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Status |
Public on Feb 12, 2014 |
Title |
B-myb is Essential Regulator of Hematopoietic Stem Cell and Myeloid Progenitor Cell Development |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
The B-myb (MYBL2) gene is a member of the MYB family of transcription factors and is involved in cell cycle regulation, DNA replication and maintenance of genomic integrity. However, its function during adult development and hematopoiesis is unknown. We show here that conditional inactivation of B-myb in vivo results in depletion of the HSC pool, leading to profound reductions in mature lymphoid, erythroid and myeloid cells. This defect is autonomous to the bone marrow and is first evident in the HSCs, which accumulate in the S and G2/M phases. B-myb inactivation also causes defects in the myeloid progenitor compartment and results in an accumulation of GMPs. Microarray studies indicate that B-myb null LKS+ cells differentially express genes that direct myeloid lineage development and commitment, suggesting that B-myb is a key player in controlling cell fate. Collectively, these studies demonstrate that B-myb is essential for HSC and progenitor maintenance and survival during hematopoiesis. Total RNA was isolated from FACS purified LKS+ cells isolated from pIpC-treated control and B-myb floxed-MxCre mice.
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Overall design |
Each sample is derived from a pool of 3-5 mice. 2 samples were analyzed for each genotype.
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Contributor(s) |
Baker SJ, Reddy EP |
Citation(s) |
24516162 |
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Submission date |
Jan 07, 2014 |
Last update date |
Nov 24, 2017 |
Contact name |
Stacey J Baker |
Organization name |
Icahn School of Medicine at Mount Sinai
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Department |
Oncological Sciences
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Street address |
One Gustave L. Levy Place, Box 1130
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City |
New York |
State/province |
NY |
ZIP/Postal code |
10029 |
Country |
USA |
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Platforms (1) |
GPL17543 |
Illumina MouseWG-6 v2.0 R2 expression beadchip |
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Samples (4)
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Relations |
BioProject |
PRJNA233615 |