Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012872 (DNA marker)
 929 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A high-oleate trait in the cultivated peanut ( Arachis hypogaea L.) was reported to rely on the allelic composition of the two homeologous, microsomal oleoyl-PC desaturase genes ( ahFAD2A or ahFAD2B). The enzyme activity of either ahFAD2A or ahFAD2B is sufficient for a normal oleate phenotype, and a significant reduction in the levels of ahFAD2B and a mutation in ahFAD2A were reported to be responsible for the high-oleate phenotype in one chemically induced mutant (M2-225) and one derived from a naturally occurring (8-2122) mutant. Here, we report an insertion of the same miniature inverted-repeat transposable element (MITE) in the ahFAD2B gene in another chemically induced mutant (Mycogen-Flavo) and the previously characterized M2-225 mutant. In both cases, this MITE insertion in ahFAD2B causes a frameshift, resulting in a putatively truncated protein sequence in both mutants. The insertion of this MITE in ahFAD2B, in addition to the point mutation in ahFAD2A, appears to be the cause of the high-oleate phenotype in Mycogen-Flavo and M2-225 mutants. Utilizing sequences of the MITE, we developed a DNA marker strategy to differentiate the two insertion-containing mutants from the normal oleate peanut variety (AT-108) and the naturally occurring, high-oleate mutant 8-2122. Reverse transcript-PCR/differential digestion results reveal the expression of both ahFAD2A and ahFAD2B genes in Mycogen-Flavo mutant. This result is in contrast to the observation that ahFAD2B transcripts are greatly reduced in the M2-225 mutant having the MITE insertion further 3' in ahFAD2B gene.
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PMID:High-oleate peanut mutants result from a MITE insertion into the FAD2 gene. 1496 7

Indole-3-carbinol (I3C) has a liver tumor promoting activity in rats, and is also known as a cytochrome p450 1A (CYP1A) inducer. The generation of reactive oxygen species (ROS) resulting from CYP1A induction due to I3C, is probably involved in the tumor promotion. To clarify whether ROS generation contributes to I3C's induction of hepatocellular altered foci, partially hepatectomized rats were fed a diet containing 0.5% of I3C for 8 weeks with or without 0.3% N-acetyl-L-cysteine (NAC), an antioxidant, in their drinking water after N-diethylnitrosamine (DEN) initiation. Immunohistochemical analysis showed that the glutathione-S-transferase placental form (GST-P) positive foci promoted by I3C were suppressed by the administration of NAC. The mRNAs of members of the phase II nuclear factor, erythroid derived 2, like 2 (Nrf2) gene batteries, whose promoter region is called as antioxidant response element (ARE), were down-regulated in the DEN-I3C-NAC group compared to the DEN-I3C group, but Cyp1a1 was not suppressed in the DEN-I3C-NAC group compared to the DEN-I3C group. There was no marked difference in production of microsomal ROS and genomic 8-hydroxy-2'-deoxygunosine (8-OHdG) as an oxidative DNA marker between the DEN-I3C-NAC and DEN-I3C groups, while mapkapk3 and Myc were decreased by the NAC treatment. These results indicate that oxidative stress plays an important role for I3C's tumor promotion, and NAC suppresses induction of hepatocellular altered foci with suppressed cytoplasmic oxidative stress.
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PMID:Antioxidant N-acetyl-L-cysteine (NAC) supplementation reduces reactive oxygen species (ROS)-mediated hepatocellular tumor promotion of indole-3-carbinol (I3C) in rats. 2212 41