Category: 443-72-1

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 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

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