Hasan, Mehedi Md et al. published their research in Briefings in Functional Genomics in 2021 |CAS: 443-72-1

The Article related to review dna methyladenine distant sequence, dna n6-methyladenine site, machine learning, prediction model, sequence analysis, web servers, Placeholder for records without volume info and other aspects.Recommanded Product: 443-72-1

Hasan, Mehedi Md; Shoombuatong, Watshara; Kurata, Hiroyuki; Manavalan, Balachandran published an article in 2021, the title of the article was Critical evaluation of web-based DNA N6-methyladenine site prediction tools.Recommanded Product: 443-72-1 And the article contains the following content:

A review. The accurate genome-wide identification of 6mA is a challenging task that leads to understanding the biol. functions. For the last 5 years, a number of bioinformatics approaches and tools for 6mA site prediction have been established, and some of them are easily accessible as web application. Nevertheless, the accurate genome-wide identification of 6mA is still one of the challenging works that lead to understanding the biol. functions. Especially in practical applications, these tools have implemented diverse encoding schemes, machine learning algorithms and feature selection methods, whereas few systematic performance comparisons of 6mA site predictors have been reported. In this review, 11 publicly available 6mA predictors evaluated with seven different species-specific datasets (Arabidopsis thaliana, Tolypocladium, Diospyros lotus, Saccharomyces cerevisiae, Drosophila melanogaster, Caenorhabditis elegans and Escherichia coli). Of those, few species are close homologs, and the remaining datasets are distant sequences. Our independent, validation tests demonstrated that Meta-i6mA and MM-6mAPred models for A. thaliana, Tolypocladium, S. cerevisiae and D. melanogaster achieved excellent overall performance when compared with their counterparts. However, none of the existing methods were suitable for E. coli, C. elegans and D. lotus. A feasibility of the existing predictors is also discussed for the seven species. Our evaluation provides useful guidelines for the development of 6mA site predictors and helps biologists selecting suitable prediction tools. Methylation of DNA N6-methyladenosine (6mA) is a type of epigenetic modification that plays pivotal roles in various biol. processes. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Recommanded Product: 443-72-1

The Article related to review dna methyladenine distant sequence, dna n6-methyladenine site, machine learning, prediction model, sequence analysis, web servers, Placeholder for records without volume info and other aspects.Recommanded Product: 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Goh, Yeek Teck et al. published their research in Nucleic Acids Research in 2020 |CAS: 443-72-1

The Article related to mettl4 m6am transcriptome rna methylation u2snrna premrna splicing, human rna sequence adenosine methylome catalytic site splice site, Placeholder for records without volume info and other aspects.Category: imidazoles-derivatives

Goh, Yeek Teck; Koh, Casslynn W. Q.; Sim, Donald Yuhui; Roca, Xavier; Goh, W. S. Sho published an article in 2020, the title of the article was METTL4 catalyzes m6Am methylation in U2 snRNA to regulate pre-mRNA splicing.Category: imidazoles-derivatives And the article contains the following content:

N6-methylation of 2è·?O-methyladenosine (Am) in RNA occurs in eukaryotic cells to generate N6,2éˆ?O-dimethyladenosine (m6Am). Identification of the methyltransferase responsible for m6Am catalysis has accelerated studies on the function of m6Am in RNA processing. While m6Am is generally found in the first transcribed nucleotide of mRNAs, the modification is also found internally within U2 snRNA. However, the writer required for catalyzing internal m6Am formation had remained elusive. By sequencing transcriptome-wide RNA methylation at single-base-resolution, we identified human METTL4 as the writer that directly methylates Am at U2 snRNA position 30 into m6Am. We found that METTL4 localizes to the nucleus and its conserved methyltransferase catalytic site is required for U2 snRNA methylation. By sequencing human cells with overexpressed Mettl4, we determined METTL4鈥瞫 in vivo target RNA motif specificity. In the absence of Mettl4 in human cells, U2 snRNA lacks m6Am thereby affecting a subset of splicing events that exhibit specific features such as 3éˆ?splice-site weakness and an increase in exon inclusion. These findings suggest that METTL4 methylation of U2 snRNA regulates splicing of specific pre-mRNA transcripts. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Category: imidazoles-derivatives

The Article related to mettl4 m6am transcriptome rna methylation u2snrna premrna splicing, human rna sequence adenosine methylome catalytic site splice site, Placeholder for records without volume info and other aspects.Category: imidazoles-derivatives

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Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Sheng, Yalan et al. published their research in mSphere in 2021 |CAS: 443-72-1

The Article related to tetrahymena environmental stress n6 methyladenine dna modification, 6ma, tetrahymena thermophila, starvation, unicellular eukaryote, Placeholder for records without volume info and other aspects.Application In Synthesis of N-Methyl-7H-purin-6-amine

Sheng, Yalan; Pan, Bo; Wei, Fan; Wang, Yuanyuan; Gao, Shan published an article in 2021, the title of the article was Case study of the response of N6-methyladenine DNA modification to environmental stressors in the unicellular eukaryote Tetrahymena thermophila.Application In Synthesis of N-Methyl-7H-purin-6-amine And the article contains the following content:

Study on the dynamic changes of 6mA under starvation in the unicellular model organism Tetrahymena thermophila. Single-mol., real-time (SMRT) sequencing reveals that DNA 6mA levels in starved cells are significantly reduced, especially sym. 6mA, compared to those in vegetatively growing cells. Despite a global 6mA reduction, the fraction of asym. 6mA with a high methylation level was increased, which might be the driving force for stronger nucleosome positioning in starved cells. Starvation affects expression of many metabolism-related genes, the expression level change of which is associated with the amount of 6mA change, thereby linking 6mA with global transcription and starvation adaptation. These results demonstrated that a regulated 6mA response to environmental cues is evolutionarily conserved in eukaryotes. Increasing evidence indicated that 6mA could respond to environmental stressors in multicellular eukaryotes. As 6mA distribution and function differ significantly in multicellular and unicellular organisms, whether and how 6mA in unicellular eukaryotes responds to environmental stress remains elusive. In the present work, we characterized the dynamic changes of 6mA under starvation in the unicellular model organism Tetrahymena thermophila. Our results provide insights into how Tetrahymena fine-tunes its 6mA level and composition upon starvation, suggesting that a regulated 6mA response to environmental cues is evolutionarily conserved in eukaryotes. 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 tetrahymena environmental stress n6 methyladenine dna modification, 6ma, tetrahymena thermophila, starvation, unicellular eukaryote, Placeholder for records without volume info and other aspects.Application In Synthesis of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Gao, Chundi et al. published their research in Future Oncology in 2022 |CAS: 443-72-1

The Article related to expression pattern clin relevance regulator cancer type, n6-methyladenine, correlation, pan-cancer, regulatory factor, survival, Placeholder for records without volume info and other aspects.Quality Control of N-Methyl-7H-purin-6-amine

Gao, Chundi; Yu, Haiyang; Li, Huayao; Liu, Cun; Ma, Xiaoran; Zhuang, Jing; Sun, Changgang published an article in 2022, the title of the article was Analysis of the expression patterns and clinical relevance of m6A regulators in 33 cancer types.Quality Control of N-Methyl-7H-purin-6-amine And the article contains the following content:

The role of N6-methyladenine (m6A) RNA methylation in a variety of biol. processes is gradually being revealed. Here, we systematically describe the correlation between the expression pattern of m6A RNA methylation regulatory factors and clin. phenotype, immunity, drug sensitivity, stem cells and prognosis in more than 10,000 samples of 33 types of cancer. The results show that there are significant differences in the expression of 20 m6A RNA methylation regulatory factors in different cancers, and there was a significant correlation with the anal. indicators. In this study, the m6A RNA methylation regulatory factor was found not only to potentially assist in stratifying the prognosis but also to predict or improve the sensitivity of clin. drug therapy. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Quality Control of N-Methyl-7H-purin-6-amine

The Article related to expression pattern clin relevance regulator cancer type, n6-methyladenine, correlation, pan-cancer, regulatory factor, survival, Placeholder for records without volume info and other aspects.Quality Control of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Liu, Mengya et al. published their research in Briefings in Bioinformatics in 2022 |CAS: 443-72-1

The Article related to dna n methyladenine mol graph rice, dna n6-methyladenine, dna molecular graph feature, smiles, residual block, rice genome, Placeholder for records without volume info and other aspects.Quality Control of N-Methyl-7H-purin-6-amine

Liu, Mengya; Sun, Zhan-Li; Zeng, Zhigang; Lam, Kin-Man published an article in 2022, the title of the article was MGF6mARice: prediction of DNA N6-methyladenine sites in rice by exploiting molecular graph feature and residual block.Quality Control of N-Methyl-7H-purin-6-amine And the article contains the following content:

DNA N6-methyladenine (6mA) is produced by the N6 position of the adenine being methylated, which occurs at the mol. level, and is involved in numerous vital biol. processes in the rice genome. Given the shortcomings of biol. experiments, researchers have developed many computational methods to predict 6mA sites and achieved good performance. However, the existing methods do not consider the occurrence mechanism of 6mA to extract features from the mol. structure. In this paper, a novel deep learning method is proposed by devising DNA mol. graph feature and residual block structure for 6mA sites prediction in rice, named MGF6mARice. Firstly, the DNA sequence is changed into a simplified mol. input line entry system (SMILES) format, which ref lects chem. mol. structure. Secondly, for the mol. structure data, we construct the DNA mol. graph feature based on the principle of graph convolutional network. Then, the residual block is designed to extract higher level, distinguishable features from mol. graph features. Finally, the prediction module is used to obtain the result of whether it is a 6mA site. By means of 10-fold cross-validation, MGF6mARice outperforms the state-of-the-art approaches. Multiple experiments have shown that the mol. graph feature and residual block can promote the performance of MGF6mARice in 6mA prediction. To the best of our knowledge, it is the first time to derive a feature of DNA sequence by considering the chem. mol. structure. We hope that MGF6mARice will be helpful for researchers to analyze 6mA sites in rice. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Quality Control of N-Methyl-7H-purin-6-amine

The Article related to dna n methyladenine mol graph rice, dna n6-methyladenine, dna molecular graph feature, smiles, residual block, rice genome, Placeholder for records without volume info and other aspects.Quality Control of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Drennen, Brandon’s team published research in RSC Medicinal Chemistry in 2022 | CAS: 5805-53-8

RSC Medicinal Chemistry published new progress about Animal gene, Bcl-2 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 5805-53-8 belongs to class imidazoles-derivatives, name is Methyl 1H-benzo[d]imidazole-2-carboxylate, and the molecular formula is C9H8N2O2, Product Details of C9H8N2O2.

Drennen, Brandon published the artcileScaffold hopping from indoles to indazoles yields dual MCL-1/BCL-2 inhibitors from MCL-1 selective leads, Product Details of C9H8N2O2, the main research area is indole indazole MCL1 BCL2 inhibitor scaffold hopping.

Overexpression of the anti-apoptotic BCL-2 proteins is associated with the development and progression of a range of cancers. Venetoclax, an FDA-approved BCL-2 inhibitor, is fast becoming the standard-of-care for acute myeloid leukemia and chronic lymphocytic leukemia. However, the median survival offered by venetoclax is only 18 mo (as part of a combination therapy regimen), and one of the primary culprits for this is the concomitant upregulation of sister anti-apoptotic proteins, in particular MCL-1 (and BCL-xL), which provides an escape route that manifests as venetoclax resistance. Since inhibition of BCL-xL leads to thrombocytopenia, we believe that a dual MCL-1/BCL-2 inhibitor may provide an enhanced therapeutic effect relative to a selective BCL-2 inhibitor. Beginning with a carboxylic acid-containing literature compound that is a potent inhibitor of MCL-1 and a moderate inhibitor of BCL-2, we herein describe our efforts to develop dual inhibitors of MCL-1 and BCL-2 by scaffold hopping from an indole core to an indazole framework. Subsequently, further elaboration of our novel N2-substituted, indazole-3-carboxylic acid lead into a family of indazole-3-acylsulfonamides resulted in improved inhibition of both MCL-1 and BCL-2, possibly through occupation of the p4 pocket, with minimal or no inhibition of BCL-xL.

RSC Medicinal Chemistry published new progress about Animal gene, Bcl-2 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 5805-53-8 belongs to class imidazoles-derivatives, name is Methyl 1H-benzo[d]imidazole-2-carboxylate, and the molecular formula is C9H8N2O2, Product Details of C9H8N2O2.

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Dabiri, Yasamin’s team published research in iScience in 2019-02-22 | CAS: 1023-01-4

iScience published new progress about Cadherin CDH1 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1023-01-4 belongs to class imidazoles-derivatives, name is 2-(4-Bromophenyl)-6-methylimidazo[1,2-a]pyridine, and the molecular formula is C14H11BrN2, Product Details of C14H11BrN2.

Dabiri, Yasamin published the artcileImidazopyridines as Potent KDM5 Demethylase Inhibitors Promoting Reprogramming Efficiency of Human iPSCs, Product Details of C14H11BrN2, the main research area is induced pluripotent stem cell reprogramming efficiency imidazopyridine KDM5 demethylation; Biochemistry; Biological Sciences; Molecular Biology.

Pioneering human induced pluripotent stem cell (iPSC)-based pre-clin. studies have raised safety concerns and pinpointed the need for safer and more efficient approaches to generate and maintain patient-specific iPSCs. One approach is searching for compounds that influence pluripotent stem cell reprogramming using functional screens of known drugs. Our high-throughput screening of drug-like hits showed that imidazopyridines-analogs of zolpidem, a sedative-hypnotic drug-are able to improve reprogramming efficiency and facilitate reprogramming of resistant human primary fibroblasts. The lead compound (O4I3) showed a remarkable OCT4 induction, which at least in part is due to the inhibition of H3K4 demethylase (KDM5, also known as JARID1). Experiments demonstrated that KDM5A, but not its homolog KDM5B, serves as a reprogramming barrier by interfering with the enrichment of H3K4Me3 at the OCT4 promoter. Thus our results introduce a new class of KDM5 chem. inhibitors and provide further insight into the pluripotency-related properties of KDM5 family members.

iScience published new progress about Cadherin CDH1 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1023-01-4 belongs to class imidazoles-derivatives, name is 2-(4-Bromophenyl)-6-methylimidazo[1,2-a]pyridine, and the molecular formula is C14H11BrN2, Product Details of C14H11BrN2.

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Mangericha, Aswin et al. published their research in Proceedings of the National Academy of Sciences of the United States of America in 2012 |CAS: 55662-66-3

The Article related to gene expression helicobacter infection stress dna damage colon carcinoma, Mammalian Pathological Biochemistry: Oncology and other aspects.SDS of cas: 55662-66-3

On July 3, 2012, Mangericha, Aswin; Knutson, Charles G.; Parry, Nicola M.; Muthupalani, Sureshkumar; Ye, Wenjie; Prestwich, Erin; Cui, Liang; McFaline, Jose L.; Mobley, Melissa; Ge, Zhongming; Taghizadeh, Koli; Wishnok, John S.; Wogan, Gerald N.; Fox, James G.; Tannenbaum, Steven R.; Dedon, Peter C. published an article.SDS of cas: 55662-66-3 The title of the article was Infection-induced colitis in mice causes dynamic and tissue-specific changes in stress response and DNA damage leading to colon cancer. And the article contained the following:

Helicobacter hepaticus-infected Rag2-/- mice emulate many aspects of human inflammatory bowel disease, including the development of colitis and colon cancer. To elucidate mechanisms of inflammation-induced carcinogenesis, we undertook a comprehensive anal. of histopathol., mol. damage, and gene expression changes during disease progression in these mice. Infected mice developed severe colitis and hepatitis by 10 wk post-infection, progressing into colon carcinoma by 20 wk post-infection, with pronounced pathol. in the cecum and proximal colon marked by infiltration of neutrophils and macrophages. Transcriptional profiling revealed decreased expression of DNA repair and oxidative stress response genes in colon, but not in liver. Mass spectrometric anal. revealed higher levels of DNA and RNA damage products in liver compared to colon and infection-induced increases in 5-chlorocytosine in DNA and RNA and hypoxanthine in DNA. Paradoxically, infection was associated with decreased levels of DNA etheno adducts. Levels of nucleic acid damage from the same chem. class were strongly correlated in both liver and colon. The results support a model of inflammation-mediated carcinogenesis involving infiltration of phagocytes and generation of reactive species that cause local mol. damage leading to cell dysfunction, mutation, and cell death. There are strong correlations among histopathol., phagocyte infiltration, and damage chem. that suggest a major role for neutrophils in inflammation-associated cancer progression. Further, paradoxical changes in nucleic acid damage were observed in tissue- and chem.-specific patterns. The results also reveal features of cell stress response that point to microbial pathophysiol. and mechanisms of cell senescence as important mechanistic links to cancer. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).SDS of cas: 55662-66-3

The Article related to gene expression helicobacter infection stress dna damage colon carcinoma, Mammalian Pathological Biochemistry: Oncology and other aspects.SDS of cas: 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Obtulowicz, Tomasz et al. published their research in Free Radical Biology & Medicine in 2010 |CAS: 55662-66-3

The Article related to colon cancer base excision repair etheno dna adduct leukocyte, Mammalian Pathological Biochemistry: Oncology and other aspects.Category: imidazoles-derivatives

On September 15, 2010, Obtulowicz, Tomasz; Winczura, Alicja; Speina, Elzbieta; Swoboda, Maja; Janik, Justyna; Janowska, Beata; Ciesla, Jaroslaw M.; Kowalczyk, Pawel; Jawien, Arkadiusz; Gackowski, Daniel; Banaszkiewicz, Zbigniew; Krasnodebski, Ireneusz; Chaber, Andrzej; Olinski, Ryszard; Nair, Jagadesaan; Bartsch, Helmut; Douki, Thierry; Cadet, Jean; Tudek, Barbara published an article.Category: imidazoles-derivatives The title of the article was Aberrant repair of etheno-DNA adducts in leukocytes and colon tissue of colon cancer patients. And the article contained the following:

To assess the role of lipid peroxidation-induced DNA damage and repair in colon carcinogenesis, the excision rates and levels of 1,N6-etheno-2′-deoxyadenosine (蔚dA), 3,N4-etheno-2′-deoxycytidine (蔚dC), and 1,N2-etheno-2′-deoxyguanosine (1,N2-蔚dG) were analyzed in polymorphic blood leukocytes (PBL) and resected colon tissues of 54 colorectal carcinoma (CRC) patients and PBL of 56 healthy individuals. In PBL the excision rates of 1,N6-ethenoadenine (蔚Ade) and 3,N4-ethenocytosine (蔚Cyt), measured by the nicking of oligodeoxynucleotide duplexes with single lesions, and unexpectedly also the levels of 蔚dA and 1,N2-蔚dG, measured by LC/MS/MS, were lower in CRC patients than in controls. In contrast the mRNA levels of repair enzymes, alkylpurine- and thymine-DNA glycosylases and a basic site endonuclease (APE1), were higher in PBL of CRC patients than in those of controls, as measured by QPCR. In the target colon tissues 蔚Ade and 蔚Cyt excision rates were higher, whereas the 蔚dA and 蔚dC levels in DNA, measured by 32P-postlabeling, were lower in tumor than in adjacent colon tissue, although a higher mRNA level was observed only for APE1. This suggests that during the onset of carcinogenesis, etheno adduct repair in the colon seems to be under a complex transcriptional and posttranscriptional control, whereby deregulation may act as a driving force for malignancy. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Category: imidazoles-derivatives

The Article related to colon cancer base excision repair etheno dna adduct leukocyte, Mammalian Pathological Biochemistry: Oncology and other aspects.Category: imidazoles-derivatives

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Liu, Zhifeng et al. published their research in Neurochemical Research in 2021 |CAS: 443-72-1

The Article related to alkbh5 g6pd glioma, alkbh5, g6pd, glioma, m6a modification, Mammalian Pathological Biochemistry: Oncology and other aspects.Related Products of 443-72-1

On November 30, 2021, Liu, Zhifeng; Chen, Yonghan; Wang, Leilei; Ji, Suzhen published an article.Related Products of 443-72-1 The title of the article was ALKBH5 Promotes the Proliferation of Glioma Cells via Enhancing the mRNA Stability of G6PD. And the article contained the following:

To investigate the biol. role of 6-methyladenine (m6A) methylation in inducing the carcinogenesis of glioma and its proliferation. Relative levels of ALKBH5 and glucose-6-phosphate dehydrogenase (G6PD) in glioma tissues and cell lines were determined by quant real-time polymerase chain reaction (qRT-PCR) and Western blot. Gain-of-function and loss-of-function approaches were used to investigate the role of ALKBH5 in mediating proliferation and energy metabolism of glioma cells. The regulatory effect of ALKBH5 on G6PD was analyzed using m6A-qRT-PCR. Our showed that ALKBH5 was upregulated in glioma, which stimulated glioma cells to proliferate. Serving as a m6A eraser, ALKBH5 demethylated the target transcript G6PD and enhanced its mRNA stability, thereby promoting G6PD translation and activating the pentose phosphate pathway (PPP). Collectively, ALKBH5 stimulates glioma cells to proliferate through erasing the m6A methylation of G6PD, which can be utilized as a potential therapeutic target for glioma. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Related Products of 443-72-1

The Article related to alkbh5 g6pd glioma, alkbh5, g6pd, glioma, m6a modification, Mammalian Pathological Biochemistry: Oncology and other aspects.Related Products of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem