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β-Arrestin2 mediates progression of murine primary myelofibrosis

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Figure

Figure 1. β< 0.0001 for time/row factor, mice receiving White blood cells (WBCs) were lower over time in mice receiving receiving -Arrestin2 is necessary for development of primary myelofibrosis in a murine disease model
Figure 2. Donor KLS cells from WT, βtative images of WT, In vivo imaging performed +20 hours after engraftment
Figure 3. βsetting of MPLW515L-mutant retrovirus. -Arrestin2–knockout KLS cells demonstrate no differences in proliferation, increased apoptosis, and decreased self-renewal in the (A) 5-Ethynyl-2′-deoxyuridine (EdU) incorporation to measure proliferation w
Figure 4. Loss of β-arrestin2 has effects on KLS cells independent of MPLW515L-mutant retrovirus
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