Cloning of an Inr- and E-box-binding protein, TFII-I, that interacts physically and functionally with USF1

Roy, Ananda L.; Du, Hong; Gregor, Polly D.; Novina, Carl D.; Martinez, Ernest; Roeder, Robert G.

doi:10.1093/emboj/16.23.7091

Cited by 186 publications

(228 citation statements)

References 60 publications

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“…Strong activation of transcription was observed both in vitro and in vivo following binding of USF to speci®c sites in gene promoters (Sawadogo and Roeder, 1985;Luo and Sawadogo, 1996b;Roy et al, 1997). This transcriptional activity requires, in addition to the Cterminal DNA-binding domain, activation domains present in the N-terminal region of the USF proteins.…”

Section: Introductionmentioning

confidence: 99%

Loss of USF transcriptional activity in breast cancer cell lines

1999

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USF is a family of transcription factors that are structurally related to the Myc oncoproteins and also share with Myc a common DNA-binding speci®city. USF overexpression can prevent c-Myc-dependent cellular transformation and also inhibit the proliferation of certain transformed cells. These antiproliferative activities suggest that USF inactivation could be implicated in carcinogenesis. To explore this possibility, we compared the activities of the ubiquitous USF1 and USF2 proteins in several cell lines derived from either normal breast epithelium or breast tumors. The DNAbinding activities of USF1 and USF2 were present at similar levels in all cell lines. In the non-tumorigenic MCF-10A cells, USF in general, and USF2 in particular, exhibited strong transcriptional activities. In contrast, USF1 and USF2 were completely inactive in three out of six transformed breast cell lines investigated, while the other three transformed cell lines exhibited loss of USF2 activity. Analyses in cells cultured from healthy tissue con®rmed the transcriptional activity of USF in normal human mammary epithelial cells. These results demonstrate that a partial or complete loss of USF function is a common event in breast cancer cell lines, perhaps because, like Myc overexpression, it favors rapid proliferation.

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Section: Introductionmentioning

confidence: 99%

Loss of USF transcriptional activity in breast cancer cell lines

1999

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“…Consistently, submicroscopic deletion and duplication were shown to modify the expression levels of some of their flanking genes. [34][35][36][37][38] We could also not rule out the possibility that abnormally low levels of LIMK1 combined with reduced levels of other proteins involved in brain function (eg CLIP2) could affect spatial impairment, as suggested previously. 35 GTF2I, GTF2IRD1 and GTF2IRD2 belong to the TFII-I gene family of transcription factors.…”

Section: Discussionmentioning

confidence: 87%

An atypical 7q11.23 deletion in a normal IQ Williams–Beuren syndrome patient

et al. 2009

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Williams-Beuren syndrome (WBS; OMIM no. 194050) is a multisystemic neurodevelopmental disorder caused by a hemizygous deletion of 1.55 Mb on chromosome 7q11.23 spanning 28 genes. Haploinsufficiency of the ELN gene was shown to be responsible for supravalvular aortic stenosis and generalized arteriopathy, whereas LIMK1, CLIP2, GTF2IRD1 and GTF2I genes were suggested to be linked to the specific cognitive profile and craniofacial features. These insights for genotype-phenotype correlations came from the molecular and clinical analysis of patients with atypical deletions and mice models. Here we report a patient showing mild WBS physical phenotype and normal IQ, who carries a shorter 1 Mb atypical deletion. This rearrangement does not include the GTF2IRD1 and GTF2I genes and only partially the BAZ1B gene. Our results are consistent with the hypothesis that hemizygosity of the GTF2IRD1 and GTF2I genes might be involved in the facial dysmorphisms and in the specific motor and cognitive deficits observed in WBS patients.

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“…TFII-I is a ubiquitously expressed transcription factor that is postulated to facilitate communication between upstream regulatory factors and the basal machinery (21)(22)(23)(24)(25). TFII-I belongs to a family of vertebrate specific transcription factors, each characterized by the presence of reiterated 90 amino acids domains (designated as R1-R6 in Figure 1) and multiple alternatively spliced isoforms (26,27 reviewed in 25).…”

Section: Transcriptional Regulation Of C-fos By Tfii-imentioning

confidence: 99%

“…TFII-I belongs to a family of vertebrate specific transcription factors, each characterized by the presence of reiterated 90 amino acids domains (designated as R1-R6 in Figure 1) and multiple alternatively spliced isoforms (26,27 reviewed in 25). The most conserved region within these repeats is called the I-repeat (23). There are four characterized alternatively spliced isoforms of TFII-I: Δ (957 amino acids), α (977 amino acids), β (978 amino acids) and γ (998 amino acids) (26,27).…”

Section: Transcriptional Regulation Of C-fos By Tfii-imentioning

confidence: 99%

“…Although TFII-I was functionally identified and characterized based on its ability to bind the core promoter sequence element (Inr) and activate transcription (21)(22)(23)(24), later on it was demonstrated that it also functions as a signal-induced multifunctional transcription factor that is tyrosine phosphorylated in response to B cell receptor (BCR) and growth factor signaling (29)(30)(31)(32)(33)(34). Importantly, induced tyrosine phosphorylation of TFII-I is necessary for its transcriptional function (32).…”

Section: Transcriptional Regulation Of C-fos By Tfii-imentioning

confidence: 99%

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Signal-induced functions of the transcription factor TFII-I

Roy

2007

Biochimica et Biophysica Acta (BBA) - Gene Structure and Expres

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We have learned a great deal over the last several years about the molecular mechanisms that govern cell growth, cell division and cell death. Normal cells pass through cell cycle (growth) and divide in response to mitogenic signals that are transduced through their cognate cell surface receptors to the nucleus. Despite the fact that cellular growth and division are mechanistically distinct steps, they are usually coordinately regulated, which is critical for normal cellular proliferation. The precise mechanistic basis for this coordinated regulation is unclear. TFII-I is a unique, signal induced multifunctional transcription factor that is activated upon a variety of signaling pathways and appears to participate in distinct phases of cell growth. For instance, TFII-I is required for growth factorinduced transcriptional activation of the c-fos gene, which is essential for cell cycle entry. Two alternatively spliced isoforms of TFII-I exhibit opposing but necessary functions for mitogen-induced transcriptional activation of c-fos. Besides transcriptional activation of the c-fos proto-oncogene and eventual entry into cell cycle, TFII-I also appears to have a role in later phases of the cell cycle and cell division. Here we discuss how a multitude of signaling inputs target TFII-I isoforms, which may exert their functions in distinct phases of the cell cycle and play a key role in the coordinated regulation of cellular proliferation.

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Cloning of an Inr- and E-box-binding protein, TFII-I, that interacts physically and functionally with USF1

Cited by 186 publications

References 60 publications

Loss of USF transcriptional activity in breast cancer cell lines

Loss of USF transcriptional activity in breast cancer cell lines

An atypical 7q11.23 deletion in a normal IQ Williams–Beuren syndrome patient

Signal-induced functions of the transcription factor TFII-I

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