumor size, TNM stage, lymph node metastasis, smoking, alcohol intake, or family history (all P>0.05). In conclusion, DNA 6mA epigenetic modification increased in human ESCC and may serve as a prognostic marker. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Product Details of 443-72-1

The Article related to adenine: analogs & derivatives, adenine: analysis, adenine: metabolism, adult, aged, aged, 80 and over, biomarkers, tumor: analysis, biomarkers, tumor: metabolism, dna methylation, epigenesis, genetic, esophageal mucosa: pathology, esophageal neoplasms: diagnosis, esophageal neoplasms: genetics and other aspects.Product Details of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On September 17, 2021, Mathur, Lavina; Jung, Sunhee; Jang, Cholsoon; Lee, Gina published an article.Safety of N-Methyl-7H-purin-6-amine The title of the article was Quantitative analysis of m6A RNA modification by LC-MS. And the article contained the following:

N6-adenosine methylation (m6A) of mRNA (mRNA) plays key regulatory roles in gene expression. Accurate measurement of m6A levels is thus critical to understand its dynamic changes in various biol. settings. Here, we provide a protocol to quantitate the levels of adenosine and m6A in cellular mRNAs. Using nuclease and phosphatase, we digest mRNA into nucleosides, which are subsequently quantified using liquid chromatog. mass spectrometry. For complete details on the use and execution of this protocol, please refer to Cho et al. (2021). The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Safety of N-Methyl-7H-purin-6-amine

The Article related to adenine: analogs & derivatives, adenine: analysis, adenine: chemistry, adenosine: analogs & derivatives, adenosine: chemistry, adenosine: metabolism, biochemical phenomena, chromatography, liquid: methods, methylation, nucleosides: analysis, rna: chemistry, rna, messenger: chemistry, rna and other aspects.Safety of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem