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Search results for: Lipoxidase CAS Number [9029 60 1]

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#32372640   2020/05/06 To Up

CRISPR/Cas9-Mediated Mutagenesis Adverse to Tomato Plant Growth and MeJA-Induced Fruit Resistance to .

Methyl jasmonate (MeJA), a natural phytohormone, played a critical role not only in plant growth but also in plant defense response to biotic and abiotic stresses. MYC2, a basic helix-loop-helix transcription factor, is a master regulator in MeJA signaling pathway. In the present work, mutants were generated by the clustered regularly interspaced short palindromic repeats and associated Cas9 protein (CRISPR/Cas9) system to investigate the role of in tomato plant growth and fruit disease resistance induced by exogenous MeJA. The results showed that mutants possessed a higher number of flowers and a lower fruit setting rate in comparison with wild-type plants. In addition, the fruit shape of s mutant was prolate, while the control fruits were oblate. Knockout of significantly decreased the activities of disease defensive and antioxidant enzymes, as well as the expression levels of pathogen-related (PR) genes ( and ) and the key genes related to jasmonic acid (JA) biosynthesis and signaling pathway including (), (), , and (), and consequently aggravated the disease symptoms. By contrast, the disease symptoms were largely reduced in MeJA-treated fruit that possessed higher activities of these enzymes and expression levels of genes. However, the induction effects of MeJA on fruit disease resistance and these enzymes' activities and genes' expressions were significantly attenuated by knockout of . Therefore, the results indicated that played positive regulatory roles not only in the growth of tomato plants but also in MeJA-induced disease resistance and the antioxidant process in tomato fruits.
Pan Shu, Ziye Li, Dedong Min, Xinhua Zhang, Wen Ai, Jiaozhuo Li, Jingxiang Zhou, Zilong Li, Fujun Li, Xiaoan Li

1117 related Products with: CRISPR/Cas9-Mediated Mutagenesis Adverse to Tomato Plant Growth and MeJA-Induced Fruit Resistance to .

200assays961 kit(96 Wells)200 ug96T202 modules1000 100 G5x96 well plate0.2 mg

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#7779147   // To Up

Studies on the in vitro and in vivo genotoxicity of [2,2-dimethyl-6- (4-chlorophenyl)-7-phenyl-2,3-dihydro-1H-pyrrolizine-5-yl]-acetic acid.

[2,2-Dimethyl-6-(4-chlorophenyl)-7-phenyl-2,3-dihydro-1H-pyrrolizine-5- yl]-acetic acid (CAS 156897-06-2, ML 3000) was examined for genotoxic activity in bacteria and mammalian cells in vitro as well as in vivo. The substance did not increase gene mutation frequencies either in a bacterial system or in a cultured V79 cell line of the Chinese hamster. Both in vitro tests were conducted in the presence and absence of S9-mix. In the unscheduled DNA synthesis assay in vitro with primary rat hepatocytes, negative results were also obtained. A cytogenetic analysis of the bone marrow of male and female Wistar rats was performed. After oral application ML 3000 did not increase the number of cells with structural chromosomal aberrations. The results suggest that ML 3000 has no genotoxic potential in vitro and in vivo.
A Heidemann, S Tries, S Laufer, J Augustin

1072 related Products with: Studies on the in vitro and in vivo genotoxicity of [2,2-dimethyl-6- (4-chlorophenyl)-7-phenyl-2,3-dihydro-1H-pyrrolizine-5-yl]-acetic acid.

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#7907874   // To Up

Mechanism of anti-inflammatory action of fepradinol.

The mechanism of the anti-inflammatory activity of fepradinol (CAS 67704-50-1) has been investigated. The effect of fepradinol was compared with that of indometacin and other non-steroidal anti-inflammatory drugs. Oral dosing of fepradinol and cyproheptadine suppressed zymosan-induced paw edema in rats. Indometacin and piroxicam were without effect. Fepradinol inhibited the early and late stages of concanavalin A-induced edema in rats; indometacin and piroxicam only inhibited the late stage. Fepradinol and indometacin prevented the carrageenin-induced inflammation in rats: they acted on the exudate, on the increase of protein and gamma-glutamyltransferase levels, and also reduced the number of leucocytes. But, in contrast to indometacin, fepradinol did not inhibit prostaglandin E2 biosynthesis. Fepradinol and indometacin prevented diarrhoea induced by intravenous injection of endotoxin in mice or by oral administration of castor oil in rats. In in vitro tests, fepradinol did not inhibit prostaglandin biosynthesis from arachidonic acid by bovine seminal vesicle microsomal enzyme or 15-lipoxygenase. These results indicate that fepradinol possesses a potent inhibitory activity on the acute inflammation in rodents and that its anti-inflammatory activity does not seem to be related to an inhibitory effect on prostaglandin biosynthesis.
J M Massó, A M Villar, J R Conde, J Martorell

1087 related Products with: Mechanism of anti-inflammatory action of fepradinol.

0.1ml (1mg/ml) 5 G100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100 25 100 μg100ug Lyophilized1ml1 mg

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