The HeLa cell protein TEF-1 binds specifically and cooperatively to two SV40 enhancer motifs of unrelated sequence

Davidson, Irwin; Xiao, Jiumei; Rosales, Ricardo; Staub, Adrien; Chambon, Pierre

doi:10.1016/0092-8674(88)90108-0

Cited by 301 publications

(265 citation statements)

References 49 publications

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“…We next employed the TEAD reporter GTIIC luciferase plasmid 27 to investigate the c-Abl inhibitory role. Constitutively active c-Abl (Δ1-81 c-Abl) 28 Consistent with previous studies, 18 when overexpressed in MCF10A cells, YAP induced EMT, as evidenced by a fibroblast-like appearance and a dispersed cell distribution on a regular culture dish (Figure 2d, left panels).…”

Section: Resultsmentioning

confidence: 99%

c-Abl antagonizes the YAP oncogenic function

et al. 2014

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YES-associated protein (YAP) is a central transcription coactivator that functions as an oncogene in a number of experimental systems. However, under DNA damage, YAP activates pro-apoptotic genes in conjunction with p73. This program switching is mediated by c-Abl (Abelson murine leukemia viral oncogene) via phosphorylation of YAP at the Y357 residue (pY357). YAP as an oncogene coactivates the TEAD (transcriptional enhancer activator domain) family transcription factors. Here we asked whether c-Abl regulates the YAP-TEAD functional module. We found that DNA damage, through c-Abl activation, specifically depressed YAP-TEAD-induced transcription. Remarkably, c-Abl counteracts YAP-induced transformation by interfering with the YAP-TEAD transcriptional program. c-Abl induced TEAD1 phosphorylation, but the YAP-TEAD complex remained unaffected. In contrast, TEAD coactivation was compromised by phosphomimetic YAP Y357E mutation but not Y357F, as demonstrated at the level of reporter genes and endogenous TEAD target genes. Furthermore, YAP Y357E also severely compromised the role of YAP in cell transformation, migration, anchorage-independent growth, and epithelial-to-mesenchymal transition (EMT) in human mammary MCF10A cells. These results suggest that YAP pY357 lost TEAD transcription activation function. Our results demonstrate that YAP pY357 inactivates YAP oncogenic function and establish a role for YAP Y357 phosphorylation in cell-fate decision.

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Section: Resultsmentioning

confidence: 99%

c-Abl antagonizes the YAP oncogenic function

et al. 2014

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“…A consensus Pu.1 binding site oligonucleotide did not compete for any of the ARE-1 complexes (lane 5). Homology searches also indicated a 9 of 11 match with a region of the SV40 promoter that contains overlapping binding sites for AP3 and TEF-2 (41,42). In addition, an earlier study suggested homology with a c-Myb or c-Myc binding sequence (10).…”

Section: In Vivo Genomic Footprinting Analysis In B-lymphocytes Detecmentioning

confidence: 95%

A Novel Element and a TEF-2-like Element Activate the Major Histocompatibility Complex Class II Transactivator in B-lymphocytes

Ghosh

Piskurich

Wright

et al. 1999

Journal of Biological Chemistry

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Major histocompatibility complex (MHC) class II molecules play a central role in immune responses, and transcription of this family of genes requires the MHC class II transactivator (CIITA). CIITA has four promoters, which are transcribed in a tissue-specific manner. CIITA promoter III is constitutively active in mature B-lymphocytes. This report now describes the minimal 319-base pair promoter region necessary for maximal transcriptional activity in B-lymphocytes. Ultraviolet light and dimethylsulfate in vivo genomic footprinting analyses reveal five occupied DNA sequence elements present in intact B-lymphocytes. Functional analysis of these elements using promoter deletions and site-specific mutations demonstrates that at least two of the sites occupied in vivo are critical for transcriptional activity. In vitro protein/DNA analysis suggests that one of the sites is a TEF-2-like element and the other is occupied by a novel transcription activator. In addition, nuclear factor-1 associates with the promoter both in vivo and in vitro. In myeloma cell lines, loss of CIITA transcription correlates with a completely unoccupied CIITA promoter III. These findings suggest that CIITA transcription in B-lymphocytes is activated through at least two strong promoter elements, while loss of expression in myeloma cells is mediated through changes in promoter assembly.Major histocompatibility complex (MHC) 1 class II molecules play a fundamental role in presenting exogenous antigenic peptides to CD4 ϩ helper T lymphocytes (1). These activated CD4 ϩ T cells release stimulatory cytokines that augment the response of CD8 ϩ cytotoxic T lymphocytes (2). Constitutive expression of MHC class II molecules is restricted to professional antigen-presenting cells, such as B lymphocytes and dendritic cells, and can be induced by interferon-␥ (IFN-␥) in macrophages, endothelial cells, and fibroblasts (3, 4). The MHC class II family of genes are coordinately regulated at the level of transcription through a conserved trimeric promoter motif (3, 5). A major component of this transcription complex was cloned by genetic complementation of an in vitro mutagenized MHC class II negative B cell line, RJ2.2.5. This component was named the MHC class II transactivator (CIITA) and restored MHC class II cell surface expression in one subgroup of bare lymphocyte syndrome patient cells (6). CIITA has since been shown to be a key regulatory molecule in the expression of all the known genes involved in the MHC class II antigen-presenting pathway (6 -9). CIITA is required for constitutive expression of MHC class II on B-lymphocytes (10) and with a few exceptions, such as in respiratory epithelial cells and dendritic cells (11,12), is required for cytokine-induced expression in other cell types. Mice in which functional CIITA protein was ablated clearly demonstrated an absolute requirement for CI-ITA in B cell expression of MHC class II (13). It has been shown that the CIITA gene has four distinct promoters each transcribing a unique first exon, which are lo...

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“…Mammals express four closely related and evolutionarily conserved transcription factors, the prototype for which was isolated from human cells as TEF1 (Davidson et al, 1988) and later renamed TEAD1 by the human genome project. A mouse homologue was subsequently identified (TEAD1/TEF1; Blatt and DePamphilis, 1993;Shimizu et al, 1993), as well as three additional members of the TEAD family (TEAD2/TEF4; Jacquemin et al, 1996;Kaneko et al, 1997;Yasunami et al, 1995, TEAD3/TEF5;Kaneko et al, 1997;Yasunami et al, 1996, and TEAD4/TEF3;Jacquemin et al, 1996;Yasunami et al, 1996;Yockey et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…Tead2 may be involved in the production or maintenance of the stem cells responsible for embryonic development, because it is expressed in embryonic, neural, and hematopoietic stem cells (Ramalho-Santos et al, 2002). Moreover, since these analyses compared transcripts expressed preferentially in proliferating stem cells relative to terminally differentiated cells, a common thread ties together all of the Tead2 expression studies: Tead2 appears to be expressed specifically in proliferating cells, although the absence of Tead2 expression in proliferating lymphoma and myeloma cell lines (Davidson et al, 1988;Kaneko et al, 2004) suggests that TEAD2 protein is not required for cells to proliferate per se but facilitates the process.…”

Section: Introductionmentioning

confidence: 99%

Transcription factor TEAD2 is involved in neural tube closure

Kaneko

Kohn

Liu

et al. 2007

Genesis

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Summary-TEAD2, one of the first transcription factors expressed at the beginning of mammalian development, appears to be required during neural development. For example, Tead2 expression is greatest in the dorsal neural crest where it appears to regulate expression of Pax3, a gene essential for brain development. Consistent with this hypothesis, we found that inactivation of the Tead2 gene in mice significantly increased the risk of exencephaly (a defect in neural tube closure). However, none of the embryos exhibited spina bifida, the major phenotype of Pax3 nullizygous embryos, and expression of Pax3 in E11.5 Tead2 nullizygous embryos was normal. Thus, Tead2 plays a role in neural tube closure that is independent of its putative role in Pax3 regulation. In addition, the risk of exencephaly was greatest with Tead2 nullizygous females, and could be suppressed either by folic acid or pifithrin-α. These results reveal a maternal genetic contribution to neural tube closure, and suggest that Tead2-deficient mice provide a model for anencephaly, a common human birth defect that can be prevented by folic acid. genesis 45:577-587, 2007.

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The HeLa cell protein TEF-1 binds specifically and cooperatively to two SV40 enhancer motifs of unrelated sequence

Cited by 301 publications

References 49 publications

c-Abl antagonizes the YAP oncogenic function

c-Abl antagonizes the YAP oncogenic function

A Novel Element and a TEF-2-like Element Activate the Major Histocompatibility Complex Class II Transactivator in B-lymphocytes

Transcription factor TEAD2 is involved in neural tube closure

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