• <code id="tvhzc"><ol id="tvhzc"></ol></code>
    <big id="tvhzc"><span id="tvhzc"></span></big>
  • <object id="tvhzc"><strong id="tvhzc"></strong></object>
    首頁> 外文期刊>Biochimica et Biophysica Acta. General Subjects >Selenium-binding protein 1: Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8- tetrachlorodibenzo-p-dioxin
    【24h】

    Selenium-binding protein 1: Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8- tetrachlorodibenzo-p-dioxin

    機譯:硒結合蛋白1:其生理功能,對芳烴受體的依賴性以及在2,3,7,8-四氯二苯并-p-二惡英的消瘦綜合征中的作用

    獲取原文
    獲取原文并翻譯 | 示例
               

    摘要

    Background Selenium-binding protein 1 (Selenbp1) is suggested to play a role in tumor suppression, and may be involved in the toxicity produced by dioxin, an activator of aryl hydrocarbon receptors (AhR). However, the mechanism or likelihood is largely unknown because of the limited information available about the physiological role of Selenbp1. Methods To address this issue, we generated Selenbp1-null [Selenbp1 (-/-)] mice, and examined the toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in this mouse model. Results Selenbp1 (-/-) mice exhibited only a few differences from wild-type mice in their apparent phenotypes. However, a DNA microarray experiment showed that many genes including Notch1 and Cdk1, which are known to be enhanced in ovarian carcinoma, are also increased in the ovaries of Selenbp1 (-/-) mice. Based on the different responses to TCDD between C57BL/6J and DBA/2J strains of mice, the expression of Selenbp1 is suggested to be under the control of AhR. However, wasting syndrome by TCDD occurred equally in Selenbp1 (-/-) and (+/+) mice. Conclusions The above pieces of evidence suggest that 1) Selenbp1 suppresses the expression of tumor-promoting genes although a reduction in Selenbp1 alone is not very serious as far as the animals are concerned; and 2) Selenbp1 induction by TCDD is neither a pre-requisite for toxicity nor a protective response for combating TCDD toxicity. General significance Selenbp1 (-/-) mice exhibit little difference in their apparent phenotype and responsiveness to dioxin compared with the wild-type. This may be due to the compensation of Selenbp1 function by a closely-related protein, Selenbp2.
    機譯:背景技術硒結合蛋白1(Selenbp1)被認為在腫瘤抑制中發揮作用,并可能參與芳烴受體(AhR)活化劑二惡英產生的毒性。但是,由于有關Selenbp1的生理作用的可用信息有限,因此該機制或可能性很大程度上未知。方法為了解決這個問題,我們產生了Selenbp1-null [Selenbp1(-/-)]小鼠,并檢查了2,3,7,8-四氯二苯并-p-二惡英(TCDD)的毒性作用。結果Selenbp1(-/-)小鼠的表型與野生型小鼠僅表現出少量差異。但是,DNA微陣列實驗顯示,包括Notch1和Cdk1在內的許多基因在Selenbp1(-/-)小鼠的卵巢中也會增加,這些基因在卵巢癌中被稱為增強。根據C57BL / 6J和DBA / 2J小鼠對TCDD的不同反應,提示Selenbp1的表達受AhR的控制。但是,在Selenbp1(-/-)和(+ / +)小鼠中,TCDD造成的浪費綜合征也同樣發生。結論以上證據表明:1)Selenbp1抑制腫瘤促進基因的表達,盡管就動物而言,單獨減少Selenbp1并不嚴重; 2)TCDD誘導Selenbp1既不是毒性的先決條件,也不是對抗TCDD毒性的保護性反應。一般意義Selenbp1(-/-)小鼠的表型和對二惡英的反應性與野生型相比幾乎沒有差異。這可能是由于緊密相關的蛋白質Selenbp2對Selenbp1功能的補償。

    著錄項

    相似文獻

    • 外文文獻
    • 中文文獻
    • 專利
    獲取原文

    客服郵箱:kefu@zhangqiaokeyan.com

    京公網安備:11010802029741號 ICP備案號:京ICP備15016152號-6 六維聯合信息科技 (北京) 有限公司?版權所有
    • 客服微信

    • 服務號

    在线中文字幕日本无码欧美_国产萝控精品福利视频_2020黄色三级片电影_人妻系列在线亚洲
  • <code id="tvhzc"><ol id="tvhzc"></ol></code>
    <big id="tvhzc"><span id="tvhzc"></span></big>
  • <object id="tvhzc"><strong id="tvhzc"></strong></object>