mnng 中文意思是什麼

mnng 解釋
n-甲基-n-亞硝基胍
  1. Comprehensive cellular responses was found in human amnion fl cells following exposure to low concentration of mnng, such as the lowering of dna replication fidelity resulted from alteration of dna polymerase profile ; activation of a lot of transcription factors, such as api, creb, nf - kb etc ; clustering of egfr ( epidermal growth factor receptor ) and tnfr ( tumor necrosis factor receptor ) and activation of camp - pka - creb and jnk / sapk signal pathways

    我們發現，低劑量mnng處理后的人羊膜fl細胞有廣泛的細胞反應，並有多個信號轉導通路的激活和基因表達的改變。例如dna復制保真度下降， dna聚合酶譜發生改變，應用報告基因技術和底物磷酸化檢出技術證明細胞一系列轉錄因子如ap1 、 creb 、 nf b等被激活，細胞表面受體如表皮生長因子受體、腫瘤壞死因子受體發生聚簇，細胞信號轉導通路camp - pka - creb和jnk sapk被激活。
  2. For example, we have found the clustering of egfr ( epidermic growth factor receptor ) and tnfr ( tumor necrosis factor receptor ) and the activation of camp - pka - creb and jnk / sapk pathways after mnng treatment

    例如細胞表面受體如表皮生長因子受體、腫瘤壞死因子受體發生聚簇，細胞信號轉導通路camp kacgyb和jnk sapk被激活。
  3. Our previous work identified delayed mutation occurred at target supf trna gene in plasmid transfected into cells pretreated with low concentration of alkylating agent n - methyl - n ' - nitro - n - nitrosoguanidine ( mnng )

    在收回的質粒上我們檢測到了延遲發生的、高於對照5倍以上的突變。由於w在細胞中的半壽期僅為1
  4. Monofunctional alkylating agent n - methyl - n ' - nitro - n - nitrosoguanidine ( mnng ) is a widely spread environmental mutagen and carcinogen that targets dna and proteins to generate adducts. among the adducts, o6 - alkyl guanine is the predominant mutagenic lesion because of its mispairing properties, which can eventually lead to chromosomal aberrations, point mutations, and cell death. this lesion also appears to be involved in tumor initiation, particularly in gastric carcinogenesis

    單功能烷化劑n -甲基- n -硝基- n -亞硝基胍（ mnng ）是一種在環境中廣泛存在的化學誘變劑和致癌劑，它能和dna及蛋白質等生物大分子形成加合物（ adduct ） ，其引起的與突變有關的主要dna損傷類型是o ~ 6 -甲基鳥嘌呤，這種損傷與腫瘤尤其是胃癌的發生密切相關。
  5. In our laboratory, a unique mutation detection system using a shuttle vector plasmid has been established to demonstrate that a low concentration of mnng ( 0. 2 m ) can induce nontargeted mutation in mammalian cells : the mammalian cells were exposed to 0. 2m mnng for 2. 5h, then a shuttle plasmid pz189 carrying supf trna gene was transfected into cells after 24h culture. we found a 5 - fold higher mutation frequency of the plasmid replicated in pretreated cells than the spontaneous mutation frequency of the plasmid replicated in control cells. this kind of mutation did not occur immediately after mnng exposure

    我們實驗室曾用一特殊的突變檢測系統，直接證明dna損傷劑可在哺乳動物細胞誘發非定標性突變：首先用低濃度（ 0 . 2 m ）的短壽烷化劑mnng （半壽期為1 . 1hr ）處理細胞2 . 5h后，繼續培養24h ，將重組有用作突變檢測的靶基因supftrna基因的穿梭質粒pz189轉入細胞復制，發現在未受致癌物直接攻擊的穿梭質粒中有較自發突變率高5倍以上的靶基因突變。
  6. Direct damage on supf trna gene can be neglected because half - life of mnng is 1. 1 hour and the interval between treatment and transfection was as long as 12 - 24 hours. therefore the mutagenesis is not lesion directed

    20m的mnng經洗滌后的極微量殘留經過10 ? 20多個半衰期的降解后，己不足攻擊轉人的qdna分子，因此這種突變顯然是發生在mnng直接攻擊部位以外的正常堿基上。
  7. Time - course analysis showed that the frequency of mnng induced nontargeted mutation increased gradually, reached the peak at 12 h after mnng treatment, and then declined

    且突變譜明顯不同於由mnng直接攻擊引起的定標性突變，有其突變好發部位的序列特異性。
  8. An expression vector with fragment 9 in antisense orientation was constructed to block the expression of the relevant gene ( fragment 9 related gene, fnr gene ) in vero cells. interestingly, we found that the nontargeted mutation frequency induced by mnng was increased significantly, implicating that the product of the blocked gene may be involved in the inhibition of nontargeted mutation

    利用反義核酸技術構建含反向插入9號片段的真核細胞表達重組體並轉染細胞，以獲得反義rna阻斷vero細胞中相應基因的表達，發現mn 』 ng誘發的非定標性突變頻率顯著增高，提示被阻斷的相關基因的表達產物可能參與抑制非定標性突變的發生。
  9. Thus, we hypothesized that pol p might be involved in mnng induced untargeted mutagenesis. establishment of pol p down - regulated cell line : to verify the hypothesis, a human pol p down - regulated cell line was established using an antisense rna strategy

    Lp表達阻斷的細胞系：為驗證此假設，我們用反義na技術3一i浙江大學博士學位論文王谷亮1建立了pcid表達下調的轉基因細胞系。
  10. The specific nontargeted mutation spectrum is different from that of targeted mutation, whereas the mutation occurs at damaged dna site. furthermore, we have demonstrated that low concentration mnng exposure induced comprehensive cellular responses

    進一步地，我們還證明了低濃度mnng的作用下有廣泛的細胞反應，尤其是在信號轉導通路的激活和基因表達的改變的研究中取得了一些突破性的進展。
  11. A review on the toxicological study of chemicals using gene - analytic techniques in china was introduced in the paper, main chemicals concerned are lead, cadmium, nickel, chromium, manganese, benzene, benzo ( a ) pyrene, vinyl chloride, trichlorethylene, alcohol, octyl phenol, ethyl nitrosocarbamide, mnng etc

    摘要按化學毒物的類別，概略地介紹了近年來我國基因分析技術在化學物（包括鉛、鎘、鎳、鉻、苯、苯? （ a ）芘、氯乙烯、三氯乙烯、酒精、辛基酚、乙基亞硝基脲、 mnng等）毒性檢測中的應用情況。
  12. In this research, the expression of dna polymerase p was examined in mnng treated cells, where untargeted mutation had been proved arisen

    Lp的表達：我們用western印跡方法檢測了經mnng處理后細胞中的p 。
  13. Furthermore, we found the mutagenesis relies on the alteration on gene expression profile induced by mnng treatment ; and also, the expression of dna polymerase p ( pol p ) was proved increased after mnng treatment

    這種不依賴于dna損傷的非定標性突變隨后被證明依賴于mn 』 ng引起的細胞內基因表達的變化。進一步我們用rtpcr技術證明dna聚合酶e （ p 。 lp ）的表達在mn 』 ng處理后顯著升高。
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