Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding of aflatoxin B1, AFB1, a potent hepatocarcinogen, to various high molecular weight (HMW) DNAs from human normal liver and two liver cancer cell lines, Alexander primary liver carcinoma (PLC) and Mahlavu hepatocellular carcinoma (hHC) and from NIH/3T3 cell have been investigated. The kinetics of AFB1 binding to these DNAs showed similar initial rates but the extents of binding to the PLC and hHC DNAs seemed to be slightly higher. Preferential AFB1 bindings were identified in both PLC and hHC DNAs compared to normal liver DNA when analyzed by restriction endonuclease digestions and agarose gel electrophoresis. A critical AFB1 binding dosage, ranging 100 to 460 fmole/microgram DNA, was found to activate the carcinogenic effect of the Mahlavu hHC HMW DNA, but not normal liver HMW DNA, rendering it capable of inducing focal transformation in NIH/3T3 cell. Excessive AFB1 binding on the hHC and PLC HMW DNAs resulted in an "over-kill" of both cell transformation capability and templating activity of the DNA.
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PMID:Dose dependency of aflatoxin B1 binding on human high molecular weight DNA in the activation of proto-oncogene. 300 75

Long interspersed nucleotide element (LINE-1; L1) as an autonomous retrotransposon is localized usually in AT-rich, low-recombined, and gene-poor regions of genome. It is transiently activated in embryonic development and continuously activated in all tumor cells tested so far. Full-length L1 gene contains 5' untranslated region, two open reading frames (ORFs) encoded L1ORF1p and L1ORF2p, and a 3' terminal polyadenylation site. Compared with L1ORF2p, a protein encompassing reverse transcriptase and endonuclease activities, L1ORF1p remains to be elucidated. With liver cancer cells and tissues, the expression and sub-localization of L1ORF1p were investigated and shown that L1-ORF1p expresses just in liver cancer cells and tissues but not in normal liver cells and almost not in adjacent tissues. To characterize L1ORF1p, the strategies for over-expression and down-regulation of L1ORF1p in transfected cells were implemented. The phenomenon of promoting cell proliferation and colony formation was observed in transfected cells with L1ORF1p over-expression and vice versa. Down-regulation of L1ORF1p suppresses tumorigenesis in vitro and in vivo. Smad4 as an interaction protein of L1ORF1p is identified for the first time, while L1ORF1p is responsible for Smad4 sequestration in the cytoplasm. Thus, L1ORF1p contributed to tumorigenesis and may attribute to, at least partly, its participation in Smad4-signaling regulation.
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PMID:L1-ORF1p, a Smad4 interaction protein, promotes proliferation of HepG2 cells and tumorigenesis in mice. 2386 96