Figure 2.
Figure 2. Absence of GATA1 leads to differential protein tyrosine phosphorylation. Platelets from wild-type (WT) and ΔneoΔHS (KO) mice were aggregated with thrombin (1.0 U/mL), collagen (10 μg/mL), or CRP (10 μg/mL) prior to lysis with 2 × Lysis buffer. Proteins were separated on SDS-PAGE, using 4% to 12% precast gradient gels, transferred onto PVDF membranes, and blotted with anti-phosphotyrosine Ab, 4G10. Bands of interest are highlighted by arrows, including a constitutively tyrosine phosphorylated band at approximately 26 to 28 kDa, and phosphorylated proteins at 40, 62, 70, 80, and 140 kDa. Molecular weight (MW) markers are provided on the left-hand side.

Absence of GATA1 leads to differential protein tyrosine phosphorylation. Platelets from wild-type (WT) and ΔneoΔHS (KO) mice were aggregated with thrombin (1.0 U/mL), collagen (10 μg/mL), or CRP (10 μg/mL) prior to lysis with 2 × Lysis buffer. Proteins were separated on SDS-PAGE, using 4% to 12% precast gradient gels, transferred onto PVDF membranes, and blotted with anti-phosphotyrosine Ab, 4G10. Bands of interest are highlighted by arrows, including a constitutively tyrosine phosphorylated band at approximately 26 to 28 kDa, and phosphorylated proteins at 40, 62, 70, 80, and 140 kDa. Molecular weight (MW) markers are provided on the left-hand side.

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