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   myc oncogene 的翻译结果: 查询用时:0.205秒
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肿瘤学
眼科与耳鼻咽喉科
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myc oncogene     
相关语句
  myc癌基因
     Co operative Expression of P 53 、 ras P 21 and C myc Oncogene proteins in Brain Astrocytomas
     脑星形细胞瘤P~(53)、ras-P~(21)、C-myc癌基因蛋白协同表达的观测
短句来源
     Ocular metastasis of neuroblastoma and amplification of N myc oncogene
     神经母细胞瘤眼部转移与N-myc癌基因扩增的临床意义
短句来源
     Detection of c myc Oncogene Amplification During Induced Differentiation of HL 60 Cells
     应用PCR检测HL-60细胞诱导分化前后c-myc癌基因的扩增
短句来源
     Conclusion (1) Hypoxia may lead to activation of C myc oncogene and increase of FGF b expression in lung tissue.
     结论(1)缺氧可激活C-myc癌基因以及增强FGF-b的表达;
短句来源
     Methods The relationship between molecular chaperone Grp94 and c myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX 1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c myc cDNA probe spot bybridization and RT PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3′ end oligonucletide primers was investigated.
     方法应用地高辛标记c-myccDNA探针的斑点杂交,和以Grp94基因近3′端一对寡核苷酸为引物的RT-PCR技术,比较了人大肠癌细胞系CCL229、CX-1以及经维甲酸诱导的CCL229细胞中Grp94和c-myc癌基因在表达上的关系。
短句来源
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  myc基因
     Apoptosis Induced by Etoposide in PC-3 Cells with bcl-2 and c myc Oncogene Expression
     VP-16诱导PC-3细胞凋亡和bcl-2及c-myc基因表达的研究
短句来源
     )Objective To study the changes of PCNA and C myc oncogene overexpression and it's clinical value in CIN and cervical squamous carcinoma.
     目的:研究增殖细胞核抗原(PCNA)及C-myc基因过度表达在子宫颈上皮内瘤变(CIN)及子宫颈鳞癌中的变化及其临床意义。
短句来源
     Methods A series of 59 lung cancer specimens were analyzed for p53, myc oncogene family and mdrl gene by DNA/PCR sequencing, immunohistochemistry and RT PCR methods.
     方法采用免疫组化、DNA/PCR直接测序及RT-PCR方法对59例原发性肺癌组织p53、myc基因和mdrl基因进行检测。
短句来源
     Objective To study the effects of amplification of N myc oncogene on the oculometastasis and prognosis of neuroblastoma (NB).
     目的通过定量研究小儿神经母细胞瘤(NB)N-myc基因扩增倍数,观察NB眼部转移以及与预后的关系。
短句来源
     olymerase chain reaction(PCR) was used to study c myc oncogene amplification of HL 60 cells during the differential induction by retinoic acid(RA) and dimethyl sulfoxido(DMSO).
     应用PCR方法研究了维甲酸(RA)和二甲基亚砜(DMSO)诱导HL-60细胞分化过程中c-myc基因扩增的变化。
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  myc原癌基因
     Conclusion Losartan possesses inhibitive effects on the proliferation of VSMC and the expression of c myc oncogene.
     结论  Losartan 抑制 V S M C 的增殖及cmyc原癌基因的表达。
短句来源
  myc族癌基因
     The relationship between myc oncogene and metastasis and invasion of esophygeal carcinoma
     myc族癌基因与食管癌浸润和转移的关系
短句来源
     A relative study on the expression of myc oncogene and esophageal carcinoma
     Myc族癌基因与食管癌相关性的研究
短句来源
     Objective To study the relationship between myc oncogene and the biologic behavior and prognosis of esophageal carcinoma.
     目的 通过检测食管癌组织中myc族癌基因的扩增情况探讨myc族癌基因与食管癌发生、发展及预后的关系。
短句来源
     Conclusion myc gene had close relationship with metastasis and invasion of esophygeal carcinoma the expression of myc oncogene may be a new indicator to assess the prognosis of esophygeal carcinoma.
     结论 :myc族癌基因的过表达与食管癌的浸润和转移关系密切 ,m yc基因的表达情况可作为评价食管癌预后新的指标。
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      myc oncogene
    In a previous study, a replication-defective recombinant Moloney murine leukemia virus containing the v-myc oncogene was generated (M-MuLV(myc); Brightman B.K., Pattengale P.K., and Fan H., J Virol 60: 68-81, 1986).
          
    On the other hand, the combine treatment of 18:1/DHA-PE and dbcAMP markedly reduced the expression level of c-myc oncogene during 48 h incubation.
          
    In this paper, we studied the interaction of the human isoform B of nucleoside diphosphatekinase (NDP kinase B) with the nuclease hypersensitive element (NHE) present in the promoterelement of the c-myc oncogene.
          
    The cyclopentenone PGs inhibit myc oncogene expression while inhibiting the cell cycle progression and results in apoptotic cell death and growth inhibition.
          
    The CTCF gene encodes for a transcriptional repressor of the c-myc oncogene and has previously been mapped to one of the smallest regions of overlapping interstitial deletions on chromosome 16q22.1 in invasive breast cancer.
          
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    Expression of c-myc oncogene of myeloma cells and their changes after hybridization in homo-and hetero-cellular cybrid and hybrid were studied with Northern-blot and dot-blot techniques, using cloned c-myc gene as a probe. Results indicated that c-myc oncogene transcripts could not be detected in cybrids of mouse X mouse (BW-RM), mouse X rabbit (BW-RR) and human X mouse (HMy-RM) hybridization. However, weak transcription of this oncogene was shown to be active in cybrids after 15th passages...

    Expression of c-myc oncogene of myeloma cells and their changes after hybridization in homo-and hetero-cellular cybrid and hybrid were studied with Northern-blot and dot-blot techniques, using cloned c-myc gene as a probe. Results indicated that c-myc oncogene transcripts could not be detected in cybrids of mouse X mouse (BW-RM), mouse X rabbit (BW-RR) and human X mouse (HMy-RM) hybridization. However, weak transcription of this oncogene was shown to be active in cybrids after 15th passages with a tendency of increasing expression activity noted during later subcultures. Similarly, no detectable c-myc gene transcript was seen in 4th and 7th subcultures of hetero-cellular hybrids (mouse plasmocytoma Sp 2/0 X rat erythroblasts, SP-ER), suggesting that "cy-toplasmic factor" of erythroid cells could inhibit or reduce expression of originally active c-myc, the inhibition being nonspecific in both cybrid and hybrid and reduction of expression of oncogene closely related to decrease or reversion of malignancy of tumor cells. Mechanisms of regulatory effects of erythroid cell cytoplasmic factors and molecular basis for oncogene repression in tumor cells were discussed.

    本实验用Northern杂交方法,以c-myc癌基因为探针,对人和小鼠骨髓瘤细胞以及杂交后的同种和异种胞质体杂交细胞和异种杂交细胞进行了癌基因表达的核酸分子杂交分析。结果表明,在小鼠-小鼠,小鼠-兔及人-小鼠的胞质体杂交细胞(BW-RM,BW-RR,HMy-RM)中均未检测到myc癌基因的表达产物。但自15代以后开始出现微弱或可测的表达活性,并随传代而有上升的趋向。同样,在小鼠浆细胞瘤(Sp2/o)与大鼠有核红细胞(ER)的异种杂交中,杂交细胞(SpER)的第4代和第7代细胞中亦未检查到myc基因转录物。表明细胞杂交后,myc基因受到了抑制。这种抑制作用似无种属特异性。这一结果提示红系细胞内“胞质因子”对肿瘤细胞原来活化的myc基因具有抑制作用,并与杂交细胞的恶性下降有关。论文对胞质因子对癌基因表达的调控作用及其分子生物学机理进行了讨论。

    A human promyelocytic leukemia cell mutant (HL-60-AR) with characteristics of resistance to 8-azagunine and deficient in hy-poxanthine and guanine phosphoribosyltrans-ferase had been established from HL-60 cell line in our laboratory.The previous study showed that HL-60-AR mutant cells main-tained the basic biological characteristics and potence of differentiation induced by various compounds of their parental HL-60 cells.In order to investigate the dependence of inducer presence for HL-60-AR cell differentiation,the...

    A human promyelocytic leukemia cell mutant (HL-60-AR) with characteristics of resistance to 8-azagunine and deficient in hy-poxanthine and guanine phosphoribosyltrans-ferase had been established from HL-60 cell line in our laboratory.The previous study showed that HL-60-AR mutant cells main-tained the basic biological characteristics and potence of differentiation induced by various compounds of their parental HL-60 cells.In order to investigate the dependence of inducer presence for HL-60-AR cell differentiation,the present experiment was designed that HL-60-AR cells were washed for 3 times to re-move inducer after treatment for various pe-riod,and suspended in medium without indu-cer,then assayed expression of cell differen-tiated characters.Meanwhile,the cultures in which inducer was removed were passaged se-veral generations and assayed to determine the passage hereditary stablization of cell dif-ferentiated characters. Experimental results showed that when HL-60-AR cells incubated in medium without inducer after they had a previous treatment with 10~(-6)M RA for 24 hours,the cell dif-ferentiated characters could be continuous ex-pression and the number of differentiated cells was progressively increased.The increase of NBT reduction positive cells and cell mem-brane C_3 complement receptor positive cells de-tected by YC rosette formation was indepen-dent on the duration of incubation between cells and RA,but it does depend on the ad-ditive duration of cell exposure to RA-contai-ning medium and RA-free medium.The cells which exposed to RA for 24 hours and rein-cubated in RA-free medium for another 120 hours showed kinetics of numbers of differen-tiated cells similar to cells exposed RA for 144 hours (Fig.3,4).This result indicated that cellular commitment to differentiation re-quired an approximately 24 hour exposure to RA.Following this,committed cells continued to differentiate.However,cell differentiated characters induced by DMSO was unstable and reversible. A notable result happened when RA-induced cells were suspended in conventional culture medium and passaged for 3 times,the number of differentiated cells could be de-tected as high as 50 percent.Taken togather the results indicate that after exposure to RA for 24 hours,a significant cell differentiation could be required and cell in populations re-moved from RA thereafter continued to diffe-rentiate.The expression of differentiated cha-racters was irreversible and heritable,exten-ding from parent to daughter cells. It was showed that a cell proliferative arrest could be assayed as HL-60-AR cell dif-ferentiation.The differentiated cells decreasedcell DNA synthesis and number of colony-forming in soft agar medium,and lost the ability of tumor-producing in nude mice.A rapid decrease of c-myc oncogene expression detected by molecular hybridization at the ear-ly stage of RA-treatment indicated that the inhibition of c-myc gene expression might provide some clues for explaining the primary-process and molecular mechanism of HL-60-AR cell differentiation.

    HGPRT~-人早幼粒白血病细胞突变株(HL-60-AR)与RA保温一定时间后,洗去药物继续培养,细胞分化性状(NBT还原能力、细胞膜C_3补体受体及形态变化)不但继续存在,而且能持续表达。撤去RA后连续传代培养,至少在传三代后细胞分化性状仍高度表达。然而,DMSO对HL-60-AR细胞的作用特点明显不同于RA。HL-60-AR细胞分化伴随增殖能力的降低。核酸分子杂交结果表明,细胞c-myc癌基因表达受抑先于细胞分化性状的获得和增殖能力的下降。

    Expression of the C-myc oncogene is tightly regulated in a normal cell, but is often, although not always, enhanced in some types of tnmor cells. We have previously suggested that a normal cell is equipped with a secure mechanism, possibly a cis-acting gene-to-gene interaction, ensuring that constitutive or excessive C-myc activity does not occur. In the present experiment, we examined this possibility using a mouse genomic C-myc clone. We present evidence that a novel transcription unit (...

    Expression of the C-myc oncogene is tightly regulated in a normal cell, but is often, although not always, enhanced in some types of tnmor cells. We have previously suggested that a normal cell is equipped with a secure mechanism, possibly a cis-acting gene-to-gene interaction, ensuring that constitutive or excessive C-myc activity does not occur. In the present experiment, we examined this possibility using a mouse genomic C-myc clone. We present evidence that a novel transcription unit ( "gene" ) , presumably 15-30 kb long, lies 2.4-3.4 kb upstream from C-myc in the same transcriptional orientation and actively produces a single species of 5.8 kb transcript in normal cells where C-myc RNA is hardly detected. The observed intergenic distance between the C-myc and tne neighbouring "gene" is much shorter than the length defined as necessary for a pair of simultaneously active genes.Consequently, C-myc is thought to be under transcriptional interference from the neighbouring "gene" .

    本文利用cDNA探针,以Southern杂交在C-myc 5′上游区域发现了一段活跃转录的序列(文中称“旁侧基因”)。对该基因克隆及进一步分析表明,能与cDNA杂交的序列存在于距C-myc 5′端约2.4kb的Sma Ⅰ片段中。Northern杂交显示,该旁侧基因在不同组织均有表达,产物为5.8kb,推断该基因为15~3.5kb。以旁侧基因部分序列为探针,在不同种属的基因组中检测出单拷贝序列,提示该基因在进化上的保守性。RNase Mapping分析发现此旁侧基因与C-myc转录方向相同,转录终止在C-myc5’上游约2.4~3.4kb区域。根据基因领域效应及本文结果,我们推测,在正常细胞中,由于旁侧基因的领域效应,使C-myc保持相对静止状态,而在肿瘤细胞中,染色体转位或原病毒插入,破坏了旁侧基因的领域效应,使C-myc表达增高。

     
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