Promoter occlusion prevents transcription of adenovirus polypeptide IX mRNA until after DNA replication.

Vales, L D; Darnell, James

doi:10.1101/gad.3.1.49

Cited by 61 publications

(63 citation statements)

References 32 publications

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“…Expression of INK4a was also widespread in humans and mice in contrast to a previous study of murine tissues (Quelle et al, 1995). Clearly both transcripts were capable of being co-expressed, making it unlikely that transcriptional interference (Proudfoot, 1986;Vales and Darnell, 1989;Wu et al, 1990) was operational unless an as yet unknown mechanism was allowing for allelespeci®c transcription. Human INK4a and ARF expression patterns were unique in the pancreas because: (i) no ARF mRNA was detectable; (ii) INK4a mRNA was present at high levels; and (iii) an alternatively spliced INK4a transcript, termed p12, was detected at high levels.…”

Section: Discussionmentioning

confidence: 62%

Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus

1999

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The INK4a/ARF locus on human chromosome 9p resides at the nexus of two critical cell cycle regulatory pathways, the p53 pathway and the retinoblastoma (pRb) gene pathway. Through the use of shared coding regions and alternative reading frames two distinct proteins are produced: INK4a is a cyclin-dependent kinase inhibitor whereas ARF binds the MDM2 protooncogene and stabilizes p53. We have examined the expression patterns of the INK4a/ARF locus at the RNA level in normal human and murine tissues to determine if these genes are coordinately regulated. We found that both INK4a and ARF were expressed in most tissues at low levels detectable only by RT ± PCR. The pancreas was an exception in that it expressed no detectable ARF mRNA but expressed high levels of INK4a mRNA. Furthermore, human pancreas expressed an additional previously unrecognized splice variant of INK4a, termed p12, through the use of an alternative splice donor site within intron 1. The p12 transcript produced a 12 kD protein composed of INK4a exon 1a and a novel intronderived C-terminus. This novel protein did not interact with cdk4 but was capable of suppressing growth in a pRb-independent manner. The implications of the capacity of the INK4a/ARF locus to encode a third transcript, and for pancreatic cancer, in which the INK4a/ARF locus is nearly always altered, are considered.

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Section: Discussionmentioning

confidence: 62%

Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus

1999

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“…The dominant negative p53 plasmid (aa 320 -393) was a kind gift from Dr. Ute Moll (Stony Brook University) (43). Plasmid encoding adenoviral E1B-19K was a kind gift of Dr. Lynne Vales (University of Medicine and Dentistry, New Jersey) (44). Plasmids encoding adenoviral E1B-55K and E4-Orf6 were kind gifts of Dr. Patrick Hearing (Stony Brook University).…”

Section: Methodsmentioning

confidence: 99%

The Interferon Stimulated Gene 54 Promotes Apoptosis

Stawowczyk

Scoy

Kumar

et al. 2011

Journal of Biological Chemistry

149

153

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The ability of interferons (IFNs) to inhibit viral replication and cellular proliferation is well established, but the specific contribution of each IFN-stimulated gene (ISG) to these biological responses remains to be completely understood. In this report we demonstrate that ISG54, also known as IFN-induced protein with tetratricopeptide repeats 2 (IFIT2), is a mediator of apoptosis. Expression of ISG54, independent of IFN stimulation, elicits apoptotic cell death. Cell death and apoptosis were quantified by propidium iodide uptake and annexin-V staining, respectively. The activation of caspase-3, a key mediator of the execution phase of apoptosis, was clearly apparent in cells expressing ISG54.

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“…Subsequently, samples were extracted with phenol-chloroform and chloroform and ethanol precipitated with an Sp6 antisense probe synthesized from pSP73␤Pol which had been digested with HindIII. Samples were then hybridized at 63°C and digested with RNase T 2 as previously described (62). Protected fragments and products from the primer extension reaction were denatured and fractionated by electrophoresis in 8 M urea-6% polyacrylamide sequencing gels.…”

Section: Methodsmentioning

confidence: 99%

Accurate Positioning of RNA Polymerase II on a Natural TATA-Less Promoter Is Independent of TATA-Binding-Protein-Associated Factors and Initiator-Binding Proteins

Weis

Reinberg

1997

Molecular and Cellular Biology

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Two promoter elements, the TATA element and initiator (Inr), are capable of directing specific transcription initiation of protein-encoding genes by RNA polymerase II (RNAPII). Although binding to the TATA element by the TATA-binding protein (TBP) has been shown to be the initial recognition step in transcription complex formation in vitro, the mechanism through which the basal machinery assembles into a functional complex on TATA-less promoters is controversial. Evidence supporting numerous models of Inr-mediated transcription complex formation exists, including the nucleation of a complex by Inr-binding proteins, a component of the TFIID complex, or a specific upstream activator common to many TATA-less promoters, Sp1. Using various techniques, we have undertaken a systematic analysis of the natural TATA-less human DNA polymerase ␤ (␤-pol) gene promoter. Although the ␤-pol promoter contains upstream Sp1 elements and a functional Inr that binds YY1, neither of these factors is essential for Inr-mediated transcription complex formation. A complex containing TBP, TFIIB, TFIIF, and RNAPII (DBPolF complex) is capable of forming on the promoter in an Inr-dependent manner. A single point mutation within the Inr that affects DBPolF complex formation diminishes ␤-pol transcriptional activity.Transcription initiation of protein-encoding genes is a complex process requiring the precise positioning of RNA polymerase II (RNAPII) on promoter DNA. This is accomplished via a series of interactions between RNAPII and at least six accessory proteins, TFIIA, TFIIB, TFIID, TFIIE, TFIIF, and TFIIH, termed the general transcription factors (GTFs) (37, 70). Additionally, nucleation of an initiation complex occurs by recognition of a specific core element (31,54,66). In many genes, the TATA element is the primary core element responsible for positioning the basal transcription machinery on the promoter. TFIID, a multisubunit protein complex consisting of the TATA-binding protein (TBP) and TBP-associated factors (TAFs), nucleates the formation of the transcription initiation complex by binding to the TATA element (8,22,59). In vitro experiments have shown that preinitiation complex assembly proceeds by sequential recruitment of TFIIB followed by RNAPII together with TFIIF, TFIIE, and TFIIH to the promoter-bound TFIID. This multistep model has recently been challenged by the isolation of an RNAPII complex containing a subset of the GTFs, SRB (suppressor of RNAP B) proteins, and additional polypeptides capable of interacting with each other in the absence of promoter DNA (29). Under the appropriate conditions, this complex is capable of specifically initiating transcription and mediating a response to transcriptional activators in vitro (30, 38).As more promoters of protein-encoding genes have been characterized, it has been found that many lack a TATA element (31,54,66). Studies using the TATA-less murine terminal deoxynucleotidyltransferase (TdT) promoter identified a second core element, the initiator (Inr), which encompasses the tra...

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Promoter occlusion prevents transcription of adenovirus polypeptide IX mRNA until after DNA replication.

Cited by 61 publications

References 32 publications

Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus

Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus

The Interferon Stimulated Gene 54 Promotes Apoptosis

Accurate Positioning of RNA Polymerase II on a Natural TATA-Less Promoter Is Independent of TATA-Binding-Protein-Associated Factors and Initiator-Binding Proteins

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