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1.  Direct Reprogramming of Murine Fibroblasts to Hematopoietic Progenitor Cells 
Cell Reports  2014;9(5):1871-1884.
Recent reports have shown that somatic cells, under appropriate culture conditions, could be directly reprogrammed to cardiac, hepatic, or neuronal phenotype by lineage-specific transcription factors. In this study, we demonstrate that both embryonic and adult somatic fibroblasts can be efficiently reprogrammed to clonal multilineage hematopoietic progenitors by the ectopic expression of the transcription factors ERG, GATA2, LMO2, RUNX1c, and SCL. These reprogrammed cells were stably expanded on stromal cells and possessed short-term reconstitution ability in vivo. Loss of p53 function facilitated reprogramming to blood, and p53−/− reprogrammed cells efficiently generated erythroid, megakaryocytic, myeloid, and lymphoid lineages. Genome-wide analyses revealed that generation of hematopoietic progenitors was preceded by the appearance of hemogenic endothelial cells expressing endothelial and hematopoietic genes. Altogether, our findings suggest that direct reprogramming could represent a valid alternative approach to the differentiation of embryonic stem cells (ESCs) or induced pluripotent stem cells (iPSCs) for disease modeling and autologous blood cell therapies.
Graphical Abstract
•ERG, GATA2, LMO2, RUNX1c, and SCL reprogram fibroblasts to blood•Reprogrammed fibroblasts have multilineage hematopoietic potential•Loss of p53 increases efficiency and multilineage potential of reprogrammed cells•Generation of blood progenitors is preceded by the appearance of hemogenic cells
Batta et al. demonstrate that murine fibroblasts are reprogrammed to hematopoietic progenitors, with erythroid, megakaryocyte, and myeloid potential, by ectopic expression of hematopoietic transcription factors. Reprogramming efficiency is increased by loss of p53 function, and generation of blood cells is preceded by the appearance of hemogenic endothelium.
PMCID: PMC4542300  PMID: 25466247
2.  EGF activates TTP expression by activation of ELK-1 and EGR-1 transcription factors 
Tristetraprolin (TTP) is a key mediator of processes such as inflammation resolution, the inhibition of autoimmunity and in cancer. It carries out this role by the binding and degradation of mRNA transcripts, thereby decreasing their half-life. Transcripts modulated by TTP encode proteins such as cytokines, pro-inflammatory agents and immediate-early response proteins. TTP can also modulate neoplastic phenotypes in many cancers. TTP is induced and functionally regulated by a spectrum of both pro- and anti-inflammatory cytokines, mitogens and drugs in a MAPK-dependent manner. So far the contribution of p38 MAPK to the regulation of TTP expression and function has been best described.
Our results demonstrate the induction of the gene coding TTP (ZFP36) by EGF through the ERK1/2-dependent pathway and implicates the transcription factor ELK-1 in this process. We show that ELK-1 regulates ZFP36 expression by two mechanisms: by binding the ZFP36 promoter directly through ETS-binding site (+ 883 to +905 bp) and by inducing expression of EGR-1, which in turn increases ZFP36 expression through sequences located between -111 and -103 bp.
EGF activates TTP expression via ELK-1 and EGR-1 transcription factors.
PMCID: PMC3342124  PMID: 22433566

Results 1-2 (2)