TAZ is a coactivator for Pax8 and TTF-1, two transcription factors involved in thyroid differentiation

Palma, Tina Di; D’Andrea, Barbara; Liguori, Giovanna L.; Liguoro, Annamaria; Cristofaro, Tiziana de; D, Del Prete; Pappalardo, Andrea A.; Mascia, Anna; Zannini, Mariastella

doi:10.1016/j.yexcr.2008.10.016

Cited by 65 publications

(55 citation statements)

References 56 publications

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“…Previous studies have shown that TAZ and its paralog, YAP, act as coactivators of numerous TFs (Yagi et al 1999;Vassilev et al 2001;Basu et al 2003;Komuro et al 2003;Hong et al 2005;Murakami et al 2005Murakami et al , 2006Varelas et al 2008;Di Palma et al 2009;Zhang et al 2009). Of particular interest is the association of TAZ/ YAP with the TEAD family of TFs, as elucidated by the Guan group (Zhao et al 2008b, Zhang et al 2009).…”

Section: Mes Transition Is Induced By the Taz/tead Complexmentioning

confidence: 99%

“…TAZ functions by transactivating numerous TFs, including runt-related transcription factor 2 (RUNX2), paired box-3 (PAX3), PAX8, transcription termination factor-1 (TTF-1), T-box 5 (TBX5), mothers against decapentaplegic homologs (SMADs), and TEA domain family members (TEAD) (Hong et al 2005;Murakami et al 2005Murakami et al , 2006Varelas et al 2008;Di Palma et al 2009;Zhang et al 2009). The regulation of TAZ and its paralog, Yes-associated protein (YAP), occurs primarily via HIPPO tumor suppressor pathway, many components of which are conserved from flies to humans (Zhao et al 2008a;Pan 2010;Halder and Johnson 2011).…”

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confidence: 99%

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The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma

Bhat¹,

Salazar²,

et al. 2011

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Recent molecular classification of glioblastoma (GBM) has shown that patients with a mesenchymal (MES) gene expression signature exhibit poor overall survival and treatment resistance. Using regulatory network analysis of available expression microarray data sets of GBM, including The Cancer Genome Atlas (TCGA), we identified the transcriptional coactivator with PDZ-binding motif (TAZ ), to be highly associated with the MES network. TAZ expression was lower in proneural (PN) GBMs and lower-grade gliomas, which correlated with CpG island hypermethylation of the TAZ promoter compared with MES GBMs. Silencing of TAZ in MES glioma stem cells (GSCs) decreased expression of MES markers, invasion, self-renewal, and tumor formation. Conversely, overexpression of TAZ in PN GSCs as well as murine neural stem cells (NSCs) induced MES marker expression and aberrant osteoblastic and chondrocytic differentiation in a TEAD-dependent fashion. Using chromatin immunoprecipitation (ChIP), we show that TAZ is directly recruited to a majority of MES gene promoters in a complex with TEAD2. The coexpression of TAZ, but not a mutated form of TAZ that lacks TEAD binding, with plateletderived growth factor-B (PDGF-B) resulted in high-grade tumors with MES features in a murine model of glioma. Our studies uncover a direct role for TAZ and TEAD in driving the MES differentiation of malignant glioma.

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Section: Mes Transition Is Induced By the Taz/tead Complexmentioning

confidence: 99%

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confidence: 99%

The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma

Bhat¹,

Salazar²,

et al. 2011

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“…Different isoforms of TAZ and YAP exist that possess either one or two WW domains, and this has been shown to provide differential activity (Komuro et al, 2003;Webb et al, 2011). Some of the TAZ/YAP nuclear DNA-binding partners that interact with the WW domain include RUNX1, RUNX2, p73, PAX3, PAX8, TTF-1 (also known as NKX2.1), TBX5 (also known as NKX2.5), PPARg and SMAD1 (Strano et al, 2001;Cui et al, 2003;Park et al, 2004;Murakami et al, 2005Murakami et al, , 2006Hong and Yaffe, 2006;Alarcon et al, 2009;Di Palma et al, 2009). TAZ/YAP possess additional domains that are important for transcription factor binding, including a coiled-coil domain that facilitates interactions with the TGFb-regulated SMADs (Varelas et al, 2008), and an N-terminal domain that binds to the TEAD family of transcription factors (Vassilev et al, 2001;Zhao et al, 2008).…”

Section: Hippo Signaling In Contextmentioning

confidence: 99%

Integrating developmental signals: a Hippo in the (path)way

2011

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The Hippo pathway, a signaling cascade that controls cell cycle progression, apoptosis and cell differentiation, has emerged as a fundamental regulator of many physiological and pathological processes. Recent studies have revealed a complex network of interactions directing Hippo pathway activity, and have connected this pathway with other key signaling pathways. Such crosstalk has uncovered novel roles for Hippo signaling, including regulation of TGFb/SMAD and WNT/b-catenin pathways. This review highlights some of the recent findings in the Hippo field with an emphasis on how the Hippo pathway is integrated with other pathways to mediate diverse processes.

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“…An example of this is the transcriptional coactivator TAZ, recently shown to enhance in vitro the activity of PAX8 and NKX2-1 on the thyroglobulin (TG) promoter (Di Palma et al 2009). Interestingly, TAZ is first expressed in the mouse embryonic thyroid at E14.5 coinciding with the onset of TG biosynthesis (Di Palma et al 2009). Lack of TAZ prior to this time point may thus explain why PAX8 and NKX2-1 already expressed from E9 and onward are unable to activate the TG promoter.…”

Section: Introductionmentioning

confidence: 99%

Morphogenetics of early thyroid development

Fagman¹,

Nilsson²

2010

Journal of Molecular Endocrinology

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The thyroid develops from the foregut endoderm. Yet uncharacterized inductive signals specify endoderm progenitors to a thyroid cell fate that assembles in the pharyngeal floor from which the primordium buds and migrates to the final position of the gland. The morphogenetic process is regulated by both cell-autonomous (e.g. activated by NKX2-1, FOXE1, PAX8, and HHEX) and mesoderm-derived (e.g. mediated by TBX1 and fibroblast growth factors) mechanisms acting in concert to promote growth and survival of progenitor cells. The developmental role of TSH is limited to thyroid differentiation set to work after the gross anatomy of the gland is already sculptured. This review summarizes recent advances on the molecular genetics of thyroid morphogenesis put into context of endoderm developmental traits and highlights established and novel mechanisms of thyroid dysgenesis of potential relevance to congenital hypothyroidism in man.

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TAZ is a coactivator for Pax8 and TTF-1, two transcription factors involved in thyroid differentiation

Cited by 65 publications

References 56 publications

The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma

The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma

Integrating developmental signals: a Hippo in the (path)way

Morphogenetics of early thyroid development

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