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c myc     
相关语句
  c-myc
     However c myc and met D highly expressed in OS 732 cells after and before 1,25(OH) 2D 3 treatment.
     而在1,25(OH)2D3作用前后OS-732细胞c-myc和metD基因均处于高度活跃表达状态。
短句来源
     The intensity of bcl 2 and C MYC gene expression in colorectal carcinoma was significantly higher than that in colorectal adenoma or normal mucosa ( χ 2 = 4.98 - 16.84 ,P <0.05).
     大肠癌bcl-2和C-MYC的表达强度均显著高于大肠腺瘤或正常大肠黏膜(χ2=4.98~16.84,P<0.05)。
短句来源
     The results demonstrated that the expression of c myc and CDK4 is lower in HTB1 than that in HT29 cells.
     其结果表明:c-myc和CDK4在HTB1中的表达低于在HT29中的表达;
短句来源
     The molecular mechanisms of TGF β 1 inducing HL 60 cell apoptosis maybe that TGF β 1 can effectively down regulate the expression of bcl 2 gene and c myc gene in HL 60 cells.
     实验发现TGF-β1可显著诱导HL-60细胞凋亡,TGF-β1下调HL-60细胞bcl-2、c-myc基因的表达可能是其诱导凋亡的分子机制之一。
短句来源
     p 53 overexpression correlated with overexpression of C erbB 2 and C myc.
     p53与C-erbB2及C-myc过度表达间呈正相关。
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  cmyc
     The expression intensity of c myc gene was markedly higher in GC+DENA group that in DENA group.
     cmyc基因表达强度GC+DENA组明显高于DENA组。
短句来源
     Conclusion:As2O3 can induce GLC 82 cell apoptosis mainly with regulation of c myc,p53 and p16 gene expression.
     结论:As2 O3 能显著抑制GLC82 细胞生长、诱导细胞凋亡,并主要通过调节cmyc,p16 和p53 等基因的表达来实现。
短句来源
     Detection of P53 and c myc with immunohistochemical technique were carried out for 34 surgical specimens of malignant tumor of adrenal gland,25 adrenal benign tumors and in 12 adrenal tissues free of tumor.
     为探讨肾上腺肿瘤发病机理,为鉴别肿瘤良恶性及其分级分期提供依据,收集34例肾上腺恶性肿瘤应用SP法作P53及cmyc免疫组化检测,并与25例肾上腺良性瘤及12例非瘤肾上腺组织对比。
短句来源
     Methods The pathological features of EPS were observed in 17 cases, and the expressions of HCG, HPL, EMA, PRL, PLAP, Vim, actin, c erbB 2 and c myc were analyzed immunohistochemically.
     方法:对17 例经病理检查诊断为EPS的病例进行病理学形态观察,采用免疫组化方法标记滋养细胞HCG、HPL、EMA、PRL、PLAP、Vim 、actin、cerbB2 和cmyc
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     Results: The positive expression rates of P 53 , ras P 21 and C myc were 26%, 44% and 36% respectively.
     结果:星形细胞瘤P53、P21、Cmyc基因蛋白的表达率分别为26%、44%及36%。
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  cmyc基因
     Positive expression of c myc in grade 1 to 2 was 68.2% (15/22), and 27.3% (3/11) in grade 1 (P<0.05).
     ⅡⅢ度睑板腺癌c myc基因阳性表达率为 68.2 % ( 15 / 2 2 ) ,Ⅰ度为 2 7.3 % ( 3 / 11) ,P <0 .0 5 ;
短句来源
     Results The rates of positive staining for p16, p53 and c myc were 34.8%, 95.7% and 100% for malignant GST,and 45.5%, 77.3% and 90.9% for borderline GST,and 65.4%, 73.1% and 65.4% for benign GST respectively.
     结果  71例GST中p1 6、p53、c myc基因蛋白阳性表达率分别为 :恶性 34 .8%、95 .7%、1 0 0 % ; 交界性 45 .5 %、77.3 %、90 .9% ;
短句来源
     Purpose:To investigate Fas&FasL、C myc expression and testicular germ cell apoptosis in experimental cryptorchidism.
     目的 :探讨Fas/FasL和C myc基因表达与隐睾生殖细胞凋亡的关系 ,以及C myc与Fas/FasL介导的细胞凋亡途径之间的关系。
短句来源
     Positive rate of c myc in poorly differentiated group was 69.6% (16/23) and 20% (2/10) in well differentiated group(P<0.05).
     中低分化睑板腺癌c myc基因阳性表达率为 69.6% ( 16/ 2 3 ) ,高分化癌为 2 0 % ( 2 / 10 ) ,P <0 .0 5。
短句来源
     Results: Positive rate of nm23 mRNA in meibomian gland carcinoma was 48.5% (16/33), and positive rate of c myc expression was 54.6% (18/33).
     结果 :睑板腺癌nm2 3基因mRNA阳性表达率为 4 8.5 % ( 16/ 3 3 ) ,c myc基因阳性表达率为 5 4 .5 % ( 18/ 3 3 )。
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  cmyc蛋白
     Results:The rates of positive immunostaining of cyclin D1,P53 and c myc in gastric carcinoma were 32.75% ,25.40% and 52.38%,respectively.
     结果 :63例胃癌中cyclinD1、P53及c myc蛋白染色阳性率分别为 32 .75 %、2 5 .40 %及 52 .38% ;
短句来源
     Methods After treatment of HepG 2 cells with 0~1.5 g/L matrine for 3 d, the protein expressions of AFP, PCNA, wp53, Rb, N ras and c myc were detected with immunocytochemical method, mRNA expressions of wp53, c myc with in situ hybridization;
     方法  0~ 1 5g/L苦参碱作用HepG2 细胞 3d ,免疫组化检测AFP、PCNA、wp5 3、Rb、N ras、c myc蛋白的表达 ,原位杂交法检测wp5 3、c mycmRNA的表达 ,真彩色图像定量分析检测结果 ,Microsoft-Excel软件统计学处理结果 ;
短句来源
     The results show that ox LDL could upregulate the gene expression of c fos,c jun and c myc, which induced the apoptosis of U937 cells.
     ox LDL可以上调c fos、c jun和c myc基因表达 ,使c fos、c jun和c myc蛋白合成增多 ,最终诱导U937细胞凋亡 .
短句来源
     The expression of bcl 2 was positively correlated with the expression of c myc(γ=0.517,γ=0.636, P <0.05) in MAWPL and IM.
     bcl 2和c myc蛋白表达在癌旁伴癌前病变粘膜和移行粘膜呈正相关 (γ =0 .5 17,γ =0 .6 36 ,P <0 .0 5 )。
短句来源
     The expression of cyclin D1,P53 and c myc proteins in gastric carcinoma ≥ 4 cm in diameter was significantly higher than those <4 cm.
     最大径≥ 4cm胃癌cyclinD1、P53及c myc蛋白染色阳性率明显高于 <4cm的胃癌 (P <0 .0 5) ;
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      c myc
    We have not known the reason why expression of c-myc on SGC-7901 cells is lower than that in negative control, and this needs further studies.
          
    Western blotting was performed to confirm the expression of the fusion protein using anti-c-myc monoclonal antibody.
          
    We have shown here that TIS7 inhibits OPN as well as c-Myc gene expression.
          
    Western blot analysis was performed with mouse monoclonal anti-c-Myc or anti-HA antibodies, as indicated on the left side of the figure.
          
    We map bvr-l and pvt-l about 140 and 260 kilobase pairs, respectively, distal from c-myc.
          
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    Expression of seven oncogenes and their cha nges after induced differentiation in a HGPRT- human promyelocytic leukemia cell mutant (HL-60-AR) were studied by Northern blot and dot blot techniques. Results indicated that in HL-60-AR cells, the c-myc gene was highly expressed, while oncogenes of H-ras, fos, sis, abl and erb-B although expressed actively, yet lower than that of c-myc. The expression of K-ras gene, however, was weak or undetectable. When HL-60-AR cells were chemically induced...

    Expression of seven oncogenes and their cha nges after induced differentiation in a HGPRT- human promyelocytic leukemia cell mutant (HL-60-AR) were studied by Northern blot and dot blot techniques. Results indicated that in HL-60-AR cells, the c-myc gene was highly expressed, while oncogenes of H-ras, fos, sis, abl and erb-B although expressed actively, yet lower than that of c-myc. The expression of K-ras gene, however, was weak or undetectable. When HL-60-AR cells were chemically induced to differentiate, the expression of c-myc was significantly decreased. Decrease in expression of H-ras, fos, sis, abl and erb-B oncogenes could also be observed, but without change of K-ras during cell differentiation. Our data also indicated that the decrease in c-myc gene expression after induced differentiation was not due to the decrease of number of c-myc gene copy, but mainly a transcriptional regulation pf c-myc.

    用Northern杂交和斑点杂交方法分别探测HL-60-AR细胞中七种癌基因的表达及其在诱导分化后的变化。结果表明,在HL-60-AR细胞中c-myc基因高度活跃表达,H-ras基因次之,fos、sis、abl和erb-B基因表达微弱,而K-ras基因表达极微弱或检测不出。当HL-60-AR细胞被药物诱导成熟分化后,c-myc基因表达大为下降,H-ras、fos、sis、abl和erb-B基因表达亦相应降低,而K-ras的表达则无变化。对诱导分化前后c-myc基因拷贝数的比较分析表明,c-myc基因表达下降可能主要发生在基因的转录或/和转录后调节水平。

    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...

    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。

     
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