Cloning and chromosomal localization of the rat &lt;i&gt;Stat5&lt;/i&gt; and Y&lt;i&gt;γ&lt;/i&gt;1 genes

Chen, K. S.; Paladugu, Abhaya; Aldaz, C. Marcelo; Gould, Michael N.

doi:10.1159/000134434

Cited by 7 publications

(2 citation statements)

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“…YY1 is ubiquitously expressed in all tissues and highly conserved among different species. Currently, YY1 cDNAs have been cloned from many species, including human (7), mouse (10,12), rat (13), chicken (14), zebrafish (15) and xenopus (16). Drosophila has two orthologs of YY1, pleiohomeotic (pho) and pho like (phol) (17,18), which have high degrees of similarity in the zinc finger regions with those of human YY1.…”

Section: Expression and General Function Of Yy1mentioning

confidence: 99%

The Regulation of YY1 in Tumorigenesis and its Targeting Potential in Cancer Therapy

Sui¹

2009

Mol Cell Pharmacol

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Yin Yang 1 (YY1) is a multifunctional protein and regulates various processes of development and differentiation. Increasing evidence indicates an essential role of YY1 in tumorigenesis. As a transcription factor, YY1 regulates the expression of numerous genes that are mostly involved in cancers. YY1 can either activate or repress the target genes, depending on the cofactors that it recruits. Importantly, most studies to date suggest a proliferative or oncogenic role of YY1 in cancer development. Meanwhile, overexpression of YY1 has been observed in different types of cancers and YY1 has been proposed as a potential prognostic marker of these cancers. A reasonable hypothesis is that upregulated YY1 leads to unbalanced expression of its target genes and in turn initiates or arguments tumorigenesis. Ample studies indicate that YY1 exerts broad regulation in various epigenetic events, especially histone acetylation and methylation. Since most cancers exhibit deregulated epigenetics, overexpressed YY1 may contribute to these aberrant epigenetic statuses in cancer cells. The epigenetic processes regulated by YY1 are reversible. Therefore, it is possible that targeting YY1 may adjust various deregulated epigenetic events in cancer cells, restore the normal epigenetic conditions and consequently block cancer development. This review summarizes cancer-related studies of YY1 and discusses the potential of YY1 as a target of cancer therapy.

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Section: Expression and General Function Of Yy1mentioning

confidence: 99%

The Regulation of YY1 in Tumorigenesis and its Targeting Potential in Cancer Therapy

Sui¹

2009

Mol Cell Pharmacol

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“…Given the profound effects of mutation of either GATA-4 or FOG-2 proteins on heart morphogenesis in mice, it is worth considering their potential relevance to human congenital heart defects, such as the Tetralogy of Fallot or the double-outlet right ventricle (Walters et al 2000). Whereas mutation of several genes, such as Jmj (Jumanji), Sox4, and Egfr/Shp2, give rise to the double-outlet right ventricle defect in mice (Chen et al 1996;Ya et al 1998;Lee et al 2000), and defects in other genes for transcription factors, such as FOG-2, NF1, neurotrophin 3, and RXR␣, result in all or a subset of the Tetralogy of Fallot (Jacks et al 1994;Donovan et al 1996;Gruber et al 1996;Lee et al 1997;Tevosian et al 2000), the consistent and combined phenotype seen in the Gata4 ki/ki mice is unique. Although it is sometimes difficult to distinguish between double-outlet right ventricle with associated pulmonary stenosis and the Tetralogy of Fallot, it is clear that the defects in the GATA-4 ki/ki hearts are different in the outflow tracts than those observed in Fog2-deficient embryos.…”

Section: Fog-noninteracting Gata-4 Knock-in Mouse Genes and Developmentmentioning

confidence: 99%

Proper coronary vascular development and heart morphogenesis depend on interaction of GATA-4 with FOG cofactors

Crispino¹,

Lodish²,

Thurberg³

et al. 2001

Genes Dev.

291

240

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GATA-family transcription factors are critical to the development of diverse tissues. In particular, GATA-4 has been implicated in formation of the vertebrate heart. As the mouse Gata-4 knock-out is early embryonic lethal because of a defect in ventral morphogenesis, the in vivo function of this factor in heart development remains unresolved. To search for a requirement for Gata4 in heart development, we created mice harboring a single amino acid replacement in GATA-4 that impairs its physical interaction with its presumptive cardiac cofactor FOG-2. Gata4ki/ki mice die just after embryonic day (E) 12.5 exhibiting features in common with Fog2 −/− embryos as well as additional semilunar cardiac valve defects and a double-outlet right ventricle. These findings establish an intrinsic requirement for GATA-4 in heart development. We also infer that GATA-4 function is dependent on interaction with FOG-2 and, very likely, an additional FOG protein for distinct aspects of heart formation. Transcriptional activity of the GATA-factors is modulated through interaction with nuclear proteins, including zinc finger proteins of the Kruppel and FOG/Ushaped families, general coactivators (p300 and CBP), the myocardial-expressed protein Nkx2.5, and NF-AT3 (Durocher and Nemer 1998;Mackay and Crossley 1998;Blobel 2000;Molkentin 2000). Whereas the specificity and in vivo functional relevance of many of these interactions are incompletely defined, the association of GATA-1 with FOG-1 has been examined in detail. FOG-1 interacts with GATA-1 in hematopoietic cells and regulates the ability of GATA-1 to promote terminal differentiation of erythroid cells and megakaryocytes (Tsang et al. 1997). Mutation of specific residues within the conserved N-terminal zinc finger of GATA-1, such as V205G, disrupts binding to FOG-1, preserves DNA-binding properties of GATA-1, and renders GATA-1 unable to promote terminal differentiation of red blood cells (Crispino et al. 1999). Furthermore, mutation of Val 205 in humans leads to congenital dyserythropoietic anemia and thrombocytopenia (Nichols et al. 2000). Taken together, these findings demonstrate that direct physical association of GATA-1 and FOG-1 is essential for GATA-1's roles in transcription and, critical for the experiments reported herein, identifies a specific residue of the N finger that mediates cofactor interaction.GATA-4, GATA-5, and GATA-6, nonhematopoietic expressed factors, are implicated in development of heart, endoderm, and intestinal epithelia, where they are expressed in an overlapping and dynamic fashion Bossard and Zaret 1998;Gao et al. 1998;Koutsourakis et al. 1999;Parmacek and Leiden 1999;Molkentin 2000). GATA-4 has been extensively studied in the context of heart development, as it is present in precardiac splanchnic mesoderm and binds to and activates promoters and enhancers of numerous myocardial-expressed genes . In its absence, mouse embryos die by E7.0-9.5, with failure of ventral morphogenesis leading to cardiac bifida (Kuo et al. 1997;Molkentin et al. 1997). The deat...

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Angiotensin II Activates Stat5 Through Jak2 Kinase in Cardiac Myocytes

McWhinney

Dostal

Baker

1998

Journal of Molecular and Cellular Cardiology

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Cloning and chromosomal localization of the rat <i>Stat5</i> and Y<i>γ</i>1 genes

Cited by 7 publications

References 8 publications

The Regulation of YY1 in Tumorigenesis and its Targeting Potential in Cancer Therapy

The Regulation of YY1 in Tumorigenesis and its Targeting Potential in Cancer Therapy

Proper coronary vascular development and heart morphogenesis depend on interaction of GATA-4 with FOG cofactors

Angiotensin II Activates Stat5 Through Jak2 Kinase in Cardiac Myocytes

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