Fig. 7.
Fig. 7. Lack of gp120-induced MAPK activation following lipid raft disruption. / (A) Jurkat 77-6.8 cells were treated with 10 mM MβCD for 20 minutes at 37°C, washed, and then resuspended in serum-free media. Surface expression of CD4 and CXCR4 was analyzed on a FACScan using PE-conjugated mAbs. The expression profiles of these 2 proteins were then assessed using PE-conjugated αCD4 and αCXCR4 mAbs as indicated. Isotype control staining is shown by a filled histogram. (B) Untreated and MβCD-treated cells were then stimulated with gp120, SDF-1, an αCD3 mAb, or an αCD4 mAb, as described in the legend to Figure 1. Membranes immunoblotted with the pAb recognizing dually phosphorylated Erk1/Erk2 are shown. Blots were reprobed with an αZAP-70 mAb to assess expression of a T-cell–specific protein. Results are representative of data obtained in 1 of 2 independent experiments.

Lack of gp120-induced MAPK activation following lipid raft disruption.

(A) Jurkat 77-6.8 cells were treated with 10 mM MβCD for 20 minutes at 37°C, washed, and then resuspended in serum-free media. Surface expression of CD4 and CXCR4 was analyzed on a FACScan using PE-conjugated mAbs. The expression profiles of these 2 proteins were then assessed using PE-conjugated αCD4 and αCXCR4 mAbs as indicated. Isotype control staining is shown by a filled histogram. (B) Untreated and MβCD-treated cells were then stimulated with gp120, SDF-1, an αCD3 mAb, or an αCD4 mAb, as described in the legend to Figure 1. Membranes immunoblotted with the pAb recognizing dually phosphorylated Erk1/Erk2 are shown. Blots were reprobed with an αZAP-70 mAb to assess expression of a T-cell–specific protein. Results are representative of data obtained in 1 of 2 independent experiments.

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