Month: October 2022

On August 31, 2022, Le, Nguyen Quoc Khanh; Ho, Quang-Thai published an article.Recommanded Product: 443-72-1 The title of the article was Deep transformers and convolutional neural network in identifying DNA N6-methyladenine sites in cross-species genomes. And the article contained the following:

As one of the most common post-transcriptional epigenetic modifications, N6-methyladenine (6 mA), plays an essential role in various cellular processes and disease pathogenesis. Therefore, accurately identifying 6 mA modifications is necessary for a deep understanding of cellular processes and other possible functional mechanisms. Although a few computational methods have been proposed, their resp. models were developed with small training datasets. Hence, their practical application is quite limited in genome-wide detection. To overcome the existing limitations, we present a novel model based on transformer architecture and deep learning to identify DNA 6 mA sites from the cross-species genome. The model is constructed on a benchmark dataset and explored a feature derived from pre-trained transformer word embedding approaches. Subsequently, a convolutional neural network was employed to learn the generated features and generate the prediction outcomes. As a result, our predictor achieved excellent performance during independent test with the accuracy and Matthews correlation coefficient (MCC) of 79.3% and 0.58, resp. Overall, its performance achieved better accuracy than the baseline models and significantly outperformed the existing predictors, demonstrating the effectiveness of our proposed hybrid framework. Furthermore, our model is expected to assist biologists in accurately identifying 6mAs and formulate the novel testable biol. hypothesis. We also release source codes and datasets freely at https://github.com/khanhlee/bert-dna for front-end users. 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 methyladenine pathogenesis deep learning convolutional neural network, contextualized word embedding, dna sequence analysis, deep learning, n6-methyladenine site, natural language processing, post-translational modification and other aspects.Recommanded Product: 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On September 30, 2017, Jahan, Humera; Choudhary, Muhammad I.; Shah, Zarbad; Khan, Khalid M.; Atta-ur-Rahman published an article.Recommanded Product: 2-Nitro-1H-benzo[d]imidazole The title of the article was Derivatives of 6-Nitrobenzimidazole Inhibit Fructose-Mediated Protein Glycation and Intracellular Reactive Oxygen Species Production. And the article contained the following:

Background: Benzimidazoles are important pharmacophores in drug discovery, and currently its derivatives such as flubendazole, omeprazole, and astemizole are used for the treatment of anthelmintic, ulcerative, and histaminic diseases, resp.

Objectives: The aim of the current study was to investigate the antiglycation activity of nitrobenzimidazole derivatives against fructose-mediated human serum albumin (HSA) glycation. The study was also aimed at investigating the effects of newly identified antiglycation inhibitors on AGEsinduced intracellular reactive oxygen species (ROS) production, and associated impaired proliferation of the hepatocytes.

Methods: The present study focuses on the antiglycation activity of 6-nitrobenzimidazole derivatives 1-13 in in-vitro human serum albumin (HSA)- fructose model. These derivatives were also identified as non-toxic against 3T3 mouse fibroblast cell-line in MTT-based assay. The effect of the most promising derivative 5, 4-(6-nitro-1H-benzimidazol-2-yl)-1,2,3-benzenetriol, was studied in a dose dependent manner, co-incubated with fructose-derived AGEs (0- 200 g/mL) on rat hepatocytes proliferation and associated intracellular generation of ROS via MTT-based assay and DCFHDA technique, resp.

Results: We found that derivative 5 ameliorates the elevated intracellular oxidative stress and associated diminished proliferation of the hepatocytes in response to AGEs.

Conclusion: In conclusion, we identified novel 6-nitrobenzimidazole derivatives as antiglycation agents through in-vitro, and cell-based models. The experimental process involved the reaction of 2-Nitro-1H-benzo[d]imidazole(cas: 5709-67-1).Recommanded Product: 2-Nitro-1H-benzo[d]imidazole

The Article related to fibroblast cell proliferation ros protein glycation 6 nitrobenzimidazole derivative, 6-nitrobenzimidazole derivatives, advanced glycation end products, fructose-derived ages, intracellular oxidative stress, protein glycation and other aspects.Recommanded Product: 2-Nitro-1H-benzo[d]imidazole

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 25, 2021, Ma, Mingxuan; Chen, Cheng; Zhu, Xinqi; Li, Xiaoqi; Du, Yingxiang; Zhang, Liu; Gan, Jie published an article.Product Details of 5036-48-6 The title of the article was A porous layer open-tubular capillary column supported with pepsin and zeolitic imidazolate framework for enantioseparation of four basic drugs in capillary electrochromatography. And the article contained the following:

New material zeolitic imidazolate framework-4, 5-imidazoledicarboxylic acid (ZIF-IMD) located on the pore surface of porous layer open-tubular (PLOT) column previously functionalized with N-(3-aminopropyl)-imidazole have been prepared via a layer-by-layer self-assembly strategy. This new ZIF-IMD coating hybrids are used as solid-phase carriers for chiral selector pepsin immobilization. The ZIF-IMD material was characterized by SEM, energy-dispersive spectroscopy, transmission electron microscope and X-ray diffraction. The synthesized pepsin@ZIF-IMD@POLT column achieved the baseline separation of hydroxychloroquine (HCQ), chloroquine (CHQ) and hydroxyzine (HXY) (the resolution of HCQ: 2.19; CHQ: 1.84; HXY: 1.53). Compared with the pepsin@PLOT column (without ZIF-IMD material), the chiral separation capability of the pepsin@ZIF-IMD@POLT column can be remarkably improved. Several key parameters including concentration of chiral selector, buffer pH, applied voltage and buffer concentration were systematically evaluated to provide the optimal enantioseparation condition. The relative standard deviations (RSDs) of intra-day, inter-day, column-to-column and inter-batch of migration time and Rs of the HCQ were evaluated in detail, resp. (RSD < 7.21%). Addnl., the potential mechanism of increased resolution was discussed in the article. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Product Details of 5036-48-6

The Article related to zeolitic imidazolate framework chromatog column drug electrochromatog separation, 4,5-imidazoledicarboxylic acid, capillary electrochromatography, chiral separation, organic hybrid coating, plot, zeolitic imidazolate framework and other aspects.Product Details of 5036-48-6

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Matkarimov, Bakhyt T.; Saparbaev, Murat K. published an article in 2020, the title of the article was DNA Repair and Mutagenesis in Vertebrate Mitochondria: Evidence for Asymmetric DNA Strand Inheritance.Electric Literature of 55662-66-3 And the article contains the following content:

A variety of endogenous and exogenous factors induce chem. and structural alterations in cellular DNA in addition to the errors occurring throughout DNA synthesis. These types of DNA damage are cytotoxic, miscoding or both and are believed to be at the origin of cancer and other age-related diseases. A human cell, aside from nuclear DNA, contains thousands of copies of mitochondrial DNA (mtDNA), a double-stranded, circular mol. of 16,569 bp. It has been proposed that mtDNA is a critical target of reactive oxygen species: byproducts of oxidative phosphorylation that are generated in the organelle during aerobic respiration. Indeed, oxidative damage to mtDNA is more extensive and persistent as compared to that to nuclear DNA. Although transversions are the hallmark of mutations induced by reactive oxygen species, paradoxically, the majority of mtDNA mutations that occur during aging and cancer are transitions. Furthermore, these mutations show a striking strand orientation bias: T→C/G→A transitions preferentially occur on the light strand, whereas C→T/A→G on the heavy strand of mtDNA. Here, we propose that the majority of mtDNA progenies, created after multiple rounds of DNA replication, are derived from the heavy strand only, owing to asym. replication of the DNA strand anchored to the inner membrane via the D-loop structure. 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 mitochondrial dna mismatch repair damage mutagenesis oxidative phosphorylation, review2 ros nucleotide excision uracil, abasic sites, dna excision repair, dna glycosylases, mitochondrial dna, oxidative dna damage, uracil and other aspects.Electric Literature of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On April 24, 2020, Yoneda, Ryoma; Ueda, Naomi; Uranishi, Kousuke; Hirasaki, Masataka; Kurokawa, Riki published an article.Formula: C6H7N5 The title of the article was Long noncoding RNA pncRNA-D reduces cyclin D1 gene expression and arrests cell cycle through RNA m6A modification. And the article contained the following:

PncRNA-D is an irradiation-induced 602-nt long noncoding RNA transcribed from the promoter region of the cyclin D1 (CCND1) gene. CCND1 expression is predicted to be inhibited through an interplay between pncRNA-D and RNA-binding protein TLS/FUS. Because the pncRNA-D-TLS interaction is essential for pncRNA-D-stimulated CCND1 inhibition, here we studied the possible role of RNA modification in this interaction in HeLa cells. We found that osmotic stress induces pncRNA-D by recruiting RNA polymerase II to its promoter. pncRNA-D was highly m6A-methylated in control cells, but osmotic stress reduced the methylation and also arginine methylation of TLS in the nucleus. Knockdown of the m6A modification enzyme methyltransferase-like 3 (METTL3) prolonged the half-life of pncRNA-D, and among the known m6A recognition proteins, YTH domain-containing 1 (YTHDC1) was responsible for binding m6A of pncRNA-D. Knockdown of METTL3 or YTHDC1 also enhanced the interaction of pncRNA-D with TLS, and results from RNA pulldown assays implicated YTHDC1 in the inhibitory effect on the TLS-pncRNA-D interaction. CRISPR/Cas9-mediated deletion of candidate m6A site decreased the m6A level in pncRNA-D and altered its interaction with the RNA-binding proteins. Of note, a reduction in the m6A modification arrested the cell cycle at the G0/G1 phase, and pncRNA-D knockdown partially reversed this arrest. Moreover, pncRNA-D induction in HeLa cells significantly suppressed cell growth. Collectively, these findings suggest that m6A modification of the long noncoding RNA pncRNA-D plays a role in the regulation of CCND1 gene expression and cell cycle progression. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Formula: C6H7N5

The Article related to lncrna pncrnad ccnd1 gene repression cell cycle m6a modification, rna methylation, translocated in liposarcoma (tls), cell cycle, cyclin d1, epigenetics, fused in sarcoma (fus), long noncoding rna (long ncrna, lncrna), m6a, pncrna-d and other aspects.Formula: C6H7N5

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On February 7, 2020, Thelen, Adam Z.; O’Brien, Patrick J. published an article.Recommanded Product: Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Recognition of 1,N2-ethenoguanine by alkyladenine DNA glycosylase is restricted by a conserved active-site residue. And the article contained the following:

The adenine, cytosine, and guanine bases of DNA are susceptible to alkylation by the aldehyde products of lipid peroxidation and by the metabolic byproducts of vinyl chloride pollutants. The resulting adducts spontaneously cyclize to form harmful etheno lesions. Cells employ a variety of DNA repair pathways to protect themselves from these pro-mutagenic modifications. Human alkyladenine DNA glycosylase (AAG) is thought to initiate base excision repair of both 1,N6-ethenoadenine (εA) and 1,N2-ethenoguanine (εG). However, it is not clear how AAG might accommodate εG in an active site that is complementary to εA. This prompted a thorough investigation of AAG-catalyzed excision of εG from several relevant contexts. Using single-turnover and multiple-turnover kinetic analyses, we found that εG in its natural εG·εC context is very poorly recognized relative to εA·εT. Bulged and mispaired εG contexts, which can form during DNA replication, were similarly poor substrates for AAG. Furthermore, AAG could not recognize an εG site in competition with excess undamaged DNA sites. Guided by previous structural studies, we hypothesized that Asn-169, a conserved residue in the AAG active-site pocket, contributes to discrimination against εG. Consistent with this model, the N169S variant of AAG was 7-fold more active for excision of εG compared with the wildtype (WT) enzyme. Taken together, these findings suggest that εG is not a primary substrate of AAG, and that current models for etheno lesion repair in humans should be revised. We propose that other repair and tolerance mechanisms operate in the case of εG lesions. 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 human alkyladenine dna glycosylase active site recognition ethenoguanine repair, dna alkylation, dna damage, dna repair, alkyladenine dna glycosylase, base excision repair (ber), enzyme kinetics, ethenoguanine, substrate specificity and other aspects.Recommanded Product: Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On April 30, 2015, Shivange, Gururaj; Kodipelli, Naveena; Anindya, Roy published an article.Electric Literature of 55662-66-3 The title of the article was 2-Hydrazinobenzothiazole-based etheno-adduct repair protocol (HERP): A method for quantitative determination of direct repair of etheno-bases. And the article contained the following:

Etheno-DNA adducts are mutagenic and lead to genomic instability. Enzymes belonging to Fe(II)/2-oxoglutarate-dependent dioxygenase family repair etheno-DNA adducts by directly removing alkyl chain as glyoxal. Presently there is no simple method to assess repair reaction of etheno-adducts. We have developed a rapid and sensitive assay for studying etheno-DNA adduct repair by Fe(II)/2-oxoglutarate-dependent dioxygenases. Using AlkB as model Fe(II)/2-oxoglutarate-dependent dioxygenases, we performed in vitro repair of etheno-adducts containing DNA and detected glyoxal by reacting with 2-hydrazinobenzothiazole which forms complex yellow color compound with distinct absorption spectrum with a peak absorption at 365 nm. We refer this method as 2-hydrazinobenzothiazole-based etheno-adduct repair protocol or HERP. Our novel approach for determining repair of etheno-adducts containing DNA overcomes several drawbacks of currently available radioisotope-based assay. 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 hydrazinobenzothiazole etheno adduct repair dna alkb, 1,n(2)-ethenoguanine, 1,n(6)-ethenoadenine, 3,n(4)-ethenocytosine, chloroacetaldehyde, dna repair, etheno adduct, fe(ii)/2-oxoglutarate-dependent dioxygenase, n(2),3-ethenoguanine and other aspects.Electric Literature of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 9, 2020, Bartlett, Mark J.; Corkey, Britton Kenneth; Cosman, Jennifer Leigh; Elzein, Elfatih; Li, Xiaofen published a patent.Electric Literature of 40644-16-4 The title of the patent was Preparation of indoles, azaindoles and related bicyclic nitrogen heterocycles useful in treatment of diseases. And the patent contained the following:

The invention relates to preparation of indoles, azaindoles and related bicyclic nitrogen heterocycles of formula (I), or a pharmaceutically acceptable salt thereof, as enzyme indoleamine 2,3-dioxygenase 1 (IDO1) inhibitors. Compounds I wherein Y1 is O or N; the dotted line is a single bond that is present or absent; X1, X2 and X4 each independently is N or CH; X3 is N or CRa; Ra is H, halo, C1-4 alkyl; X5 is N, C or CRb; X6 is N or CRc; X7 is N or CRd; X8 is N or CRe; Rb-Re and R1 each independently is H, halo, or CN; R2 is C1-6 alkyl, C1-6 haloalkyl, C1-6 haloalkoxy; etc., are claimed. The example compound II was prepared via two-step synthesis using 4-bromo-3,3-dimethylindolin-2-one as starting material (procedure given). Compounds I were evaluated for IDO1-inhibitory activity (data given). Compounds I can be useful in mono- amd combination therapy of cancer and viral infections (e.g. HIV and HBV). The experimental process involved the reaction of 4-Bromo-1H-benzo[d]imidazol-2(3H)-one(cas: 40644-16-4).Electric Literature of 40644-16-4

The Article related to indole preparation ido1 inhibitor antitumor hbv hiv antiviral therapy, azaindole preparation ido1 inhibitor cancer viral infection combination therapy, bicyclic nitrogen heterocycle preparation ido1 inhibitor immunotherapy anticancer antiviral and other aspects.Electric Literature of 40644-16-4

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Fan, Xin; Zhang, Lingling; Huang, Junwen; Zhong, Yun; Fan, Yanting; Zhou, Tong; Lu, Min published an article in 2022, the title of the article was An integrated immune-related bioinformatics analysis in glioma: prognostic signature’s identification and multi-omics mechanisms’ exploration.Electric Literature of 443-72-1 And the article contains the following content:

As the traditional treatment for glioma, the most common central nervous system malignancy with poor prognosis, the efficacy of high-intensity surgery combined with radiotherapy and chemotherapy is not satisfactory. The development of individualized scientific treatment strategy urgently requires the guidance of signature with clin. predictive value. In this study, five prognosis-related differentially expressed immune-related genes (PR-DE-IRGs) (CCNA2, HMGB2, CASP3, APOBEC3C, and BMP2) highly associated with glioma were identified for a prognostic model through weighted gene co-expression network anal., univariate Cox and lasso regression. Kaplan-Meier survival curves, receiver operating characteristic curves and other methods have shown that the model has good performance in predicting the glioma patients’ prognosis. Further combined nomogram provided better predictive performance. The signature’s guiding value in clin. treatment has also been verified by multiple anal. results. We also constructed a comprehensive competing endogenous RNA (ceRNA) regulatory network based on the protective factor BMP2 to further explore its potential role in glioma progression. Numerous immune-related biol. functions and pathways were enriched in a high-risk population. Further multi-omics integrative anal. revealed a strong correlation between tumor immunosuppressive environment/IDH1 mutation and signature, suggesting that their cooperation plays an important role in glioma progression. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Electric Literature of 443-72-1

The Article related to prognosis idh1 apobec3c casp3 linc00689 snhg16 n6 methyladenine glioma, idh1 mutation, cerna regulatory network, glioma, mechanisms’ exploration, muti-omics immune-related bioinformatics research, prognostic model, tumor immunosuppressive environment and other aspects.Electric Literature of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On July 31, 1992, Seela, Frank; Gumbiowski, Rainer published an article.Category: imidazoles-derivatives The title of the article was Imidazo[1,2-a]pyrimidine 2′-deoxyribo- and 2′,3′-dideoxyribonucleosides: glycosylation of the nucleobase anion. And the article contained the following:

The synthesis of the imidazopyrimidine deoxyribonucleosides I (R = NH2, H, R1 = H, R2 = H, OH) via stereoselective glycosidation of the nucleobase anion of II, is described. The inhibitory activity of the dideoxynucleoside 5′-triphosphates I (R = H, NH2, R1 = P3O9H4, R2 = H) against HIV reverse transcriptase was tested. The experimental process involved the reaction of 7-Chloroimidazo[1,2-a]pyrimidin-5(1H)-one(cas: 57473-33-3).Category: imidazoles-derivatives

The Article related to imidazopyrimidine deoxyribonucleoside preparation phosphorylation, nucleotide dideoxy imidazopyrimidine triphosphate enzyme inhibition, nucleoside deoxy imidazopyrimidine preparation phosphorylation, stereoselective glycosidation chloroimidazopyrimidinone and other aspects.Category: imidazoles-derivatives

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem