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1 ocopy of the effect of inactivation of the c-src gene.
2 3'ss of the heterologous Rous sarcoma virus src gene.
3 from animals with targeted disruption of the src gene.
4 cell line, 10W, transfected with the avian c-src gene.
5 rfect direct repeat sequences that flank the src gene.
6 downstream control sequence (DCS) from the c-src gene.
7 these genes differed significantly from the src genes.
8 d with a recombinant retrovirus carrying a v-src gene after 2, 7, 14, 21, and 28 days of continuous g
9 ive revertants in which the src 3'ss and the src gene are deleted by homologous recombination at seve
10 g direct repeat (DR) elements that flank the src gene; at least one copy of the DR sequence is necess
13 pendent process because viruses with deleted Src gene did not induce the transcription of the PLAU ge
14 activation may be mediated by members of the Src gene family following cytokine/growth factor stimula
18 he direct repeat (DR) sequences flanking the src gene in Rous sarcoma virus are essential posttranscr
20 ion of a dominant-inhibitory Raf-1 and the v-Src genes into H19-7 cells results in an inhibition of t
21 The primary defect in mice lacking the c-src gene is osteopetrosis, a deficiency in bone resorpti
22 In addition, the presence of an oncogenic src gene or microinjected Ras protein increased drug tox
23 ern of Hydra Csk with that of STK, the Hydra Src gene orthologue, reveals that the two genes are larg
25 f mice with a disruption in both the fyn and src genes shows intrinsically reduced tyrosine phosphory
26 now known to be a retrovirus encoding the v-src gene, significant progress has been made in defining
27 irect repeat (DR) sequences flanking the RSV src gene; similar activity was observed for the upstream
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