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Blood, Vol. 109, Issue 2, 763-768, January 15, 2007
Rce1 deficiency accelerates the development of K-RAS–induced myeloproliferative disease
Blood Wahlstrom et al.
109: 763
Supplemental materials for: Wahlstrom et al, Vol 109, Issue 2, 763-768
Files in this Data Supplement:
- Table S1 (PDF, 110 KB) -
Differential counts of blood smears from Rce1fl/flKLSLM (Rce1fl/fl) and Rce1fl/+KLSLM (Rce1fl/+) mice before and after pI-pC injections (n = 6 per group). The difference in the percentage of immature cells between the two groups was evident 3 weeks after pI-pC injections. Therefore, data from 3, 5, and 7 weeks were combined. P value is from the comparison between Rce1fl/fl and Rce1fl/+ mice after pI-pC injections.
- Figure S1. Western blot analyses (PDF, 185 KB) -
(A) Western blots of total protein extracts from spleens of control mice without MPD and of pI-pC–injected Rce1fl/+KLSLM and Rce1fl/flKLSLM mice showing expression of phosphorylated ERK1/2 (p-ERK1/2), total ERK1/2, phosphorylated AKT (p-AKT), and p21CIP1. (B) Western blot showing expression of phosphorylated and total ERK1/2 in spleen extracts from 6 additional mice. (C) Expression of phosphorylated ERK1/2 in total protein extracts from liver. Sixty micrograms total protein was loaded in each well.
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