Fig. 6.
Fig. 6. Expression of 4, 5, and β1-integrins on ICSBP-deficient progenitor cells. (A) Gating of bone marrow cells according to surface expression of c-kit, as measured by FACS. (B) FACS-analysis of 4- (top panel), 5- (middle panel), and β1-integrin (lower panel) expression on c-kit+–gated (see A) bone marrow cells from ICSBP+/+ (left) and ICSBP−/− (right) mice. Filled histograms represent control traces from cells stained only with FITC-labeled secondary Ig. (C) Adhesion of CFCs to immobilized antiintegrin antibodies. Bone marrow cells from wild-type (black bars) or ICSBP−/−mice (gray bars) were incubated in 48-well plates precoated with antibodies to the indicated integrins. Adherent cells were subjected to a CFC assay as described in Materials and Methods and in the legend to Fig 5A. Data shown represent mean ± SEM of 2 independent experiments performed in triplicate with 2 mice per group.

Expression of 4, 5, and β1-integrins on ICSBP-deficient progenitor cells. (A) Gating of bone marrow cells according to surface expression of c-kit, as measured by FACS. (B) FACS-analysis of 4- (top panel), 5- (middle panel), and β1-integrin (lower panel) expression on c-kit+–gated (see A) bone marrow cells from ICSBP+/+ (left) and ICSBP−/− (right) mice. Filled histograms represent control traces from cells stained only with FITC-labeled secondary Ig. (C) Adhesion of CFCs to immobilized antiintegrin antibodies. Bone marrow cells from wild-type (black bars) or ICSBP−/−mice (gray bars) were incubated in 48-well plates precoated with antibodies to the indicated integrins. Adherent cells were subjected to a CFC assay as described in Materials and Methods and in the legend to Fig 5A. Data shown represent mean ± SEM of 2 independent experiments performed in triplicate with 2 mice per group.

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