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- myc gene
Silencing of c-myc gene expression using enzymatically and chemically synthesized siRNAs
      
The expression of c-myc gene was found pronouncedly reduced by Western blot analysis.
      
However, the inhibition of PTPase activity may block the induction oftnf-β gene and c-myc gene transcription by IL-2 and ultimately results in cell death.
      
HeLa cells overexpressing Bcl-2 partly resist As2O3 induced apoptosis, which might be relative to preventing the cells from As2O3 caused G2/M block, downregulation of c-myc gene expression and inhibition of viral gene expression was also noted.
      
CSF-1 can induce the c-myc gene expression via Ras and Ets-related proteins.
      
JAK3 mediatesc-myc gene expression induced by interleukin-2
      
C-myc gene expression can be rapidly induced by IL-2 through intracellular signal tranduction which is triggered by the interaction between IL-2 and its rccrptor (IL-2R).
      
In the transfectants coexpressing IL-2R β and α/γ/Δ NJAK3, the stimulation of IL-2 could intensively induce c-myc gene expression.
      
It is also found that the expression of the c-myc gene is inhibited, but the p53 is enhanced.
      
Induction of C-MYC gene amplification by hydroxyurea and its inhibition by homoharringtonine
      
Induction of c-myc gene amplification in L1210 cells by hydroxyurea and its inhibition by homoharringtonine were investigated using the DNA-DNA molecular hybridization technique.
      
When the cells were treated with hydroxyurea 1.0 mM for 16 hours, and incubated a further 16 hours in a drug-free medium, the c-myc gene amplified 23.5-fold.
      
cDNA-mRNA dot blot hybridization was used to detect the c-myc gene expression level of HL-60 cells after ATRA treatment.
      
C-myc gene expression was analyzed by dot blot hybridization; its expression levels of 8, 24 or 96 hours in culture with ATRA separately were higher, low, high or lower as compared with each other.
      
It was suggested that hypoxia could promote the proliferation of PC by up-regulating the expression of c-myc gene, but c-myc antisense ODNs could inhibit hypoxia-induced proliferation of PC by downregulating the expression of c-myc gene.
      
To further define the immunophenotypic and molecular genetics of these tumors, we investigated two cases of plasmablastic lymphomas of the head and neck for c-myc gene rearrangement and immunoglobulin heavy chain (IgVH) hypermutation status.
      
For the first time we report a case of AIDS-related PBL that, by fluorescence in?situ hybridization (FISH), shows a c-myc gene rearrangement.
      
Although current literature suggests that most cases of c-myc gene rearranged AIDS-NHL are Burkitt's lymphoma, our case has an immunophenotype characteristic for PBL.
      
Background: Burkitt's lymphoma is a B-cell neoplasm characterized by a chromosomal translocation involving the c-myc gene.
      
Background: Burkitt's lymphoma (BL) and B-ALL are characterized bychromosomal translocations juxtaposing the c-myc gene on chromosome 8to one of the immunoglobulin loci.
      
 

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