Fig. 2.
Fig. 2. Inhibition of AML1-MTG8–induced up-regulation of G-CSFR by AML1b. / (A) Expression of AML1b and AML1-MTG8 protein detected by Western blot analyses. L-G cells infected with LXSH or LXSH-AML1-MTG8 were further infected with LNSX-AML1b viruses and the protein extracts from the infectants were analyzed by immunodetection using anti-HA antibody. The positions of AML1 and AML1-MTG8 are indicated by arrows. (B) Northern blot analyses showing the expression of G-CSFR mRNA. Total RNAs (5 μg of RNA) were prepared from L-G infectants cultured with IL-3, blotted, and hybridized with 32P-labeled mouse G-CSFR cDNA, mouse MPO cDNA, and human G3PDH cDNA.

Inhibition of AML1-MTG8–induced up-regulation of G-CSFR by AML1b.

(A) Expression of AML1b and AML1-MTG8 protein detected by Western blot analyses. L-G cells infected with LXSH or LXSH-AML1-MTG8 were further infected with LNSX-AML1b viruses and the protein extracts from the infectants were analyzed by immunodetection using anti-HA antibody. The positions of AML1 and AML1-MTG8 are indicated by arrows. (B) Northern blot analyses showing the expression of G-CSFR mRNA. Total RNAs (5 μg of RNA) were prepared from L-G infectants cultured with IL-3, blotted, and hybridized with 32P-labeled mouse G-CSFR cDNA, mouse MPO cDNA, and human G3PDH cDNA.

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