Month: November 2022

Bera, Amit; Lewis, Stephen M. published an article in 2020, the title of the article was Regulation of epithelial-to-mesenchymal transition by alternative translation initiation mechanisms and its implications for cancer metastasis.Safety of N-Methyl-7H-purin-6-amine And the article contains the following content:

A review. Translation initiation plays a critical role in the regulation of gene expression for development and disease conditions. During the processes of development and disease, cells select specific mRNAs to be translated by controlling the use of diverse translation initiation mechanisms. Cells often switch translation initiation from a cap-dependent to a cap-independent mechanism during epithelial-to-mesenchymal transition (EMT), a process that plays an important role in both development and disease. EMT is involved in tumor metastasis because it leads to cancer cell migration and invasion, and is also associated with chemoresistance. In this review we will provide an overview of both the internal ribosome entry site (IRES)-dependent and N6-methyladenosine (m6A)-mediated translation initiation mechanisms and discuss how cap-independent translation enables cells from primary epithelial tumors to achieve a motile mesenchymal-like phenotype, which in turn drives tumor metastasis. 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 review epithelial mesenchymal cancer metastasis, ires, itaf, cancer, epithelial-to-mesenchymal transition (emt), m6a-mediated translation, metastasis, Mammalian Pathological Biochemistry: Reviews and other aspects.Safety of N-Methyl-7H-purin-6-amine

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On September 30, 2020, Zhong, Hui; Tang, Hui-Fang; Kai, Yin published an article.SDS of cas: 443-72-1 The title of the article was N6-methyladenine RNA Modification (m6A): An Emerging Regulator of Metabolic Diseases. And the article contained the following:

A review. N6-methyladenine RNA modification (m6A) is an RNA methylation modification catalyzed by methyltransferase at the 6th position nitrogen atom of adenine (A), which is the most common chem. modification of eukaryotic mRNA (mRNA). Recently, m6A has been found to play an important role in the dynamic regulation of RNA, which is crucial for some physiol. and pathophysiol. processes such as adipogenesis, cell differentiation, and the immune/inflammatory response. Metabolic diseases are a series of chronic inflammatory disorders caused by metabolic dysfunction of proteins, glucose, and lipids. Emerging studies have shown that m6A plays an important role in the process of metabolic diseases such as obesity, type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) via regulation of glucose/lipid metabolism and the immune/inflammatory response. In this review, we will summarize the role of m6A in metabolic diseases, which may provide new ideas for the prevention and treatment of metabolic diseases. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).SDS of cas: 443-72-1

The Article related to review methyladenine rna modification metabolic disease, n6-adenine methylation, cardiovascular diseases, metabolic diseases, obesity, type 2 diabetes mellitus, Mammalian Pathological Biochemistry: Reviews and other aspects.SDS of cas: 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 28, 2020, Rizzo, Carla; Cancemi, Patrizia; Mattiello, Leonardo; Marullo, Salvatore; D’Anna, Francesca published an article.HPLC of Formula: 5036-48-6 The title of the article was Naphthalimide Imidazolium-Based Supramolecular Hydrogels as Bioimaging and Theranostic Soft Materials. And the article contained the following:

1,8-Naphthalimide-based imidazolium salts differing for the alkyl chain length and the nature of the anion were synthesized and characterized to obtain fluorescent probes for bioimaging applications. First, their self-assembly behavior and gelling ability were investigated in water and water/dimethyl sulfoxide binary mixtures Only salts having longer alkyl chains were able to give supramol. hydrogels, whose properties were investigated by using a combined approach of fluorescence, resonance light scattering, and rheol. measurements. Morphol. information was obtained by SEM. In addition, conductive properties of organic salts in solution and gel state were analyzed. Imidazolium salts were successfully tested for their possible application as bioimaging and cytotoxic agents toward three cancer cell lines and a nontumoral epithelial cell line. Characterization of their behavior was performed by MTT and cell-based assays. Finally, the biol. activity of hydrogels was also investigated. Collectively, our findings showed that naphthalimide-based imidazolium salts are promising theranostic agents and they were able to preserve their biol. properties also in the gel phase. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).HPLC of Formula: 5036-48-6

The Article related to naphthalimide imidazolium pharmaceutical hydrogel bioimaging fluorescent probe, bioimaging, fluorescence, imidazolium salts, naphthalimide, supramolecular hydrogels, Pharmaceuticals: Formulation and Compounding and other aspects.HPLC of Formula: 5036-48-6

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 31, 2022, Xi, Lei; Yang, Ying; Xu, Ying; Zhang, Fangming; Li, Jinghui; Liu, Xiyang; Zhang, Zhenxi; Du, Quan published an article.Application of 443-72-1 The title of the article was The enhanced genomic 6 mA metabolism contributes to the proliferation and migration of TSCC cells. And the article contained the following:

In contrast to the well-established genomic 5-methylcytosine (5mC), the existence of N6-methyladenine (6 mA) in eukaryotic genomes was discovered only recently. Initial studies found that it was actively regulated in cancer cells, suggesting its involvement in the process of carcinogenesis. However, the contribution of 6 mA in tongue squamous cell carcinoma (TSCC) still remains uncharacterized. In this study, a pan-cancer type anal. was first performed, which revealed enhanced 6 mA metabolism in diverse cancer types. The study was then focused on the regulation of 6 mA metabolism, as well as its effects on TSCC cells. To these aspects, genome 6 mA level was found greatly increased in TSCC tissues and cultured cells. By knocking down 6 mA methylases N6AMT1 and METTL4, the level of genomic 6 mA was decreased in TSCC cells. This led to suppressed colony formation and cell migration. By contrast, knockdown of 6 mA demethylase ALKBH1 resulted in an increased 6 mA level, enhanced colony formation, and cell migration. Further study suggested that regulation of the NF-魏B pathway might contribute to the enhanced migration of TSCC cells. Therefore, in the case of TSCC, we have shown that genomic 6 mA modification is involved in the proliferation and migration of cancer cells. 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 n6methyladenine tongue squamous cell carcinoma, Mammalian Pathological Biochemistry: Oncology and other aspects.Application of 443-72-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 2003, Barbin, Alain; Ohgaki, Hiroko; Nakamura, Jun; Kurrer, Michael; Kleihues, Paul; Swenberg, James A. published an article.Recommanded Product: 55662-66-3 The title of the article was Endogenous deoxyribonucleic acid (DNA) damage in human tissues: A comparison of ethenobases with aldehydic DNA lesions. And the article contained the following:

Two types of endogenous DNA lesions, ethenobases [1,N6-ethenoadenine (蔚A), 3,N4-ethenocytosine (蔚C)] and aldehydic DNA lesions (ADLs), were measured in several tissues (liver, lung, kidney, colon, colon mucosa, cerebellum, and gray and white matter of the cerebrum) obtained postmortem during autopsy examinations of 12 individuals (6 males, 6 females; ages, 58-87 yr). Issues relating to changes in levels of DNA damage with disease and after death were addressed. The extent of DNA damage in autopsy samples was not associated with the length of the postmortem interval and was similar to levels observed in surgery samples, suggesting that endogenous, steady-state levels of etheno adducts and of ADLs are relatively stable during the hours immediately after death. In this limited series of samples, and with a few possible exceptions, the disease status before death was not associated with increased endogenous DNA damage in the affected tissue. DNA ethenobases were lowest in the cerebellum (median molar ratios: 蔚A/A = 1.0 x 10-8; 蔚C/C = 1.9 x 10-8) and highest in the gray matter (蔚A/A = 2.9 x 10-8; 蔚C/C = 4.8 x 10-8) and white matter (蔚A/A = 2.4 x 10-8; 蔚C/C = 5.2 x 10-8) of the cerebrum. In other tissues, median values were 1.2-1.9 x 10-8 for 蔚A/A and 2.0-3.3 x 10-8 for 蔚C/C. There was a good correlation between the levels of 蔚A and 蔚C (r = 0.80, P < 0.0001). Levels of ADLs were similar in the liver, lung, kidney, and white matter of the cerebrum (median values: 5.7-7.9 ADLs/106 nucleotides), higher in the colon (11.3 x 10-6) and gray matter of the cerebrum (9.0 x 10-6) and lower in the cerebellum (3.7 x 10-6). There was no correlation between levels of ethenobases and amounts of ADLs (蔚A vs. ADLs: r = 0.12, P = 0.33; 蔚C vs. ADLs: r = 0.024, P = 0.85). Although there was an interindividual variability in the extent of endogenous DNA damage (4-fold for 蔚A and 蔚C, 2-fold for ADLs), which may be determined, in part, by the capacity to repair DNA and may be related to the pathol. or treatment of the patients, these results suggest that the cerebrum contains higher endogenous DNA damage than the other tissues. These data are in line with previous studies showing that brain tissues are more susceptible to oxidative stress and lipid peroxidation than other tissues. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Recommanded Product: 55662-66-3

The Article related to dna damage aldehydic lesion ethenobase disease cancer, Mammalian Pathological Biochemistry: Oncology and other aspects.Recommanded Product: 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

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

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

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