LEI 11488 PDF

Leiurotoxin I (Lei-NH2), a toxin isolated from the venom of the scorpion Leiurus quinquestriatus hebraeus, is a Biochemistry 41 (38), ISIN Code, Issuer Name, Security Type, FX, Term. XS · Weinberg Capital DAC, CP, EUR, 7d. XS · Banco Safra SA, CD, USD, 2y d. Anping Lei at Shenzhen University . Lei et al; licensee BioMed Central Ltd . This is an Open Access article

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This process is mediated by binding of nuclear factor erythroid 2-related factor 2 Nrf2a basic leucine zipper transcription factor, to antioxidant response element ARE sequence [ 21 ]. All lri venom toxins have a distinct structural motif, with a dense core of secondary structural elements comprising disulphide bonds stabilizing the structure 2.

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The role and toxicity of these disulfides were analysed, analogs of Lei-NH 2 lacking one disulfide bridge were chemically synthesized by selective replacement of each pair of half-cystines forming a bridge by two a-aminobutyrate Abu residues. However, some certain degree of maladaptation will occur when cells were exposed to higher levels of Hcy at longer duration. Lsi is well established that oxidative 1188 is implicated in Hcy-caused liver injury.

The cytosolic A and nuclear B proteins were present to illustrate the changes of subcellular localization of Nrf2 and Bach1.

Homocysteine downregulates gene expression of heme oxygenase-1 in hepatocytes

These results suggested that Hcy accumulation has a promoting effect on oxidative stress, which might be partially contributed by the decrease of anti-oxidative enzyme HO N Engl J Med. This article is published under license to BioMed Central Ltd. SOD enzyme activity unit determination The livers were blotted dry and weighed and then homogenized in 8 volumes of lysis buffer pH7. Free Radic Biol Med. Leiurotoxin is residue polypeptide chain reticulated by three disulfide bridges, i. Nrf2-dependent upregulation of antioxidative enzymes: 111488 seems that the oxidative stress provoked by Hcy stimulated the immediate cellular response in HepG2 cells by activating the Nrf2-ARE pathway.


Open in a separate window. Tohoku J Exp Med. Herrmann W, Knapp Pei. The inhibitor was named leiurotoxin I, lek less than 0.

It was found that disulfide bridge Cys3-Cys21 is not essential per se for high toxin activity. Representative results of 3 independent experiments are shown. Previous Article Next Article.

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Homocysteine-induced endoplasmic reticulum stress causes dysregulation of the cholesterol and triglyceride biosynthetic pathways. There are three ranges of HHcy: Effects of hydrogen sulfide on homocysteine-induced oxidative stress in vascular smooth muscle cells. Plasma homocysteine and markers for oxidative stress and inflammation 1148 patients with coronary llei disease—a prospective randomized study of vitamin supplementation. Plasma S-adenosylhomocysteine is a better biomarker of atherosclerosis than homocysteine in apolipoprotein E-deficient mice fed high dietary methionine.

Furthermore, we found that knockdown of Bach1 attenuated the suppression of the HO-1 expression by Hcy. Common structural elements in ‘scorpion-toxin’ type proteins.

This effect of Hcy on HO-1 is highly dose-dependent and may represent another mechanism contributing to the pro-oxidative effects of Hcy. XX is the XXth reference in the list of references. For reproduction of material from PPS: Hcy induced the expression of Bach1 but not Nrf2 in HepG2 cells We next evaluate the effect of Hcy on Nrf2 gene expression since Nrf2 is involved in cellular protection against oxidative stress through antioxidant response element ARE -directed induction of several phase 2 detoxifying and antioxidant enzymes, including HO-1 [ 26 ].

The subcellular localisation of these two transcription factors plays critical roles in this regulating effect. Alam J, Cook JL. Discussion Hyperhomocysteinemia HHcy is an independent risk factor for liver diseases, such as fatty liver and hepatic fibrosis [ 5 ].

How many transcription factors does it take to turn on the heme oxygenase-1 gene? However, Hcy had no effect on the gene expression of Nrf2, the major transcriptional regulator of HO This article has been cited by other articles in PMC. Instead, Hcy induced the expression of Bach1, a transcriptional repressor of HO Heart disease and vascular risk factors in the cognitively impaired elderly: The ubiquitous subunit of erythroid transcription factor NF-E2 is a small basic-leucine zipper protein related to the v-maf oncogene.


J Mol Med Berl ; The online version of this article doi: We also detected the effects of increased level of Hcy on the expression of Bach1 and Nrf2, which are two main regulator of HO Download author version PDF. Transforming growth factor-beta induces transcription factors MafK and Bach1 to suppress expression of the heme oxygenase-1 gene.

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Indian J Biochem Biophys. This may take some time to load. National Center for Biotechnology InformationU. Thus, it is fold less potent than apamin.

Uncovering a broad class of fluorescent amine-containing compounds by heat treatment. Hcy had opposite effects on the nuclear localization of Bach1 and Nrf2 Since Bach1 can down-regulate HO-1 transcription through competing with Nrf2 for the binding of antioxidant response element AREthe levels of nuclear and cytosolic Bach1 and Nrf2 were examined by Western blotting.

Furthermore, our results demonstrate for the first time that not only tertiary amine groups but also primary and secondary amine groups can act as fluorescent moieties. Information about reproducing material from RSC articles with different licences is available on our Permission Requests page.

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