Fig. 4.
Fig. 4. N-glycosylation site mutations in the extracellular domain of GMRβ prevent high-affinity GM-CSF binding in transfected COS cells. / The COS cells were cotransfected with plasmids encoding wild-type GMRα and plasmids encoding mutated GMRβ at a ratio α/β = 1:6. Representative Scatchard analyses of GM-CSF binding data obtained from cotransfected cells are shown. (A) GMRβ-Ala58, kd = 4.31nmol/L. (B) GMRβ-Ala191, kd = 5.92 nmol/L. (C) GMRβ-Ala346, kd = 6.33 nmol/L. (D) GMRβ-Ala58/191/346, kd = 9.52 nmol/L. (E) GMRβ-Asp58, kd = 5.75 nmol/L. (F) GMRβ-Asp191, kd = 6.62 nmol/L. (G) GMRβ-Asp346, kd = 10.10 nmol/L. (H) GMRβ-Asp58/191/346, kd = 5.68 nmol/L.

N-glycosylation site mutations in the extracellular domain of GMRβ prevent high-affinity GM-CSF binding in transfected COS cells.

The COS cells were cotransfected with plasmids encoding wild-type GMRα and plasmids encoding mutated GMRβ at a ratio α/β = 1:6. Representative Scatchard analyses of GM-CSF binding data obtained from cotransfected cells are shown. (A) GMRβ-Ala58, kd = 4.31nmol/L. (B) GMRβ-Ala191, kd = 5.92 nmol/L. (C) GMRβ-Ala346, kd = 6.33 nmol/L. (D) GMRβ-Ala58/191/346, kd = 9.52 nmol/L. (E) GMRβ-Asp58, kd = 5.75 nmol/L. (F) GMRβ-Asp191, kd = 6.62 nmol/L. (G) GMRβ-Asp346, kd = 10.10 nmol/L. (H) GMRβ-Asp58/191/346, kd = 5.68 nmol/L.

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