Transcription profiling of murine GATA-1 wild type and mutant fetal megakaryocytes to understand the molecular basis for the megakaryocytic hyperproliferation phenotype of the GATA-1deltaN mutants

ABSTRACT: Background: Children with Down syndrome (DS) are predisposed to acute megakaryoblastic leukemia (AMKL, or AML M7) and a related myeloid disorder, referred to as transient myeloproliferative disorder (TMD), or transient leukemia (TL). Recently, acquired mutations in the erythroid/megakaryocytic lineage-specific transcription factor GATA-1 have been identified in megakaryoblasts from virtually all DS patients with AMKL (DS-AMKL), as well as in nearly all DS neonates with TMD. These mutations prevent synthesis of full-length GATA-1, but lead to synthesis of a truncated GATA-1 protein (GATA-1s) that lacks the N-terminal transactivation domain. To determine the in vivo requirement of GATA-1 N-terminal domain in hematopoiesis and to model DS megakaryocytic leukemia initiated by GATA-1 mutation,

ORGANISM(S): Mus musculus

SUBMITTER: Zhe Li 

PROVIDER: E-GEOD-2433 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress