Page last updated: 2024-11-12

methylnitronitrosoguanidine

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth

Description

Methylnitronitrosoguanidine: A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

N-methyl-N'-nitro-N-nitrosoguanidine : An N-nitroguanidine compound having nitroso and methyl substituents at the N'-position [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID135436526
CHEMBL ID440287
CHEBI ID21759
SCHEMBL ID51610
MeSH IDM0013651

Synonyms (68)

Synonym
methylnitronitrosoguanidine
MNG ,
n-methyl-n'-nitro-n-nitrosoguanidine
nsc 9369
mnng
nsc-9369
guanidine, n-methyl-n'-nitro-n-nitroso-
guanidine, 1-methyl-3-nitro-1-nitroso-
wln: wnmyum&n1&no
1-methyl-1-nitroso-3-nitroguanidine
n-methyl-n-nitrosonitroguanidin
70-25-7
n'-nitro-n-nitroso-n-methylguanidine
1-methyl-3-nitro-1-nitrosoguanidine
nsc9369
n-nitroso-n-methylnitroguanidine
n-methyl-n-nitroso-n'-nitroguanidine
NCGC00091446-01
1-methyl-3-nitro-1-nitroso-guanidine
hsdb 5104
na0473
n-metylo-n'-nitro-n-nitrozoguanidyny [polish]
einecs 200-730-1
1-nitroso-3-nitro-1-methylguanidine
rcra waste number u163
n-methylo-n'-nitro-n-nitrozoguanidyny [polish]
n-nitroso-n'-nitro-n-methylguanidine
ccris 415
nci-c01423
ai3-50851
n-methyl-n'-nitro-n-nitrosoquanidine
rcra waste no. u163
n-nitroso-n-methyl-n'-nitroguanidine
n-methyl-n-nitrosonitroguanidin [german]
CHEBI:21759 ,
n-methyl-n',2-dioxohydrazinecarboximidohydrazide 2-oxide
CHEMBL440287
NCGC00091446-03
NCGC00091446-02
tox21_201126
cas-70-25-7
dtxcid40846
NCGC00258678-01
dtxsid2020846 ,
12h3o2ugsf ,
unii-12h3o2ugsf
n-metylo-n'-nitro-n-nitrozoguanidyny
n-methylo-n'-nitro-n-nitrozoguanidyny
nitrosoguanidine [na0473] [explosive 1.1a]
BP-20462
AKOS015850792
1-methyl-1-nitroso-2-nitroguanidine
n-methyl-n'-nitro-n-nitrosoguanidine [mi]
na-0473
SCHEMBL51610
J-504927
1-methyl-3-nitro-1 -nitrosoguanidine
n-methyl-n'-nitro-n-nitroso guanidine
3-methyl-1-nitro-3-nitrosoguanidine
methyl-3-nitro-1-nitrosoguanidine
n-methyl-n-nitro-n-nitroso guanidine
n-methyl-n',2-dioxohydrazinecarboximidohydrazide 2-oxide #
na 1325
GS-6150
1-methyl-3-nitro-1-nitrosoguanidine(wetted with ca.50% water) (unit weight on dry weight basis)
HY-128612
CS-0096134
1-methyl-3-nitro-1-nitrosoguanidine (mnng)

Research Excerpts

Toxicity

ExcerptReferenceRelevance
" MTX, a non-mutagen, which induced SCE only at toxic levels, could be considered a false positive because this positivity may reflect an enhancement of incorporation of 5-BrdUrd into DNA."( Relationship between cytotoxicity and induction of sister-chromatid exchanges in mouse foetal cells exposed to several doses of carcinogenic and non-carcinogenic chemicals.
Faggin, P; Maconi, A; Parodi, S; Raffetto, G, 1979
)
0.26
" The results showed that the addition of 10-150 micrograms of NaF per ml of culture medium induced 10-75% cytotoxic effect on hamster V79 cells but had no toxic effect on human EUE cells."( Cytotoxicity and genotoxicity testing of sodium fluoride on Chinese hamster V79 cells and human EUE cells.
Gábelová, A; Ruppová, K; Slamenová, D, 1992
)
0.28
" Comparatively, the LD50 for N-methyl-N'-nitro-N-nitrosoguanidine was 3 microM."( Genotoxicity of pancreatic chemical carcinogens to propagable cultured normal pancreatic epithelial cells.
Duguid, WP; Shepherd, J; Tsao, MS, 1990
)
0.28
" Post treatment incubation of MNU-treated HeLa cells with caffeine did not increase the toxic action of MNU."( Properties of mer- HeLa cells sensitive or resistant to the cytotoxic effects of MNU; effects on DNA synthesis and of post treatment with caffeine.
Basham, C; Roberts, JJ,
)
0.13
" Qualitatively, the patterns of embryo malformations reported in treated embryos paralleled those observed in in vivo studies, especially in regard to adverse effects on central nervous system and craniofacial systems."( In vitro developmental toxicity of five direct-acting alkylating agents in rodent embryos: structure-activity patterns.
Faustman, EM; Gage, D; Kirby, Z; Varnum, M, 1989
)
0.28
"2-Chloroethyl (methylsulfonyl)methanesulfonate (ClEtSoSo) was more toxic to the BE (Mer-) cell line than to the HT-29 (Mer+) colon carcinoma."( DNA damage and cytotoxicity of 2-chloroethyl (methylsulfonyl)methanesulfonate (NSC 338947) produced in human colon carcinoma cells with or without methylating agent pretreatment.
Gibson, NW; Hartley, JA, 1986
)
0.27
" Virtually non toxic concentrations of dThd potentiated the cytotoxicity of MNNG more than 10-fold but that of MMS was potentiated only about 2-fold showing that O-alkylation of DNA was associated not only with the facilitation of mutagenesis but also with the potentiation of cytotoxicity."( Deoxyribonucleoside-induced selective modulation of cytotoxicity and mutagenesis.
Danenberg, PV; Ibric, LL; Peterson, AR; Peterson, H, 1985
)
0.27
" According to median lethalities, all three known carcinogens were substantially more toxic than nitrosocimetidine whether administered by the intravenous, intraperitoneal, or oral routes."( Comparison of the acute toxicity of N-nitrosocimetidine with three structurally related carcinogens in the rat.
Hard, GC; Jensen, DE; Magee, PN; Ogiu, T, 1986
)
0.27
"Pretreatment of H4 (rat hepatoma) cells for 48 hr with low nontoxic doses of alkylating agents [methyl methanesulfonate (MMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and N-methyl-N-nitrosourea] renders the cells more resistant to the toxic effect of these compounds."( Adaptive response in mammalian cells: crossreactivity of different pretreatments on cytotoxicity as contrasted to mutagenicity.
Laval, F; Laval, J, 1984
)
0.27
" MNNG is about 100-fold more toxic than MMS on a molar basis."( Cytotoxicity of monofunctional alkylating agents. Methyl methanesulfonate and methyl-N'-nitro-N-nitrosoguanidine have different mechanisms of toxicity for 10T1/2 cells.
Grisham, JW; Smith, GJ, 1983
)
0.27
" Acute toxic effects: DMN produced dose-dependent (0."( [Histopathological studies of the acute and chronic toxic effects of 2 N-nitroso compounds on the blue mussel (Mytilus edulis)].
Hage, E; Karlog, O; Rasmussen, LP,
)
0.13
"The toxic and mutagenic effects of the alkylating agents methylnitrosourea (MNU) and methylnitronitrosoguanidine (MNNG) and of the frameshift mutagen, ICR-191 were compared among 3 human diploid lymphoblast lines, MIT-2, WI-L2 and GM 130."( Comparison of toxicity and mutagenicity of methylnitrosourea, methylnitronitrosoguanidine and ICR-191 among human lymphoblast lines.
Andon, BM; Slapikoff, SA; Thilly, WG, 1980
)
0.26
" The maximum suspension of MNG that could be delivered, 1 mg MNG/kg body weight, produced no signs of toxic stress during the 14-day observation period."( N-methyl-N'-nitroguanidine: irritation, sensitization, and acute oral toxicity, genotoxicity, and methods for analysis in biological samples.
Brashear, WT; Godin, CS; Ketcha, MM; Kinkead, ER; Lu, PP; Salins, SA; Thilagar, A; Wolfe, RE,
)
0.13
" GTE was not toxic and no harmful effect was found during its clinical use."( Inhibitory effects and toxicity of green tea polyphenols for gastrointestinal carcinogenesis.
Iwata, Y; Kikuoka, N; Kitao, Y; Matsumoto, H; Nakatani, H; Oya, K; Takahashi, T; Yamane, T, 1996
)
0.29
" No adverse effects were seen when HWL chickens were vaccinated concurrently with MS-H and combinations of Mycoplasma gallisepticum ts-11 vaccine, IBV vaccine, and infectious laryngotracheitis virus vaccine."( Safety of a temperature-sensitive clone of Mycoplasma synoviae as a live vaccine.
Markham, JF; Morrow, CJ; Scott, PC; Whithear, KG,
)
0.13
"This report shows that hydroxyurea (HU) protected KB cells specifically against the toxic effect of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)."( Hydroxyurea: protection of KB cells against the toxic effect of N-methyl-N'-nitro-N-nitrosoguanidine.
Aujard, C; Trincal, G, 1980
)
0.26
" Regions of the Krasnodar Krai where sea and fresh waters exerted toxic action on luminescence were determined by the microbioluminescent method."( [Microbioluminescent study of the general toxicity and mutagenicity of pollutants].
Goliasnaia, NV; Maslennikova, IL,
)
0.13
"Selenite is at least 4 times as toxic as Se-enriched higher plants selected in this experiment."( [Preventive effects of 4 Se-enriched plants on rat stomach cancer induced by MNNG 2. Safety of different selenium resources for prevention of stomach cancer].
Chen, J; Chen, X; Li, W; Yang, W, 2008
)
0.35
"In both pro- and eukaryotes, the mutagenic and toxic DNA adduct O(6)-methylguanine (O(6)MeG) is subject to repair by alkyltransferase proteins via methyl group transfer."( The bacterial alkyltransferase-like (eATL) protein protects mammalian cells against methylating agent-induced toxicity.
Aasland, D; Fuchs, RP; Kaina, B; Margison, GP; Modesti, M; Pinder, SI; Tomaszowski, KH; Williams, E, 2015
)
0.42
" The aim of this work was to evaluate antidiabetic activity in Streptozotocin (STZ)-induced diabetic rats and the antioxidant effects of 3',4'-Di-O-acetyl-cis-khellactone (DOAcK), as well as its toxic potential."( Antidiabetic effect, antioxidant activity, and toxicity of 3',4'-Di-O-acetyl-cis-khellactone in Streptozotocin-induced diabetic rats.
Burgueño-Tapia, E; Cornejo-Garrido, J; Domínguez-Mendoza, EA; Ordaz-Pichardo, C, 2016
)
0.43

Compound-Compound Interactions

ExcerptReferenceRelevance
" These occurred only in the groups given MNNG in combination with stress, aspirin, or sodium taurocholate, and did not occur in experimental groups given either MNNG, stress, aspirin, or sodium taurocholate alone, and did not occur in the control group."( Experimental models for gastric leiomyosarcoma. The effects of N-methyl-N'-nitro-N-nitrosoguanidine in combination with stress, aspirin, or sodium taurocholate.
Cohen, A; Geller, SA; Horowitz, I; Toth, LS; Werther, JL, 1984
)
0.27
"A modified assay for the detection of DNA single-strand breaks (SSBs) in human mononucleated white blood cells (MWBCs) based on the nick translation (NT) reaction was developed and combined with the test for unscheduled DNA synthesis (UDS)."( A novel technique for the detection of DNA single-strand breaks in human white blood cells and its combination with the unscheduled DNA synthesis assay.
Baumgartner, E; Einhaus, M; Holz, O; Krause, T; Meissner, R; Rüdiger, HW, 1993
)
0.29
" This effect was less pronounced when FK866 was used in combination with another alkylating agent, melphalan."( Chemopotentiating effects of a novel NAD biosynthesis inhibitor, FK866, in combination with antineoplastic agents.
Azzam, K; Hasmann, M; Nüssler, V; Pelka-Fleischer, R; Pogrebniak, A; Schemainda, I, 2006
)
0.33
") was also administered along with 5-FU."( Evaluation of role of telmisartan in combination with 5-fluorouracil in gastric cancer cachexia.
Patel, BM; Patel, HJ; Sukumaran, S, 2016
)
0.43

Bioavailability

ExcerptReferenceRelevance
"We studied the characteristics and mechanisms of MNNG (N-methyl-N'-nitro-N-nitrosoguanidine) intestinal absorption and the interaction between bile acids and fatty acids and MNNG absorption rate in vivo in male Sprague-Dawley rats."( The mechanisms of intestinal absorption of the carcinogen MNNG (N-methyl-N'-nitro-N-nitrosoguanidine).
Dadufalza, V; Hollander, D; Koyama, SY, 1988
)
0.27

Dosage Studied

ExcerptRelevanceReference
" In general the magnitude of this induced variation increased with increasing dosage of the mutagen."( Induced quantitative variation for penicillin titre in clonal populations of Aspergillus nidulans.
Caten, CE; Simpson, IN, 1979
)
0.26
" A clear dose-response relationship was found in the promotion of epithelial keratinization by MNNG."( Promotion of epithelial keratinization by N-methyl-N'-nitro-N-nitrosoguanidine in rat forestomach in organ culture.
Fukamachi, H; Takayama, S, 1979
)
0.26
" Parallel studies with HeLa cells showed a similar dose-response relationship between mutagen action and immunoreactivity."( Mutagen-induced disturbances in the DNA of human lymphocytes detected by antinucleoside antibodies.
Bases, R; Elequin, F; Kadish, A; Liebeskind, D; Mendez, F; Rubinstein, A; Wittner, D, 1979
)
0.26
" Mutation frequency to 6TG R, an X-linked recessive phenotype, was inversely related to dosage whereas OUA R, a codominant phenotpye, occurred with equal frequency in both lines."( The relationship between induced mutation frequency and chromosome dosage in established mouse fibroblast lines.
Gartler, SM; Raskind, WH, 1978
)
0.26
" Dose-response relationships for recombination and mutation are discussed."( Induction of mitotic recombination with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Saccharomyces cerevisiae. A comparison between treatment in vitro and in the host-mediated assay.
Ryttman, H; Zetterberg, G, 1976
)
0.26
" Analysis of this dose-response curve suggests a one-event ("one-hit") response for transformation by this carcinogen."( Mammalian cell transformation and cell-mediated mutagenesis by carcinogenic polycyclic hydrocarbons.
Huberman, E, 1975
)
0.25
"N-methyl-N-nitroso-N'-nitroguanidine was administered as drinking water to Wistar strain and non-inbred male rats in the dosage of 100 mKg/ml for 7 months, Adenocarcinomas of the stomach were produced in about 70% of rats."( [Induction of stomach tumors in rats by N-methyl-N-nitroso-N1-nitroguanidine].
Bykorez, AI; Kartasheva, LA, 1975
)
0.25
" Dose-response studies with several mutagens indicated that the number of foci increased with concentration to the point where excessive cytotoxicity developed."( Development of an in vitro model to study carcinogen-induced neoplastic progression of initiated mouse epidermal cells.
Glick, A; Greenhalgh, D; Hennings, H; Morgan, D; Welty, D; Yuspa, SH, 1992
)
0.28
" The beta-GA, reflecting the SOS-inducing activity, of GE94 and KY946 treated with these compounds increased significantly with a clear dose-response relationship, and reached a maximum level within 60 min, while no response was seen in KY945 and KY943."( 'Rec-lac test' for detecting SOS-inducing activity of environmental genotoxic substance.
Nishioka, H; Nunoshiba, T, 1991
)
0.28
" In general, the results showed a nonlinear dose-response relationship for fiber and fat."( Interactive effects of dietary wheat bran and lard on N-methyl-N'-nitro-N-nitrosoguanidine-induced colon carcinogenesis in rats.
Bosland, MC; Hollanders, VM; Kuper, CF; Sinkeldam, EJ; Vedder, DM, 1990
)
0.28
" Histologically, GABA at the high dosage and baclofen at both dosages significantly decreased the labeling index of the antral mucosa and significantly increased the serum gastrin level."( Inhibition by gamma-amino-n-butyric acid and baclofen of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.
Baba, M; Ichii, M; Iishi, H; Nakaizumi, A; Taniguchi, H; Tatsuta, M, 1990
)
0.28
" Administration of bromocriptine alone at either dosage had no influence on gastric carcinogenesis."( Attenuating effect of bromocriptine on cysteamine anticarcinogenesis of stomach cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine.
Baba, M; Ichii, M; Iishi, H; Nakaizumi, A; Taniguchi, H; Tatsuta, M; Uehara, H, 1990
)
0.28
" In this paper we report on an automated system that successfully generates dose-response data and, moreover, reduces the labor, materials, and sample mass required to obtain such information."( Development and validation of the spiral Salmonella assay: an automated approach to bacterial mutagenicity testing.
Claxton, LD; Houk, VS; Schalkowsky, S, 1989
)
0.28
" The UV dose-response curve of mus-26 showed a characteristic plateau in the range of 100-200 J/m2."( Epistasis, photoreactivation and mutagen sensitivity of DNA repair mutants upr-1 and mus-26 in Neurospora crassa.
Inoue, H; Ishii, C, 1989
)
0.28
" The dose-response curves for enhancement of MNNG-induced transformation and induction of aryl hydrocarbon hydroxylase activity by TCDD were similar."( 2,3,7,8-Tetrachlorodibenzo-p-dioxin enhancement of N-methyl-N'-nitro-N-nitrosoguanidine-induced transformation of rat tracheal epithelial cells in culture.
Barrett, JC; Gray, T; Nelson, K; Nettesheim, P; Tanaka, N, 1989
)
0.28
" No clear dose-response curve was obtained."( Evaluation of the DNA-damaging and mutagenic activity of oxolinic and pipemidic acids by the granuloma pouch assay.
Maura, A; Pino, A, 1988
)
0.27
" The SENCAR mouse model provides a good dose-response relationship for many carcinogens used as tumor initiators and for many compounds used as tumor promoter."( SENCAR mouse skin tumorigenesis model versus other strains and stocks of mice.
Slaga, TJ, 1986
)
0.27
" Lead acetate also transformed SHE cells in a dose-response fashion following a 48-h exposure."( Genetic toxicology of lead compounds.
Costa, M; Hartwig, A; Li, JH; Rossman, TG; Wang, XW; Zelikoff, JT, 1988
)
0.27
" injection route, but a weak positive response was evident following oral gavage dosing of MNNG as an homogenate in corn oil."( The activity of MNNG in the mouse bone marrow micronucleus assay.
Ashby, J; Mirkova, E, 1987
)
0.27
" MMS and ENU both showed shouldered dose-response curves for exponentially growing asynchronous cells, and the same cell-cycle pattern for synchronous cultures with cells in early S phase being the most sensitive."( Cell killing by various monofunctional alkylating agents in Chinese hamster ovary cells.
Goth-Goldstein, R; Hughes, M, 1987
)
0.27
" and the circulating blood levels of intact and denitrosated compound 5 min after dosing quantified."( Evidence for cytosolic glutathione transferase-mediated denitrosation of nitrosocimetidine and 1-methyl-2-nitro-1-nitrosoguanidine.
Jensen, DE; Stelman, GJ, 1987
)
0.27
" As opposed to this dose-response pattern, cytotoxic alterations, regenerative hyperplastic lesions and tumours of the stomach are more frequent after medium of high MNNG doses."( The effects of different MNNG (N-methyl-N'-nitro-N-nitrosoguanidine)-doses on the stomach and the upper small intestine of the rat. II. The frequency of intestinal metaplasia.
Barten, M, 1987
)
0.27
" So the use of this orthogonal design in cell culture has many advantages: several factors can be tested simultaneously; it is easy to find the optimal protocol conditions and the dose-response relationship is stable, which enables the reproducibility to be improved."( Use of an orthogonal design method to study two-stage chemical carcinogenesis in BALB/3T3 cells.
Chouroulinkov, I; Lasne, C; Lu, YP, 1986
)
0.27
" Duplications of the pepE locus showed a gene dosage effect on levels of peptidase E, suggesting that pepE is the structural gene for this enzyme."( Aspartate-specific peptidases in Salmonella typhimurium: mutants deficient in peptidase E.
Carter, TH; Miller, CG, 1984
)
0.27
" For comparison, the DNA methylation produced by the carcinogen N-methyl-N-nitro-N-nitrosoguanidine (MNNG) dosed orally was measured."( DNA-methylation by nitrosocimetidine and N-methyl-N-nitro-N-nitrosoguanidine in the intact rat.
Gombar, CT; Magee, PN, 1982
)
0.26
"The dose-response for the induction of acentric chromosome fragments was determined in neuroblasts of the grasshopper embryo (Chortophaga viridifasciata De Geer, Orthoptera: Acrididae) exposed in vitro to four direct-acting chemical known to be mutagenic, clastogenic, and carcinogenic: 4-nitroquinoline-1-oxide (4NQO), N-methyl-N-nitro-N-nitrosoguanidine (MNNG), Adriamycin (ADM), and bleomycin (BLM)."( Neuroblast of the grasshopper embryo as a new mutagen test system. II. Chromosome breakage induced by in vitro exposure of embryos to the direct-acting mutagens 4NQO, MNNG, adriamycin, and bleomycin.
Gaulden, ME; Liang, JC, 1982
)
0.26
" Their mode of action is distinct, especially with regard to dose-response effects and reversibility."( Bile acids, but not neutral sterols, are tumor promoters in the colon in man and in rodents.
Barnes, WS; Reddy, BS; Weisburger, JH; Wynder, EL, 1983
)
0.27
" However, with a fixed experimental regimen, treatments with relatively higher doses cause a deformity of the dose-response relationship."( Proliferative kinetics and chemical-induced sister chromatid exchanges in human lymphocyte cultures.
Morimoto, K, 1984
)
0.27
" In addition, a linear dose-response curve with a slope of approximately 1 was observed when the logarithm of MNNG-induced transformation frequency was plotted versus the logarithm of MNNG dose."( High frequency of carcinogen-induced early, preneoplastic changes in rat tracheal epithelial cells in culture.
Barrett, JC; Gray, TE; Mass, MJ; Thomassen, DG, 1983
)
0.27
" A linear dose-response relationship for mutation induction was found after treatment with increasing doses of MNNG."( Mutagenesis and morphological transformation by N-methyl-N'-nitro-N-nitrosoguanidine in the BALB/3T3 clone A31-1-1 cell line.
Bignami, M; Saffiotti, U, 1983
)
0.27
" The change of gene dosage appears to be the main feature of the chromosome aberrations."( Karyological analysis of N-methyl-N'-nitro-N-nitrosoguanidine-transformed Syrian hamster cell lines using high resolution G-banding technique.
Li, S; Pathak, S,
)
0.13
" 1) Physical modifiers: Route of administration, medium (vehicle) of carcinogens, detergents, dosage (concentration), period (frequency) of administration, exposure time, and condition of mucus."( [Experimental carcinogenesis of the stomach and its modifiers].
Takahashi, M, 1983
)
0.27
" levels of O6-methylguanine (O6-MeG) in the DNA extracted from the bacteria follow a similar dose-response curve suggesting a dependency of mutagenesis on O6-MeG."( Resistance of Salmonella typhimurium TA 1535 to O6-guanine methylation and mutagenesis induced by low doses of N-methyl-N'-nitro-N-nitrosoguanidine: an apparent constitutive repair activity.
Guttenplan, JB; Milstein, S, 1982
)
0.26
" The presence of HU during chemical treatment and throughout this 18 h of incubation with [3H]dThd did not influence the dose-response curves obtained with UV, MMS, NA-AAF and BaP but it increased the input dose of MNNG, MMC, DMN and AFB1 required to give peak repair incorporation."( Chemical carcinogen induction of DNA-repair synthesis in human peripheral blood monocytes.
Igel, HJ; Kropko, ML; Lake, RS; McLachlan, S; Pezzutti, MR; Shoemaker, RH, 1980
)
0.26
" In addition, the ferret was tested for its suitability as an animal model for the induction of gastric cancer by oral dosing with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)."( Gastric disease in ferrets: effects of Helicobacter mustelae, nitrosamines and reconstructive gastric surgery.
Fox, JG, 1994
)
0.29
" Nine of 10 ferrets dosed with MNNG developed gastric adenocarcinoma (29-55 months after dosing), while none of the five historical control ferrets examined an average of 63 months after the initiation of the study developed gastric tumors."( MNNG-induced gastric carcinoma in ferrets infected with Helicobacter mustelae.
Correa, P; Fox, JG; Murphy, JC; Tannenbaum, SR; Wishnok, JS, 1993
)
0.29
", 500, 250, and 50 micrograms/ml, in the presence of bioactivation, and at the highest dosage (500 micrograms/ml) in the absence of bioactivation."( In vitro transforming effect of the fungicides metalaxyl and zineb.
Bonora, B; Colacci, A; Grilli, S; Perocco, P, 1995
)
0.29
" We conclude that the very low dose response cannot be extrapolated from usual dose-response analyses."( Response of human keratinocytes to extremely low concentrations of N-methyl-N'-nitro-N-nitrosoguanidine.
Althaus, FR; Kleczkowska, HE, 1996
)
0.29
" However, for MMS and UV light, which was included in this study for comparison, c-fos, c-jun, junB and junD mRNA as well as AP-1 induction paralleled the dose-response for induction of cell killing effects, recombination and chromosomal breakage indicating that increased expression of Fos and Jun is related to the generation of MMS and UV-induced genetic changes."( Induction of c-fos, c-jun, junB and junD mRNA and AP-1 by alkylating mutagens in cells deficient and proficient for the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) and its relationship to cell death, mutation induction and chromosomal
Dosch, J; Kaina, B, 1996
)
0.29
" However, administration of isoproterenol at either dosage had no significant effect on the incidence of gastric cancers and the labeling index of antral epithelial cells."( Promotion by the alpha-adrenoceptor agonist phenylephrine, but not by the beta-adrenoceptor agonist isoproterenol, of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.
Baba, M; Iishi, H; Iseki, K; Nakaizumi, A; Sakai, N; Tatsuta, M; Uehara, H; Yano, H, 1998
)
0.3
" Prolonged administration of genistein at a dosage of 30 mg/kg, but not 15 mg/kg, body weight significantly reduced the incidence of gastric cancers, which was increased by oral treatment with sodium chloride."( Attenuation by genistein of sodium-chloride-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.
Baba, M; Iishi, H; Nakaizumi, A; Tatsuta, M; Uehara, H; Yano, H, 1999
)
0.3
" The public health implication of this lack of linearity in the low-dose area of the dose-response curve raises the question of whether low doses of carcinogens will reduce cancer risk."( Can the concept of hormesis Be generalized to carcinogenesis?
Baldwin, LA; Calabrese, EJ, 1998
)
0.3
" In fact, the shift of the MNNG dose-response curves in the presence of increasing HU concentrations suggests that HU might interfere with the MNNG-molecule."( Hydroxyurea: protection of KB cells against the toxic effect of N-methyl-N'-nitro-N-nitrosoguanidine.
Aujard, C; Trincal, G, 1980
)
0.26
" Corn fractions tested showed evidence of anti-mutagenic activity by producing a dose-response type of relationship between a constant amount of MNNG and several concentrations of tested corn fraction."( Partial chemical/structural elucidation of anti-mutagenic compounds from corn.
Burgos-Hernández, A; López-García, R; Njapau, H; Park, DL, 2001
)
0.31
" Using this method, the mutations existed in a Psedomonas aeruginosa mutant strain were screened, indicating that A/G transitions at nt 181 and nt 314 in chloramphenicol acetyltransferase (catB7) gene conferred this strain with a high chloramphenicol dosage resistant."( Directly fishing out subtle mutations in genomic DNA with histidine-tagged Thermus thermophilus MutS.
Liu, J; Wang, J, 2004
)
0.32
" Dose-response experiments were conducted in which yeast cells were exposed in minimal medium and in the presence of 20% fetal calf serum to sublethal concentrations of an array of heavy metals, salt, and a number of stress-inducing compounds (Diclofenac, Lindane, methyl-N-nitro-N-nitrosoguanidine [MNNG], hydroxyurea, and caffeine)."( Use of PMA1 as a housekeeping biomarker for assessment of toxicant-induced stress in Saccharomyces cerevisiae.
Lichtenberg-Fraté, H; Ludwig, J; Schmitt, M; Schwanewilm, P, 2006
)
0.33
"1 ml 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) at the dosage of 800 mg/L for 10 days, whereas the rats in the normal group were similarly administered with normal saline."( Dynamic changes of Sonic Hedgehog signaling pathway in gastric mucosa of rats with MNNG-induced gastric precancerous lesions.
Cai, D; Chen, Z; He, B; Liu, Q; Qiu, J; Yan, M; Yu, J, 2019
)
0.51
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
alkylating agentHighly reactive chemical that introduces alkyl radicals into biologically active molecules and thereby prevents their proper functioning. It could be used as an antineoplastic agent, but it might be very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. It could also be used as a component of poison gases.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (1)

ClassDescription
nitroso compoundCompounds having the nitroso group, -NO, attached to carbon, or to another element, most commonly nitrogen or oxygen.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (26)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
interleukin 8Homo sapiens (human)Potency66.82420.047349.480674.9780AID651758
RAR-related orphan receptor gammaMus musculus (house mouse)Potency30.45100.006038.004119,952.5996AID1159523
GLI family zinc finger 3Homo sapiens (human)Potency1.33040.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency53.51270.000221.22318,912.5098AID1259243; AID1259247; AID588516
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency35.48130.011212.4002100.0000AID1030
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency17.12390.001022.650876.6163AID1224838; AID1224893
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency50.11870.000214.376460.0339AID588533
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency68.17130.001530.607315,848.9004AID1224842
farnesoid X nuclear receptorHomo sapiens (human)Potency55.68950.375827.485161.6524AID588526; AID743217
pregnane X nuclear receptorHomo sapiens (human)Potency60.75780.005428.02631,258.9301AID1346982
estrogen nuclear receptor alphaHomo sapiens (human)Potency37.44570.000229.305416,493.5996AID1259248; AID588513; AID588514; AID743080; AID743091
peroxisome proliferator-activated receptor deltaHomo sapiens (human)Potency39.81070.001024.504861.6448AID588534
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency51.17710.001019.414170.9645AID588536; AID588537; AID743094; AID743191
aryl hydrocarbon receptorHomo sapiens (human)Potency21.55770.000723.06741,258.9301AID743085
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency68.17130.001723.839378.1014AID743083
thyroid stimulating hormone receptorHomo sapiens (human)Potency66.88800.001628.015177.1139AID1259385; AID1259395
activating transcription factor 6Homo sapiens (human)Potency54.59840.143427.612159.8106AID1159516
nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105), isoform CRA_aHomo sapiens (human)Potency54.598419.739145.978464.9432AID1159509
v-jun sarcoma virus 17 oncogene homolog (avian)Homo sapiens (human)Potency27.02030.057821.109761.2679AID1159526; AID1159528
Histone H2A.xCricetulus griseus (Chinese hamster)Potency17.46580.039147.5451146.8240AID1224845; AID1224896
cellular tumor antigen p53 isoform aHomo sapiens (human)Potency31.62280.316212.443531.6228AID902
thyroid hormone receptor beta isoform aHomo sapiens (human)Potency50.11870.010039.53711,122.0200AID588547
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency58.51340.000323.4451159.6830AID743065; AID743067
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency66.82420.000627.21521,122.0200AID651741
Cellular tumor antigen p53Homo sapiens (human)Potency32.18450.002319.595674.0614AID651631; AID651743; AID720552
Nuclear receptor ROR-gammaHomo sapiens (human)Potency37.57800.026622.448266.8242AID651802
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (134)

Processvia Protein(s)Taxonomy
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IINuclear receptor ROR-gammaHomo sapiens (human)
xenobiotic metabolic processNuclear receptor ROR-gammaHomo sapiens (human)
regulation of glucose metabolic processNuclear receptor ROR-gammaHomo sapiens (human)
regulation of steroid metabolic processNuclear receptor ROR-gammaHomo sapiens (human)
intracellular receptor signaling pathwayNuclear receptor ROR-gammaHomo sapiens (human)
circadian regulation of gene expressionNuclear receptor ROR-gammaHomo sapiens (human)
cellular response to sterolNuclear receptor ROR-gammaHomo sapiens (human)
positive regulation of circadian rhythmNuclear receptor ROR-gammaHomo sapiens (human)
regulation of fat cell differentiationNuclear receptor ROR-gammaHomo sapiens (human)
positive regulation of DNA-templated transcriptionNuclear receptor ROR-gammaHomo sapiens (human)
adipose tissue developmentNuclear receptor ROR-gammaHomo sapiens (human)
T-helper 17 cell differentiationNuclear receptor ROR-gammaHomo sapiens (human)
regulation of transcription by RNA polymerase IINuclear receptor ROR-gammaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (38)

Processvia Protein(s)Taxonomy
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingNuclear receptor ROR-gammaHomo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificNuclear receptor ROR-gammaHomo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificNuclear receptor ROR-gammaHomo sapiens (human)
DNA-binding transcription factor activityNuclear receptor ROR-gammaHomo sapiens (human)
protein bindingNuclear receptor ROR-gammaHomo sapiens (human)
oxysterol bindingNuclear receptor ROR-gammaHomo sapiens (human)
zinc ion bindingNuclear receptor ROR-gammaHomo sapiens (human)
ligand-activated transcription factor activityNuclear receptor ROR-gammaHomo sapiens (human)
sequence-specific double-stranded DNA bindingNuclear receptor ROR-gammaHomo sapiens (human)
nuclear receptor activityNuclear receptor ROR-gammaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (19)

Processvia Protein(s)Taxonomy
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
nucleusNuclear receptor ROR-gammaHomo sapiens (human)
nucleoplasmNuclear receptor ROR-gammaHomo sapiens (human)
nuclear bodyNuclear receptor ROR-gammaHomo sapiens (human)
chromatinNuclear receptor ROR-gammaHomo sapiens (human)
nucleusNuclear receptor ROR-gammaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (9)

Assay IDTitleYearJournalArticle
AID1687883Genotoxicity in mouse RAW264.7 cells assessed as survival at 0.5 uM measured after 24 hrs by micronucleus test (Rvb = 100%)2020European journal of medicinal chemistry, Jan-15, Volume: 186Novel nitroimidazole derivatives evaluated for their trypanocidal, cytotoxic, and genotoxic activities.
AID1687881Genotoxicity in mouse RAW264.7 cells assessed as mitotic index at 0.5 uM measured after 24 hrs by micronucleus test (Rvb = 40 to 249 No_unit)2020European journal of medicinal chemistry, Jan-15, Volume: 186Novel nitroimidazole derivatives evaluated for their trypanocidal, cytotoxic, and genotoxic activities.
AID318681Anticarcinogenic activity in rat assessed as induction of tumors per day2008Bioorganic & medicinal chemistry, Mar-15, Volume: 16, Issue:6
QSAR modeling of the rodent carcinogenicity of nitrocompounds.
AID1687882Genotoxicity in mouse RAW264.7 cells assessed as number of micronucleated cells at 0.5 uM measured after 24 hrs by micronucleus test (Rvb = 12 to 15 No_unit)2020European journal of medicinal chemistry, Jan-15, Volume: 186Novel nitroimidazole derivatives evaluated for their trypanocidal, cytotoxic, and genotoxic activities.
AID9079Influence of PARP-1 cellular activity on NAD+ levels at a concentration of 25 uM of the compound2002Journal of medicinal chemistry, Nov-07, Volume: 45, Issue:23
Novel tricyclic poly(ADP-ribose) polymerase-1 inhibitors with potent anticancer chemopotentiating activity: design, synthesis, and X-ray cocrystal structure.
AID9245Effect on NAD+ depletion (% remaining versus vehicle control) 25 uM compound concentration in A549 cells2003Journal of medicinal chemistry, Jan-16, Volume: 46, Issue:2
Tricyclic benzimidazoles as potent poly(ADP-ribose) polymerase-1 inhibitors.
AID9240Percent ADP-ribose polymer formation at 25 uM compound concentration in A549 cells2003Journal of medicinal chemistry, Jan-16, Volume: 46, Issue:2
Tricyclic benzimidazoles as potent poly(ADP-ribose) polymerase-1 inhibitors.
AID1636332Mutagenicity in Salmonella typhimurium TA100 assessed as mutagenic index at 0.007 uM/plate after 48 hrs in absence of S9 fraction by Ames test relative to control2016Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16
Antidiabetic effect, antioxidant activity, and toxicity of 3',4'-Di-O-acetyl-cis-khellactone in Streptozotocin-induced diabetic rats.
AID9050Influence of PARP-1 cellular activity in human lung carcinoma A549 cells on %ADP Polymer formation at a concentration of 25 uM of the compound2002Journal of medicinal chemistry, Nov-07, Volume: 45, Issue:23
Novel tricyclic poly(ADP-ribose) polymerase-1 inhibitors with potent anticancer chemopotentiating activity: design, synthesis, and X-ray cocrystal structure.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (3,257)

TimeframeStudies, This Drug (%)All Drugs %
pre-19901770 (54.34)18.7374
1990's832 (25.54)18.2507
2000's440 (13.51)29.6817
2010's178 (5.47)24.3611
2020's37 (1.14)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials3 (0.09%)5.53%
Reviews83 (2.42%)6.00%
Case Studies4 (0.12%)4.05%
Observational0 (0.00%)0.25%
Other3,342 (97.38%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]