Category: 55662-66-3

On December 31, 2012, Prorok, Paulina; Saint-Pierre, Christine; Gasparutto, Didier; Fedorova, Olga S.; Ishchenko, Alexander A.; Leh, Herve; Buckle, Malcolm; Tudek, Barbara; Saparbaev, Murat published an article.Formula: C6H5N3O The title of the article was Highly mutagenic exocyclic DNA adducts are substrates for the human nucleotide incision repair pathway. And the article contained the following:

Background: Oxygen free radicals induce lipid peroxidation (LPO) that damages and breaks polyunsaturated fatty acids in cell membranes. LPO-derived aldehydes and hydroxyalkenals react with DNA leading to the formation of etheno(ε)-bases including 1,N6-ethenoadenine (εA) and 3,N4-ethenocytosine (εC). The εA and εC residues are highly mutagenic in mammalian cells and eliminated in the base excision repair (BER) pathway and/or by AlkB family proteins in the direct damage reversal process. BER initiated by DNA glycosylases is thought to be the major pathway for the removal of non-bulky endogenous base damage. Alternatively, in the nucleotide incision repair (NIR) pathway, the apurinic/apyrimidinic (AP) endonucleases can directly incise DNA duplex 5′ to a damaged base in a DNA glycosylase-independent manner. Methodol./Principal Findings: Here we have characterized the substrate specificity of human major AP endonuclease 1, APE1, towards εA, εC, thymine glycol (Tg) and 7,8-dihydro-8-oxoguanine (8oxoG) residues when present in duplex DNA. APE1 cleaves oligonucleotide duplexes containing εA, εC and Tg, but not those containing 8oxoG. Activity depends strongly on sequence context. The apparent kinetic parameters of the reactions suggest that APE1 has a high affinity for DNA containing ε-bases but cleaves DNA duplexes at an extremely slow rate. Consistent with this observation, oligonucleotide duplexes containing an ε-base strongly inhibit AP site nicking activity of APE1 with IC50 values in the range of 5-10 nM. MALDI-TOF MS anal. of the reaction products demonstrated that APE1-catalyzed cleavage of εA·T and εC·G duplexes generates, as expected, DNA fragments containing 5′-terminal ε-base residue. Conclusions/Significance: The fact that ε-bases and Tg in duplex DNA are recognized and cleaved by APE1 in vitro, suggests that NIR may act as a backup pathway to BER to remove a large variety of genotoxic base lesions in human cells. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Formula: C6H5N3O

The Article related to ape1 dna adduct nucleotide incision repair pathway, Enzymes: Substrates-Cofactors-Inhibitors-Activators-Coenzymes-Products and other aspects.Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Saparbaev, M.; Laval, J. published an article in 1999, the title of the article was Enzymology of the repair of etheno adducts in mammalian cells and in Escherichia coli.Application In Synthesis of Imidazo[1,2-c]pyrimidin-5(6H)-one And the article contains the following content:

Exocyclic adducts are generated in cellular DNA by reaction with epoxides that are formed metabolically from various industrial pollutants and by reaction with activated aldehydes that arise during membrane lipid peroxidation The etheno (ε) derivatives of purine and pyrimidine bases, e.g. 3,N4-ethenocytosine, 1,N6-ethenoadenine, N2,3-ethenoguanine and 1,N2-ethenoguanine, are probably involved in carcinogenesis because they are highly mutagenic and genotoxic. Therefore, the repair processes that eliminate exocyclic adducts from DNA should play a crucial role in maintaining the stability of the genetic information. The DNA glycosylases implicated in the repair of etheno adducts have been identified. Human and Escherichia coli 3-methyladenine-DNA-glycosylases excise 1,N6-ethenoadenine residues. We have identified two homologous proteins present in human cells and E. coli that remove 3,N4-ethenocytosine residues by DNA glycosylase activity. The human enzyme is an activity of the mismatch-specific thymine-DNA glycosylase, while the bacterial enzyme is an activity of the double-stranded uracil-DNA glycosylase, i.e., the homolog of the human enzyme. The fact that 1,N6-ethenoadenine and 3,N4-ethenocytosine are recognized and efficiently excised by DNA glycosylases in vitro suggests that these enzymes may be responsible for the repair of these mutagenic lesions in vivo and may contribute importantly to genetic stability. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Application In Synthesis of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to dna glycosylase etheno adduct repair, Enzymes: Substrates-Cofactors-Inhibitors-Activators-Coenzymes-Products and other aspects.Application In Synthesis of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 7, 2015, Jansa, Josef; Lycka, Antonin; Ruzicka, Ales; Grepl, Martin; Vanecek, Jan published an article.Quality Control of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Synthesis, structure and rearrangement of iodinated imidazo[1,2-c]pyrimidine-5(6H)-ones derived from cytosine. And the article contained the following:

We describe mild and selective iodination of various 8-substituted imidazo[1,2-c]pyrimidine-5(6H)-ones (ethenocytosines). Starting ethenocytosines were obtained by cyclization of 5-halogenocytosines with chloroacetaldehyde or by subsequent Suzuki-Miyaura cross-coupling between 8-iodoimidazo[1,2-c]pyrimidine-5(6H)-one 1d and corresponding arylboronic acids. When imidazo[1,2-c]pyrimidine-5(6H)-one or 8-iodoimidazo[1,2-c]pyrimidine-5(6H)-one 1d was iodinated by N-iodosuccinimide (NIS) in DMF, pure 3,8-diiododerivative 2d was obtained. Under basic or acidic conditions, this mol. is subject to rearrangement into 2,8-diododerivative 3d, which can be subsequently iodinated to 2,3,8-triododerivative 4d. Since the positions of iodine atoms on the imidazole ring could not be determined convincingly from NMR spectra only, x-ray anal. of 2d was carried out with the aim of confirming the structure undoubtedly. The same sequence of reactions was applied to another eight ethenocytosines, providing excellent regioselectivity, easy rearrangement and high yields of iodinated products. All ethenocytosines were properly characterized by 1H, 13C and 15N NMR spectroscopy. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Quality Control of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to cytosine cyclization suzuki miyaura coupling iodination dimroth rearrangement, iodinated imidazopyrimidine preparation, Heterocyclic Compounds (More Than One Hetero Atom): Pyrimidines and Quinazolines and other aspects.Quality Control of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Yanai, Mitsuji; Takeda, Shigeko; Baba, Tsuyomi; Kitagawa, Koichi published an article in 1974, the title of the article was Heterocyclic compounds. XVIII. Synthesis of imidazo[1,2-c]- and pyrimido[1,2-c]pyrimidine derivatives.Name: Imidazo[1,2-c]pyrimidin-5(6H)-one And the article contains the following content:

Reaction of the amino alcs. H2N(CH2)nOH (n = 2,3) and HN(CH2CH2OH)2 with the chloropyrimidines I (R = H, Me) and 4,6-dichloropyrimidine nII) gave the 4-substituted derivatives which, when treated with SOCl2 in THF, cyclized to give III, IV (R1 = H, Cl), V (R2 = H, Me, Cl; R3 = H, CH2CH2Cl), and VI. Treatment of V (R2 = Cl, R3 = CH2CH2Cl) with mild alk. solution gave the imidazolidines VII (R4 = H, CHO). Treatment of I and II with the amino acetal H2NCH2CH(OEt)2 gave the 4-(2,2-diethoxyethylamino) derivatives, which when treated with 6N HCl followed by concentrated H2SO4 gave III (R1 = H) and VIII resp. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Name: Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to imidazopyrimidine, pyrimidopyrimidine, amino alc chloropyrimidine cyclization, alc acetal chloropyrimidine cyclization, Heterocyclic Compounds (More Than One Hetero Atom): Pyrimidines and Quinazolines and other aspects.Name: Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Misztal, Tomasz; Kowalczyk, Pawel; Mlotkowska, Patrycja; Marciniak, Elzbieta published an article in 2020, the title of the article was The effect of allopregnanolone on enzymatic activity of the DNA base excision repair pathway in the sheep hippocampus and amygdala under natural and stressful conditions.Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one And the article contains the following content:

The neurosteroid allopregnanolone (AL) has many beneficial functions in the brain. This study tested the hypothesis that AL administered for three days into the third brain ventricle would affect the enzymic activity of the DNA base excision repair (BER) pathway in the hippocampal CA1 and CA3 fields and the central amygdala in luteal-phase sheep under both natural and stressful conditions. Acute stressful stimuli, including isolation and partial movement restriction, were used on the last day of infusion. The results showed that stressful stimuli increased N-methylpurine DNA glycosylase (MPG), thymine DNA glycosylase (TDG), 8-oxoguanine glycosylase (OGG1), and AP-endonuclease 1 (APE1) mRNA expression, as well as repair activities for 1,N6 -ethenoadenine (蔚A), 3,N4 -ethenocytosine (蔚C), and 8-oxoguanine (8-oxoG) compared to controls. The stimulated events were lower in stressed and AL-treated sheep compared to sheep that were only stressed (except MPG mRNA expression in the CA1 and amygdala, as well as TDG mRNA expression in the CA1). AL alone reduced mRNA expression of all DNA repair enzymes (except TDG in the amygdala) relative to controls and other groups. DNA repair activities varied depending on the tissue-AL alone stimulated the excision of 蔚A in the amygdala, 蔚C in the CA3 and amygdala, and 8-oxoG in all tissues studied compared to controls. However, the excision efficiency of lesioned bases in the AL group was lower than in the stressed and stressed and AL-treated groups, with the exception of 蔚A in the amygdala. In conclusion, the presented modulating effect of AL on the synthesis of BER pathway enzymes and their repair capacity, both under natural and stressful conditions, indicates another functional role of this neurosteroid in brain structures. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to allopregnanolone neuroprotectant dna base excision repair psychol stress, dna glycosylases, allopregnanolone, amygdala, base excision repair, hippocampus, stress, Pharmacology: Effects Of Nervous System- and Behavior-Affecting Drugs and Neuromuscular Agents and other aspects.Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On September 6, 2007, Kistler, Kurt A.; Matsika, Spiridoula published an article.COA of Formula: C6H5N3O The title of the article was Cytosine in Context: A Theoretical Study of Substituent Effects on the Excitation Energies of 2-Pyrimidinone Derivatives. And the article contained the following:

The ultrafast radiationless decay mechanism for cytosine has been shown to be in part dependent upon high vertical excitation, while slower fluorescence displayed in some cytosine analogs is generally linked to lower vertical excitation energies. To probe how excitation energies relate to pyrimidine structure, substituent effects on the vertical excitation energies for a number of derivatives of 2-pyrimidin-(1H)-one (2P) have been calculated using multireference configuration-interaction ab initio methods. Substitutions using groups with 蟺 electron donating, withdrawing and conjugation-extending properties at the C4 and C5 positions on the 2P system give predictive trends for the first three singlet excited-state energies. The S1 蟺蟺* energies of 2P derivatives involving C4 substitution vary linearly with the Hammett substituent parameter 蟽P+. Cytosine is shown to have the highest bright 蟺蟺* energy of the 2P derivatives presented, with that energy being strongly dependent on the position, orientation, and geometry of the C4-amino. A simple description of the predictive energetic trends for the bright 蟺蟺* energies using frontier MO theory is presented, based on the character of the HOMO and LUMO orbitals for each derivative The results of this study expand the current understanding of the photophys. behavior of the DNA pyrimidine bases and could be useful in the design of analogs where particular spectral properties are desired. 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 cytosine theory substituent effect excitation energy pyrimidinone, Physical Organic Chemistry: Theoretical Organic Chemical Concepts, Including Quantum and Molecular Mechanical Studies and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 19, 1984, Nair, Vasu; Offerman, Rick J.; Turner, Gregory A. published an article.Computed Properties of 55662-66-3 The title of the article was Structural alteration of nucleic acid bases by bromomalonaldehyde. And the article contained the following:

BrCH(CHO)2, prepared by bromination of CH2(CHO)2 with Br, has been employed to modify a number of nucleic acid bases. These reactions transform pyrimidine and purine bases into modified systems containing etheno and etheno carboxaldehyde moieties, among other products. The structures of these modified bases were established by UV, mass spectral, and high-field NMR data. Fluorescence emission data for some of the adducts are of significance. The general mechanism of modification is discussed. 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 bromomalonaldehyde purine pyrimidine base, nucleic acid base bromomalonaldehyde, Biomolecules and Their Synthetic Analogs: Others, Including Purines, Pyrimidine Nucleic Acid Bases, Flavins, Lignans and other aspects.Computed Properties of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 1996, Rahman, M. Sayeedur; Dunman, Paul M.; Wang, Ge; Murphy, Holly S.; Humayun, M. Zafri published an article.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Effect of UVM induction on mutation fixation at non-pairing and mispairing DNA lesions. And the article contained the following:

Mutation fixation at an ethenocytosine (εC) residue borne on transfected M13 single-stranded DNA is significantly enhanced in response to pretreatment of Escherichia coli cells with UV, alkylating agents, or hydrogen peroxide, a phenomenon that we have called UVM for UV modulation of mutagenesis. The UVM response does not require the E. coli SOS or adaptive responses, and is observed in cells defective for oxyR, an oxidative DNA damage-responsive regulatory gene. UVM may represent either a novel DNA-repair phenomenon, or an unrecognized feature of DNA replication in damaged cells that affects a specific class of non-coding DNA lesions. To explore the range of DNA lesions subject to the UVM effect, we have examined mutation fixation at 3,N4-ethenocytosine and 1,N6-ethenoadenine, as well as at O6-methylguanine (O6mG). M13 viral single-stranded DNA constructs bearing a single mutagenic lesion at a specific site were transfected into cells pretreated with UV or 1-methyl-3-nitro-1-nitroso-guanidine (MNNG). Survival of transfected viral DNA was measured as transfection efficiency, and mutagenesis at the lesion site was analyzed by a quant. multiplex sequence anal. technol. The results suggest that the UVM effect modulates mutagenesis at the two etheno lesions, but does not appear to significantly affect mutagenesis at O6mG. Because the modulation of mutagenesis is observed in cells incapable of the SOS response, these data are consistent with the notion that UVM may represent a previously unrecognized DNA damage-inducible response that affects the fidelity of DNA replication at certain mutagenic lesions in Escherichia coli. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to escherichia bacteriophage m13 mutation repair uv, uv induction mutation repair escherichia m13, dna damage repair uv ethenocytosine ethenoadenine, methylguanine dna damage repair uv escherichia and other aspects.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 1996, Rahman, M. Sayeedur; Dunman, Paul M.; Wang, Ge; Murphy, Holly S.; Humayun, M. Zafri published an article.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Effect of UVM induction on mutation fixation at non-pairing and mispairing DNA lesions. And the article contained the following:

Mutation fixation at an ethenocytosine (εC) residue borne on transfected M13 single-stranded DNA is significantly enhanced in response to pretreatment of Escherichia coli cells with UV, alkylating agents, or hydrogen peroxide, a phenomenon that we have called UVM for UV modulation of mutagenesis. The UVM response does not require the E. coli SOS or adaptive responses, and is observed in cells defective for oxyR, an oxidative DNA damage-responsive regulatory gene. UVM may represent either a novel DNA-repair phenomenon, or an unrecognized feature of DNA replication in damaged cells that affects a specific class of non-coding DNA lesions. To explore the range of DNA lesions subject to the UVM effect, we have examined mutation fixation at 3,N4-ethenocytosine and 1,N6-ethenoadenine, as well as at O6-methylguanine (O6mG). M13 viral single-stranded DNA constructs bearing a single mutagenic lesion at a specific site were transfected into cells pretreated with UV or 1-methyl-3-nitro-1-nitroso-guanidine (MNNG). Survival of transfected viral DNA was measured as transfection efficiency, and mutagenesis at the lesion site was analyzed by a quant. multiplex sequence anal. technol. The results suggest that the UVM effect modulates mutagenesis at the two etheno lesions, but does not appear to significantly affect mutagenesis at O6mG. Because the modulation of mutagenesis is observed in cells incapable of the SOS response, these data are consistent with the notion that UVM may represent a previously unrecognized DNA damage-inducible response that affects the fidelity of DNA replication at certain mutagenic lesions in Escherichia coli. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to escherichia bacteriophage m13 mutation repair uv, uv induction mutation repair escherichia m13, dna damage repair uv ethenocytosine ethenoadenine, methylguanine dna damage repair uv escherichia and other aspects.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On July 31, 2008, Meira, Lisiane B.; Bugni, James M.; Green, Stephanie L.; Lee, Chung-Wei; Pang, Bo; Borenshtein, Diana; Rickman, Barry H.; Rogers, Arlin B.; Moroski-Erkul, Catherine A.; McFaline, Jose L.; Schauer, David B.; Dedon, Peter C.; Fox, James G.; Samson, Leona D. published an article.Application of 55662-66-3 The title of the article was DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice. And the article contained the following:

Chronic inflammation increases cancer risk. While it is clear that cell signaling elicited by inflammatory cytokines promotes tumor development, the impact of DNA damage production resulting from inflammation-associated reactive oxygen and nitrogen species (RONS) on tumor development was not directly tested. RONS induce DNA damage that can be recognized by alkyladenine DNA glycosylase (Aag) to initiate base excision repair. Using a mouse model of episodic inflammatory bowel disease by repeated administration of dextran sulfate Na in the drinking water, we show that Aag-mediated DNA repair prevents colonic epithelial damage and reduces the severity of dextran sulfate sodium-induced colon tumorigenesis. Importantly, DNA base lesions expected to be induced by RONS and recognized by Aag accumulated to higher levels in Aag-deficient animals following stimulation of colonic inflammation. Finally, as a test of the generality of this effect we show that Aag-deficient animals display more severe gastric lesions that are precursors of gastric cancer after chronic infection with Helicobacter pylori. These data demonstrate that the repair of DNA lesions formed by RONS during chronic inflammation is important for protection against colon carcinogenesis. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Application of 55662-66-3

The Article related to dextran sulfate sodium colon inflammation carcinogenesis dna damage, alkyladenine dna glycosylase colon inflammation carcinogenesis dna damage, reactive oxygen species colon inflammation carcinogenesis dna damage, nitrogen reactive species colon inflammation carcinogenesis dna damage and other aspects.Application of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem