AN ERK-DEPENDENT FEEDBACK MECHANISM PREVENTS HEMATOPOIETIC STEM CELL EXHAUSTION

Published: 25 May 2018| Version 1 | DOI: 10.17632/7rdg6mjk5h.1
Contributor:
Manuela Baccarini

Description

This data is linked to our paper "AN ERK-DEPENDENT FEEDBACK MECHANISM PREVENTS HEMATOPOIETIC STEM CELL EXHAUSTION", DOI: 10.1016/j.stem.2018.05.003 The paper shows that MEK1 is pivotal in implementing the signaling feedback allowing hematopietic stem cells to return to quiescence after activation. We have shown this by inducing stress-dependent hematopoiesis in animals lacking MEK1 in the hematopoietic compartment (MEK1 cKO) and comparing their response with that of control animals. The data show: 1) A comparison of the hematopoietic compartment of F/F and MEK1 cKO animals. From top to bottom, young mice (2 months old); aged (12 months old) mice; mice exposed to chronic 5-FU treatment (rep 5-FU; cells harvested 12 days after the third 5-FU injection); and Ly5.1 recipients transplanted with Ly5.1 BM and Ly5.2 F/F or MEK1 cKO BM (1:1 ratio). Cells were harvested 12 weeks after transplantation. For clarity, only Ly5.2 cells are shown. The cKO underperforms in all aging/stress models. 2) Knockdown/Knockout validation of antibodies and inhibitor validation of phosphospecific antibodies used in this study. The antibodies were validated for use in phosflow by directly comparing phosflow and immunoblotting results.

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