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. 1999 Jan 18;189(2):309–318. doi: 10.1084/jem.189.2.309

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Association of PIR-A with FcRγc. (A) Assessment of cell surface PIR-A expression on LTK fibroblasts transfected with PIR-A alone (left) or with PIR-A and FcRγc (right). Viable cells were incubated with fluorochrome-labeled 6C1 anti-PIR (shaded histogram) or isotype-matched control mAb (open histogram). (B) Assessment of PIR expression in FcRγc-deficient versus normal mice. Splenocytes from FcRγc-deficient (FcRγc^−/−) or normal (FcRγc^+/+) mice were either radiolabeled with ¹²⁵I (top) or unlabeled (middle and bottom), lysed in 1% NP-40, and subjected to immunoprecipitation (IP) with the indicated mAbs. The immunoprecipitated, radiolabeled materials were resolved by SDS-PAGE and autoradiography (top). The materials isolated from unlabeled cells were resolved by SDS-PAGE, transferred onto membranes, blotted with rabbit anti-PIR (middle) or anti-FcRγc antibodies (bottom), and visualized by chemiluminescence.

Association of PIR-A with FcRγc. (A) Assessment of cell surface PIR-A expression on LTK fibroblasts transfected with PIR-A alone (left) or with PIR-A and FcRγc (right). Viable cells were incubated with fluorochrome-labeled 6C1 anti-PIR (shaded histogram) or isotype-matched control mAb (open histogram). (B) Assessment of PIR expression in FcRγc-deficient versus normal mice. Splenocytes from FcRγc-deficient (FcRγc^−/−) or normal (FcRγc^+/+) mice were either radiolabeled with ¹²⁵I (top) or unlabeled (middle and bottom), lysed in 1% NP-40, and subjected to immunoprecipitation (IP) with the indicated mAbs. The immunoprecipitated, radiolabeled materials were resolved by SDS-PAGE and autoradiography (top). The materials isolated from unlabeled cells were resolved by SDS-PAGE, transferred onto membranes, blotted with rabbit anti-PIR (middle) or anti-FcRγc antibodies (bottom), and visualized by chemiluminescence.

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