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. 2003 Feb 15;17(4):455–460. doi: 10.1101/gad.1056303

Figure 4.

Figure 4

JAK-STAT pathway is extensively activated in UBP43−/− cells upon IFN stimulation. (A) ISGF3 complex formation in UBP43-deficient cells upon IFN-β stimulation. UBP43+/+ and UBP43−/− bone marrow cells were either left untreated or stimulated for the time indicated. Total protein extracts (30 μg) were used in the gel shift assays with 32P-labeled double-stranded oligonucleotide that contains an ISGF3 binding site. (B) UBP43+/+ and UBP43−/− bone marrow cells were either left untreated or stimulated with 100 unit/mL IFN-β as described above. Total proteins (15 μg) were resolved on 7% SDS-PAGE and immunoblotted with anti-phospho-Stat1 (Tyr701) Abs. Blots were stripped and reprobed with anti-Stat1 Abs to assure equal loading. (C) Induction of ISGs in UBP43+/+ and UBP43−/− bone marrow cells. Northern blot analysis of ISG15, 2‘-5′OAS and IRF7 gene expression was performed on total RNA isolated from UBP43+/+ and UBP43−/− bone marrow cells treated with 100 unit/mL of IFN-β for the time indicated.