High GATA-2 expression inhibits human hematopoietic stem and progenitor cell function by effects on cell cycle

Tipping, Alex J.; Pina, Cristina; Castor, Anders; Hong, Dengli; Rodrigues, Neil P.; Lazzari, Lorenza; May, Gillian; Jacobsen, Sten Eirik W.; Enver, Tariq

doi:10.1182/blood-2008-06-161117

Cited by 102 publications

(117 citation statements)

References 44 publications

(56 reference statements)

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“…GATA1 inhibits expressionofCdk6andcyclinD2(Ccdn2)andinducesthecyclindependent kinase inhibitors Cdkn2c (p18 INC4c ) and Cdkn1b (p27 Kip1 ) promoting proliferation arrest during erythroid maturation (34,41,42). GATA2 inhibits the growth of hematopoietic stem/progenitor cells by regulating expression levels of Cdkn2a (p21 WAF1 ) and Cdkn1b (p27 Kip1 ) (35,43). Overexpression of Gata6 inhibits cell cycle progression of vascular smooth muscle cells by regulating expression of Cdkn2a p21 WAF1 (33).…”

Section: Gata Factors and Cell Cycle Regulation During Mousementioning

confidence: 99%

Gata4 and Gata5 Cooperatively Regulate Cardiac Myocyte Proliferation in Mice

Singh

et al. 2010

Journal of Biological Chemistry

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GATA5 is a member of the zinc finger transcription factor GATA family (GATA1-6) that plays a wide variety of roles in embryonic and adult development. Experiments in multiple model systems have emphasized the importance of the GATA family members 4 -6 in the development of the endoderm and mesoderm. Yet despite overlapping expression patterns, there is little evidence of an important role for GATA5 in mammalian cardiac development. We have generated a new Gata5 mutant allele lacking exons 2 and 3 that encodes both zinc finger domains (Gata5 tm2Eem ), and we show that although Gata5 All six members of the GATA family (GATA1-6) of zinc finger transcription factors play important roles in cell fate decision, differentiation, and morphogenesis (1). Members of this family recognize the GATA motif, which is present in the promoters of many genes. These factors have been divided into two subfamilies, Gata1/2/3 and Gata4/5/6, based on their expression patterns and amino acid sequence homology (2). Gata1, Gata2, and Gata3 are preferentially expressed in hematopoietic cells and regulate proliferation and differentiation during hematopoiesis (3). Gata4, Gata5, and Gata6 are predominantly expressed during embryonic heart development, in addition to other sites. The DNA binding domains of GATA4, GATA5, and GATA6 are ϳ85% similar at the protein level. During early cardiac development, Gata4 expression is confined to the cardiac crescent, and later the transcripts are detected throughout the myocardium and endocardium (4, 5). Gata4-deficient mice die between E8.5 4 and E10.5 because of defects in ventral morphogenesis, including a failure of the cardiac mesoderm to form a linear heart tube (6, 7). A frameshift mutation in human GATA4 (E359del) is linked to cardiac septal defects (8). Like Gata4, Gata6 is expressed in the precardiac mesoderm and later in myocardial cells. Gata6 is also expressed in vascular smooth muscle (9). Gata6 null mice die prior to cardiac development because of defects in the visceral endoderm function and extraembryonic development (10, 11).The temporal and spatial expression pattern of Gata5 suggests its involvement in tissue-specific transcriptional regulation during embryonic development (12). Gata5 is expressed in the precardiac crescent between E7 and E8 (12). By E9.5 in the heart, Gata5 is expressed at high levels in the atria with lower levels observed in the ventricle and outflow tract. By E12.5, expression is primarily restricted to endocardial cells of the atria, and by E16.5, Gata5 transcripts are no longer detected in cardiac tissues (12). In chick, GATA5 is transcribed in the cardiac crescent prior to formation of the primordial heart tube (13). In Xenopus, gata5 is expressed in both cardiac mesoderm and hepatogenic endoderm. Down-regulation of gata5 using two nonoverlapping translation-blocking and splice site-blocking morpholino causes severe reduction in the number of heart and liver precursors at the time of or shortly after their specification (14). In zebrafish, gata5 is encoded by th...

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Section: Gata Factors and Cell Cycle Regulation During Mousementioning

confidence: 99%

Gata4 and Gata5 Cooperatively Regulate Cardiac Myocyte Proliferation in Mice

Singh

et al. 2010

Journal of Biological Chemistry

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“…However, even though p57 mRNA 4 levels were robustly upregulated following treatment of hematopoietic progenitor cells with recombinant human TGF-β1 (from now on referred to as TGFβ), the response was delayed and dependent on de novo protein synthesis, indicating that p57 is not an immediate effector molecule in the TGFβ response. Instead, we have identified the transcription factor (TF) Gata2, previously described as an important regulator of HSC function with similar functions as TGFβ and p57, 19,20 as a Smaddependent, direct target of TGFβ signaling in hematopoietic progenitor cells. Our results further reveal a transcriptional network involving Gata2, p57 and members of the TGFβ signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

A network including TGFβ/Smad4, Gata2, and p57 regulates proliferation of mouse hematopoietic progenitor cells

Billing

Rörby

May

et al. 2016

Experimental Hematology

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“…The haploinsufficient GATA-2 +/-mouse model shows mildly increased quiescence of both HSCs and progenitor cells (Rodrigues et al, 2005). However, Tipping et al recently showed that enforced expression of GATA-2 in a murine cell line (Ba/F3), or human cord blood HSCs (CD34 + CD38 -) and progenitors (CD34 + CD38 + ), increases quiescence and inhibits proliferation (Tipping, et al, 2009). …”

Section: Positive Regulationmentioning

confidence: 99%

Regulation of Hematopoietic Stem Cell Fate: Self-Renewal, Quiescence and Survival

Kubota¹,

Kimura²

2012

Advances in Hematopoietic Stem Cell Research

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High GATA-2 expression inhibits human hematopoietic stem and progenitor cell function by effects on cell cycle

Abstract: Evidence suggests the transcription factor GATA-2 is a critical regulator of murine hematopoietic stem cells. Here, we explore the relation between GATA-2 and cell proliferation and show that inducing GATA-2 increases quiescence (

Cited by 102 publications

References 44 publications

Gata4 and Gata5 Cooperatively Regulate Cardiac Myocyte Proliferation in Mice

Gata4 and Gata5 Cooperatively Regulate Cardiac Myocyte Proliferation in Mice

A network including TGFβ/Smad4, Gata2, and p57 regulates proliferation of mouse hematopoietic progenitor cells

Regulation of Hematopoietic Stem Cell Fate: Self-Renewal, Quiescence and Survival

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