Figure 5
Figure 5. Jak1 overexpression sensitized pOCs to the IFN-β-mediated inhibition of osteoclastogenesis. (A) BMMs were first differentiated into pOCs by culturing with M-CSF (30 ng/mL) and RANKL (100 ng/mL). After the infection with viruses harboring empty vector (pMX), WT Jak1 (pMX-Jak1WT), or constitutively active Jak1 (pMX-Jak1CA), cells were further differentiated into OCs with RANKL in the presence or absence of IFN-β (10 U/mL). (B) At 1 day after Jak1 viral infection, total-cell lysates were investigated for Jak1 expression by Western blotting. (C) At the end of culture, cells were stained for TRAP activity. MR represents M-CSF plus RANKL. Results are representative of at least 3 experiments with similar results. (D) OC numbers in panel C were counted. Data are means (± SD) from 3 random fields in representative experiment.

Jak1 overexpression sensitized pOCs to the IFN-β-mediated inhibition of osteoclastogenesis. (A) BMMs were first differentiated into pOCs by culturing with M-CSF (30 ng/mL) and RANKL (100 ng/mL). After the infection with viruses harboring empty vector (pMX), WT Jak1 (pMX-Jak1WT), or constitutively active Jak1 (pMX-Jak1CA), cells were further differentiated into OCs with RANKL in the presence or absence of IFN-β (10 U/mL). (B) At 1 day after Jak1 viral infection, total-cell lysates were investigated for Jak1 expression by Western blotting. (C) At the end of culture, cells were stained for TRAP activity. MR represents M-CSF plus RANKL. Results are representative of at least 3 experiments with similar results. (D) OC numbers in panel C were counted. Data are means (± SD) from 3 random fields in representative experiment.

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