scholarly journals Mef2c is a direct transcriptional target of ISL1 and GATA factors in the anterior heart field during mouse embryonic development

Development ◽  
2004 ◽  
Vol 131 (16) ◽  
pp. 3931-3942 ◽  
Author(s):  
E. Dodou
Keyword(s):  
Embryonic Development ◽  
Gata Factors ◽  
Direct Transcriptional Target ◽  
Heart Field ◽  
Transcriptional Target ◽  
Anterior Heart Field

scholarly journals RUNX1/core binding factor A2 regulates platelet 12-lipoxygenase gene (ALOX12): studies in human RUNX1 haplodeficiency

Blood ◽  
2010 ◽  
Vol 115 (15) ◽  
pp. 3128-3135 ◽  
Author(s):  
Gurpreet Kaur ◽  
Gauthami Jalagadugula ◽  
Guangfen Mao ◽  
A. Koneti Rao
Keyword(s):  
Expression Profiling ◽  
Region Of Interest ◽  
Luciferase Reporter ◽  
Direct Transcriptional Target ◽  
Erythroleukemia Cells ◽  
12 Lipoxygenase ◽  
Sirna Knockdown ◽  
Induced Aggregation ◽  
Transcriptional Target

Abstract Haploinsufficiency of RUNX1 (also known as CBFA2/AML1) is associated with familial thrombocytopenia, platelet dysfunction, and predisposition to acute leukemia. We have reported on a patient with thrombocytopenia and impaired agonist-induced aggregation, secretion, and protein phosphorylation associated with a RUNX1 mutation. Expression profiling of platelets revealed approximately 5-fold decreased expression of 12-lipoxygenase (12-LO, gene ALOX12), which catalyzes 12-hydroxyeicosatetraenoic acid production from arachidonic acid. We hypothesized that ALOX12 is a direct transcriptional target gene of RUNX1. In present studies, agonist-induced platelet 12-HETE production was decreased in the patient. Four RUNX1 consensus sites were identified in the 2-kb promoter region of ALOX12 (at −1498, −1491, −708, −526 from ATG). In luciferase reporter studies in human erythroleukemia cells, mutation of each site decreased activity; overexpression of RUNX1 up-regulated promoter activity, which was abolished by mutation of RUNX1 sites. Gel shift studies, including with recombinant protein, revealed RUNX1 binding to each site. Chromatin immunoprecipitation revealed in vivo RUNX1 binding in the region of interest. siRNA knockdown of RUNX1 decreased RUNX1 and 12-LO proteins. ALOX12 is a direct transcriptional target of RUNX1. Our studies provide further proof of principle that platelet expression profiling can elucidate novel alterations in platelets with inherited dysfunction.

scholarly journals The MADS box transcription factor MEF2C regulates melanocyte development and is a direct transcriptional target and partner of SOX10

Development ◽  
2011 ◽  
Vol 138 (12) ◽  
pp. 2555-2565 ◽  
Author(s):  
P. Agarwal ◽  
M. P. Verzi ◽  
T. Nguyen ◽  
J. Hu ◽  
M. L. Ehlers ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Mads Box ◽  
Direct Transcriptional Target ◽  
Transcriptional Target

Hhex Is a Critical Gene In The Development Of Normal and Malignant Lymphoid Cells

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3788-3788
Author(s):  
Charnise Goodings ◽  
Stephen B. Smith ◽  
Elizabeth Mathias ◽  
Elizabeth Smith ◽  
Rati Tripathi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Transgenic Mice ◽  
Conflicts Of Interest ◽  
Lymphoid Cells ◽  
Conditional Knockout ◽  
Hematopoietic Stem ◽  
Direct Transcriptional Target ◽  
Cell Counts ◽  
Transcriptional Target

Abstract Hematopoietically expressed homeobox (Hhex) is a T-cell oncogene. It is frequently deregulated in murine retroviral insertional mutagenesis screens and its enforced expression induces T-cell leukemia in bone marrow transduction and transplantation experiments. We discovered that HHEX is a direct transcriptional target of an LIM domain Only-2 (LMO2)-associated protein complex. HHEX clusters with LMO2-overexpressing T-ALLs and is especially overexpressed in Early T-cell Precursor (ETP) – ALL where it is a direct transcriptional target of LMO2. To further understand Hhex's function, we induced a conditional knockout in floxed Hhex mice with the Vav-iCre transgene. Mice were viable and showed normal blood cell counts with highly efficient deletion of Hhex in all hematopoietic tissues. Thymocytes from conditional knockouts showed a normal pattern of development. Most impressively, Hhex conditional knockout markedly prolonged the latency of T-ALL onset in CD2-Lmo2 transgenic mice (figure 1). Hhex conditional knockouts (Hhex cKOs) also had a significant decrease in mature B cells in the spleen and bone marrow. Interestingly, hematopoietic stem and progenitor cells plated on OP9-GFP or OP9-DL1 stromal cells showed proliferative defects and incomplete differentiation towards both B and T lineage. Also under stress conditions such as sublethal irradiation and competitive bone marrow transplants, Hhex conditional knockouts show a marked defect in both B and T lineages but an increase in early progenitor populations. Our experiments show that Hhex is a critical transcription factor in lymphoid development and in LMO2-induced T-ALL.Figure 1Hhex conditional knockout markedly prolonged the latency of T-ALL onset in CD2-Lmo2 transgenic miceFigure 1. Hhex conditional knockout markedly prolonged the latency of T-ALL onset in CD2-Lmo2 transgenic mice Disclosures: No relevant conflicts of interest to declare.

scholarly journals GLI1 Is a Direct Transcriptional Target of EWS-FLI1 Oncoprotein

2009 ◽  
Vol 284 (14) ◽  
pp. 9074-9082 ◽  
Author(s):  
Elspeth Beauchamp ◽  
Gulay Bulut ◽  
Ogan Abaan ◽  
Kevin Chen ◽  
Akil Merchant ◽  
...  
Keyword(s):  
Direct Transcriptional Target ◽  
Transcriptional Target

scholarly journals N-cadherin prevents the premature differentiation of anterior heart field progenitors in the pharyngeal mesodermal microenvironment

Cell Research ◽  
2014 ◽  
Vol 24 (12) ◽  
pp. 1420-1432 ◽  
Author(s):  
Boon-Seng Soh ◽  
Kristina Buac ◽  
Huansheng Xu ◽  
Edward Li ◽  
Shi-Yan Ng ◽  
...  
Keyword(s):  
Heart Field ◽  
Anterior Heart Field
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