Month: November 2022

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 March 15, 2017, Chaim, Isaac A.; Gardner, Alycia; Wu, Jie; Iyama, Teruaki; Wilson, David M. III; Samson, Leona D. published an article.Computed Properties of 55662-66-3 The title of the article was A novel role for transcription-coupled nucleotide excision repair for the in vivo repair of 3,N4-ethenocytosine. And the article contained the following:

Etheno (ε) DNA base adducts are highly mutagenic lesions produced endogenously via reactions with lipid peroxidation (LPO) products. Cancer-promoting conditions, such as inflammation, can induce persistent oxidative stress and increased LPO, resulting in the accumulation of ε-adducts in different tissues. Using a recently described fluorescence multiplexed host cell reactivation assay, we show that a plasmid reporter bearing a site-specific 3,N4-ethenocytosine (εC) causes transcriptional blockage. Notably, this blockage is exacerbated in Cockayne Syndrome and xeroderma pigmentosum patient-derived lymphoblastoid and fibroblast cells. Parallel RNA-Seq expression anal. of the plasmid reporter identifies novel transcriptional mutagenesis properties of εC. Our studies reveal that beyond the known pathways, such as base excision repair, the process of transcription-coupled nucleotide excision repair plays a role in the removal of εC from the genome, and thus in the protection of cells and tissues from collateral damage induced by inflammatory responses. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Computed Properties of 55662-66-3

The Article related to transcription coupled nucleotide dna excision repair nethenocytosine, Biochemical Genetics: Genomic Processes and other aspects.Computed Properties of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Revankar, Ganapathi R.; Robins, Roland K. published an article in 1975, the title of the article was Synthesis and biological activity of some nucleosides resembling guanosine: imidazo[1,2-a]pyrimidine nucleosides.Quality Control of 7-Chloroimidazo[1,2-a]pyrimidin-5(1H)-one And the article contains the following content:

Refluxing di-Et malonate in NaOEt with 2-aminoimidazole hemisulfate gave 49.6% 5,7-dihydroxyimidazo[1,2-a]pyrimidine, which was chlorinated with POCl3 and treated with 5% aqueous NaOH to give I. Refluxing I with NH(SiMe3)2 and (NH4)2SO4 followed by addition of tetra-O-acetyl-β-D-ribofuranose and deacetylation gave II (R = Cl) (III). Amination of III with NH3 in MeOH at 100° gave 46% II (R = NH2) which showed no in vitro antiviral activity with the RNA and DNA virus tested. The experimental process involved the reaction of 7-Chloroimidazo[1,2-a]pyrimidin-5(1H)-one(cas: 57473-33-3).Quality Control of 7-Chloroimidazo[1,2-a]pyrimidin-5(1H)-one

The Article related to imidazopyrimidine nucleoside, ribofuranosylimidazopyrimidine virucide, Carbohydrates: Nucleosides, Nucleotides and other aspects.Quality Control of 7-Chloroimidazo[1,2-a]pyrimidin-5(1H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 29, 2006, Al Mamun, Abu Amar M.; Humayun, M. Zafri published an article.Related Products of 55662-66-3 The title of the article was Escherichia coli DNA polymerase II can efficiently bypass 3,N4-ethenocytosine lesions in vitro and in vivo. And the article contained the following:

Escherichia coli DNA polymerase II (pol-II) is a highly conserved protein that appears to have a role in replication restart, as well as in translesion synthesis across specific DNA adducts under some conditions. Here, we have investigated the effects of elevated expression of pol-II (without concomitant SOS induction) on translesion DNA synthesis and mutagenesis at 3,N 4-ethenocytosine (εC), a highly mutagenic DNA lesion induced by oxidative stress as well as by exposure to industrial chems. such as vinyl chloride. In normal cells, survival of transfected M13 single-stranded DNA bearing a single εC residue (εC-ssDNA) is about 20% of that of control DNA, with about 5% of the progeny phage bearing a mutation at the lesion site. Most mutations are C → A and C → T, with a slight predominance of transversions over transitions. In contrast, in cells expressing elevated levels of pol-II, survival of εC-ssDNA is close to 100%, with a concomitant mutation frequency of almost 99% suggesting highly efficient translesion DNA synthesis. Furthermore, an overwhelming majority of mutations at εC are C → T transitions. Purified pol-II efficiently catalyzes translesion synthesis at εC in vitro, accompanied by high levels of mutagenesis with the same specificity. These results suggest that the observed in vivo effects in pol-II over-expressing cells are due to pol-II-mediated DNA synthesis. Introduction of mutations in the carboxy terminus region (β interaction domain) of polB eliminates in vivo translesion synthesis at εC, suggesting that the ability of pol-II to compete with pol-III requires interaction with the β processivity subunit of pol-III. Thus, pol-II can compete with pol-III for translesion synthesis. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Related Products of 55662-66-3

The Article related to escherichia dna polymerase ii ethenocytosine lesion bypass mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 1, 2007, Al Mamun, Abu Amar M. published an article.COA of Formula: C6H5N3O The title of the article was Elevated expression of DNA polymerase II increases spontaneous mutagenesis in Escherichia coli. And the article contained the following:

Escherichia coli DNA polymerase II (Pol-II), encoded by the SOS-regulated polB gene, belongs to the highly conserved group B (α-like) family of “high-fidelity” DNA polymerases. Elevated expression of polB gene was recently shown to result in a significant elevation of translesion DNA synthesis at 3, N4-ethenocytosine lesion with concomitant increase in mutagenesis. Here, I show that elevated expression of Pol-II leads to an approx. 100-fold increase in spontaneous mutagenesis in a manner that is independent of SOS, umuDC, dinB, recA, uvrA and mutS functions. Cells grow slowly and filament with elevated expression of Pol-II. Introduction of carboxy terminus (“β interaction domain”) mutations in polB eliminates elevated spontaneous mutagenesis, as well as defects in cell growth and morphol., suggesting that these abilities require the interaction of Pol-II with the β processivity subunit of DNA polymerase III. Introduction of a mutation in the proofreading exo motif of polB elevates mutagenesis by a further 180-fold, suggesting that Pol-II can effectively compete with DNA polymerase III for DNA synthesis. Thus, Pol-II can contribute to spontaneous mutagenesis when its expression is elevated. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).COA of Formula: C6H5N3O

The Article related to escherichia dna polymerase ii expression motif spontaneous mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On July 30, 2020, Sun, Tong; Wu, Zhikun; Wang, Xiufang; Wang, Yilin; Hu, Xiaoyun; Qin, Wenyan; Lu, Senxu; Xu, Dongping; Wu, Yutong; Chen, Qiuchen; Ding, Xiangyu; Guo, Hao; Li, Yalun; Wang, Yuanhe; Fu, Boshi; Yao, Weifan; Wei, Minjie; Wu, Huizhe published an article.Quality Control of N-Methyl-7H-purin-6-amine The title of the article was LNC942 promoting METTL14-mediated m6A methylation in breast cancer cell proliferation and progression. And the article contained the following:

Abstract: Increasing evidence supports that long noncoding RNAs (lncRNAs) act as master regulators involved in tumorigenesis and development at the N6-methyladenine (m6A) epigenetic modification level. However, the underlying regulatory mechanism in breast cancer (BRCA) remains elusive. Here, we unveil that LINC00942 (LNC942) exerts its functions as an oncogene in promoting METTL14-mediated m6A methylation and regulating the expression and stability of its target genes CXCR4 and CYP1B1 in BRCA initiation and progression. Specifically, LNC942 and METTL14 were significantly upregulated accompanied with the upregulation of m6A levels in BRCA cells and our included BRCA cohorts (n = 150). Functionally, LNC942 elicits potent oncogenic effects on promoting cell proliferation and colony formation and inhibiting cell apoptosis, subsequently elevating METTL14-mediated m6A methylation levels and its associated mRNA stability and protein expression of CXCR4 and CYP1B1 in BRCA cells. Mechanistically, LNC942 directly recruits METTL14 protein by harboring the specific recognize sequence (+176-+265), thereby stabilized the expression of downstream targets of LNC942 including CXCR4 and CYP1B1 through posttranscriptional m6A methylation modification in vitro and in vivo. Therefore, our results uncover a novel LNC942-METTL14-CXCR4/CYP1B1 signaling axis, which provides new targets and crosstalk m6A epigenetic modification mechanism for BRCA prevention and treatment. 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 lnc942 mettl14 methylation human breast cancer proliferation metastasis, Biochemical Genetics: Genomic Processes and other aspects.Quality Control of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On March 4, 2021, Zhu, Pengpeng; He, Fang; Hou, Yixuan; Tu, Gang; Li, Qiao; Jin, Ting; Zeng, Huan; Qin, Yilu; Wan, Xueying; Qiao, Yina; Qiu, Yuxiang; Teng, Yong; Liu, Manran published an article.Category: imidazoles-derivatives The title of the article was A novel hypoxic long noncoding RNA KB-1980E6.3 maintains breast cancer stem cell stemness via interacting with IGF2BP1 to facilitate c-Myc mRNA stability. And the article contained the following:

Abstract: The hostile hypoxic microenvironment takes primary responsibility for the rapid expansion of breast cancer tumors. However, the underlying mechanism is not fully understood. Here, using RNA sequencing (RNA-seq) anal., we identified a hypoxia-induced long noncoding RNA (lncRNA) KB-1980E6.3, which is aberrantly upregulated in clin. breast cancer tissues and closely correlated with poor prognosis of breast cancer patients. The enhanced lncRNA KB-1980E6.3 facilitates breast cancer stem cells (BCSCs) self-renewal and tumorigenesis under hypoxic microenvironment both in vitro and in vivo. Mechanistically, lncRNA KB-1980E6.3 recruited insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) to form a lncRNA KB-1980E6.3/IGF2BP1/c-Myc signaling axis that retained the stability of c-Myc mRNA through increasing binding of IGF2BP1 with m6A-modified c-Myc coding region instability determinant (CRD) mRNA. In conclusion, we confirm that lncRNA KB-1980E6.3 maintains the stemness of BCSCs through lncRNA KB-1980E6.3/IGF2BP1/c-Myc axis and suggest that disrupting this axis might provide a new therapeutic target for refractory hypoxic tumors. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Category: imidazoles-derivatives

The Article related to hypoxia lncrnkb1980e63 breast cancer stem cell igf2bp1 cmyc transcription, Biochemical Genetics: Genomic Processes and other aspects.Category: imidazoles-derivatives

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On April 29, 2003, Sung, Jung-Suk; Mosbaugh, Dale W. published an article.Category: imidazoles-derivatives The title of the article was Escherichia coli Uracil- and Ethenocytosine-Initiated Base Excision DNA Repair: Rate-Limiting Step and Patch Size Distribution. And the article contained the following:

The rate, extent, and DNA synthesis patch size of base excision repair (BER) were measured using Escherichia coli GM31 cell-free extracts and a pGEM (form I) DNA substrate containing a site-specific uracil or ethenocytosine target. The rate of complete BER was stimulated (∼3-fold) by adding exogenous E. coli DNA ligase to the cell-free extract, whereas addition of E. coli Ung, Nfo, Fpg, or Pol I did not stimulate BER. Hence, DNA ligation was identified as the rate-limiting step in the E. coli BER pathway. The addition of exogenous DNA polymerase I caused modest inhibition of BER, which was overcome by concomitant addition of DNA ligase. Repair patch size determinations were performed to assess the distribution of DNA synthesis associated with both uracil- and ethenocytosine-initiated BER. During the early phase (0-5 min) of the BER reaction, the large majority of repair events resulted from short patch (1-nucleotide) DNA synthesis. However, during the late phase (>10 min) both short and long (2-20 nucleotide) patches were observed, with long patch BER progressively dominating the repair process. In addition, the patch size distribution was influenced by the ratio of DNA polymerase I to DNA ligase activity in the reaction. A novel mode of BER was identified that involved DNA synthesis tracts of >205 nucleotides in length and termed very-long patch BER. This BER process was dependent upon DNA polymerase I since very-long patch BER was inhibited by DNA polymerase I antibody and addition of excess DNA polymerase I reversed this inhibition. 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 escherichia uracil ethenocytosine excision repair dna ligase polymerase, dna base excision repair mechanism rate patch size escherichia, Biochemical Genetics: Genomic Processes and other aspects.Category: imidazoles-derivatives

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 31, 2021, Khanal, Jhabindra; Lim, Dae Young; Tayara, Hilal; Chong, Kil To published an article.Related Products of 443-72-1 The title of the article was A stacking ensemble-based computational prediction of DNA N6-methyladenine (6mA) sites in the Rosaceae genome. And the article contained the following:

DNA N6-methyladenine (6 mA) is an epigenetic modification that plays a vital role in a variety of cellular processes in both eukaryotes and prokaryotes. Accurate information of 6 mA sites in the Rosaceae genome may assist in understanding genomic 6 mA distributions and various biol. functions such as epigenetic inheritance. Various studies have shown the possibility of identifying 6 mA sites through experiments, but the procedures are time-consuming and costly. To overcome the drawbacks of exptl. methods, we propose an accurate computational paradigm based on a machine learning (ML) technique to identify 6 mA sites in Rosa chinensis (R.chinensis) and Fragaria vesca (F.vesca). To improve the performance of the proposed model and to avoid overfitting, a recursive feature elimination with cross-validation (RFECV) strategy is used to extract the optimal number of features (ONF) subset from five different DNA sequence encoding schemes, i.e., Binary Encoding (BE), Ring-Function-Hydrogen-Chem. Properties (RFHC), Electron-Ion-Interaction Pseudo Potentials of Nucleotides (EIIP), Dinucleotide Physicochem. Properties (DPCP), and Trinucleotide Physicochem. Properties (TPCP). Subsequently, we use the ONF subset to train a double layers of ML-based stacking model to create a bioinformatics tool named ‘i6mA-stack’. 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 rosaceae genome dna n6 methyladenine computational prediction, dna n6-methyladenine, machine learning, rfecv, sequence analysis, stacking, Biochemical Genetics: Genomic Processes and other aspects.Related Products of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 25, 1997, Hang, B.; Singer, B.; Margison, G. P.; Elder, R. H. published an article.Synthetic Route of 55662-66-3 The title of the article was Targeted deletion of alkylpurine-DNA-N-glycosylase in mice eliminates repair of 1,N6-ethenoadenine and hypoxanthine but not of 3,N4-ethenocytosine or 8-oxoguanine. And the article contained the following:

It has previously been reported that 1,N6-ethenoadenine (εA), deaminated adenine (hypoxanthine, Hx), and 7,8-dihydro-8-oxoguanine (8-oxoG), but not 3,N4-ethenocytosine (εC), are released from DNA in vitro by the DNA repair enzyme alkylpurine-DNA-N-glycosylase (APNG). To assess the potential contribution of APNG to the repair of each of these mutagenic lesions in vivo, we have used cell-free extracts of tissues from APNG-null mutant mice and wild-type controls. The ability of these extracts to cleave defined oligomers containing a single modified base was determined The results showed that both testes and liver cells of these knockout mice completely lacked activity toward oligonucleotides containing εA and Hx, but retained wild-type levels of activity for εC and 8-oxoG. These findings indicate that (i) the previously identified εA-DNA glycosylase and Hx-DNA glycosylase activities are functions of APNG; (ii) the two structurally closely related mutagenic adducts εA and εC are repaired by sep. gene products; and (iii) APNG does not contribute detectably to the repair of 8-oxoG. 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 apng glycosylase dna excision repair, ethenoadenine hypoxanthine ethenocysteine apng glycosylase repair, mouse apng glycosylase dna excision repair, Biochemical Genetics: Genomic Processes and other aspects.Synthetic Route of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem