![Figure 3. Expression of Bcr-abl signals to promote degradation and down-regulation of IFNAR1 and to attenuate IFNα signaling. (A) HeLa cells were either transfected with plasmids expressing Bcr-abl (wild type or kinase dead [KD]) or treated with TG (1μM for 30 minutes) and harvested. Phosphorylation and total levels of endogenous IFNAR1 (in IFNAR1 immunoprecipitates) or of expressed Bcr-abl (in whole cell lysates [WCL]) were determined by immunoblotting using the indicated antibodies. (B) HeLa cells expressing (or not) Bcr-abl and either FLAG-IFNAR1 or FLAG-IFNAR1S535A as indicated were treated with CHX (10 μg/mL) for the indicated time points. Immunoblotting analyses of the levels of Flag-IFNAR1 Bcr-abl and β-actin are depicted. (C) HeLa cells transfected with plasmids for expression of Bcr-abl and FLAG-tagged IFNAR1 (wild type or the phosphorylation-deficient mutant S535A) were treated or not with IFNα (250 IU/mL) as indicated. STAT1 phosphorylation and levels as well as the levels of FLAG-IFNAR1 and Bcr-abl were analyzed by immunoblotting using indicated antibodies.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/118/15/10.1182_blood-2010-12-325373/4/zh89991178750003.jpeg?Expires=1735526162&Signature=E2W~sPV6WCDV7PJmCtsVTvr6ROPd0Tum-3Yq6eavCwCATtUCM-Crcz0xjGXHOtjyxkPfZzVKBGbJpv4QvgBy7Ifdwn-pmFayIATvLtIaVjv8NOAuKilkgU2Tme0eLEH~JC2NJs64X~OghoBjY9P4cEvIn-VxcN3NH30GxvL~9Kg~UURzUkvmP~Qyhg0M3flYYiBGl8ziEFJm5KFwrOdOOHKzKlUZaxvkmLZamoqhit49pTvEYI4YbDL60FaSX20xPp3kzOUDtbGDUs36uahjtRhrjqSAf3hC-jdIzEf2t2ZOOIfiGHFmAoz1LSAwsvV93f7o9WmqYZZu6C811MuW3Q__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Expression of Bcr-abl signals to promote degradation and down-regulation of IFNAR1 and to attenuate IFNα signaling. (A) HeLa cells were either transfected with plasmids expressing Bcr-abl (wild type or kinase dead [KD]) or treated with TG (1μM for 30 minutes) and harvested. Phosphorylation and total levels of endogenous IFNAR1 (in IFNAR1 immunoprecipitates) or of expressed Bcr-abl (in whole cell lysates [WCL]) were determined by immunoblotting using the indicated antibodies. (B) HeLa cells expressing (or not) Bcr-abl and either FLAG-IFNAR1 or FLAG-IFNAR1S535A as indicated were treated with CHX (10 μg/mL) for the indicated time points. Immunoblotting analyses of the levels of Flag-IFNAR1 Bcr-abl and β-actin are depicted. (C) HeLa cells transfected with plasmids for expression of Bcr-abl and FLAG-tagged IFNAR1 (wild type or the phosphorylation-deficient mutant S535A) were treated or not with IFNα (250 IU/mL) as indicated. STAT1 phosphorylation and levels as well as the levels of FLAG-IFNAR1 and Bcr-abl were analyzed by immunoblotting using indicated antibodies.
