Fig. 5.
Fig. 5. The expression of GpIb causes p21-dependent G1 growth arrest. CHO /β/IX cells growing on vWF were serum deprived for 24 hours and then serum repleted for 20 hours, at which time BrdU incorporation and DNA content were determined. Identical measurements were made in CHO In/β/IX treated with muristerone. (A) shows that serum repletion of stable transfectants or the induced expression of GpIb inhibits BrdU incorporation and that this is reversed by the truncation of GpIb at amino acid 540 of the cytoplasmic domain. (B) shows that these cells are arrested in G1 and that G1 arrest is eliminated in cells transduced with the truncated cDNA for GpIb. (C) shows associated levels of immunoreactive p21 (n = 2). (**P< .0001 compared with V/β/IX; *P < .001 compared with V/β/IX; n = 3.)

The expression of GpIb causes p21-dependent G1 growth arrest. CHO /β/IX cells growing on vWF were serum deprived for 24 hours and then serum repleted for 20 hours, at which time BrdU incorporation and DNA content were determined. Identical measurements were made in CHO In/β/IX treated with muristerone. (A) shows that serum repletion of stable transfectants or the induced expression of GpIb inhibits BrdU incorporation and that this is reversed by the truncation of GpIb at amino acid 540 of the cytoplasmic domain. (B) shows that these cells are arrested in G1 and that G1 arrest is eliminated in cells transduced with the truncated cDNA for GpIb. (C) shows associated levels of immunoreactive p21 (n = 2). (**P< .0001 compared with V/β/IX; *P < .001 compared with V/β/IX; n = 3.)

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