Role of Adenovirus E1B Proteins in Transformation: Altered Organization of Intermediate Filaments in Transformed Cells That Express the 19-Kilodalton Protein

White, Eileen; Cipriani, Ralph

doi:10.1128/mcb.10.1.120-130.1990

Cited by 15 publications

(2 citation statements)

References 60 publications

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“…The CrmA cDNA was a gift from Yuri Lazebnik (Cold Spring Harbor Laboratory, N.Y.) and was subcloned into pcDNA3. Adenovirus E1B 19 K protein cDNA was a gift from Eileen White (Rutgers University, New Brunswick, N.J.) (29) was subcloned into pcDNA3.1(Ϫ). The expression plasmids encoding FLAG-tagged p53 mutant (F320 -393) and p53 were gifts from Ute Moll (SUNY Stony Brook, New York) (30).…”

Section: Plasmid Constructsmentioning

confidence: 99%

Apoptosis is promoted by the dsRNA‐activated factor (DRAF1) during viral infection independent of the action of interferon or p53

et al. 2001

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An apoptotic cellular defense mechanism is triggered in response to viral dsRNA generated during the course of infection by many DNA and RNA viruses. We demonstrate that apoptosis induced by dsRNA or a paramyxovirus is independent of the action of interferon as it can proceed in a variety of cell lines and primary cells deficient in an interferon response. Initiation of apoptosis appears to be triggered by activation of a cellular transcription factor, the dsRNA-activated factor (DRAF1). DRAF1 is composed of interferon regulatory factor 3 (IRF-3) and the transcriptional coactivators CREB binding protein (CBP) or p300. We find that activation of IRF-3 in the absence of viral infection stimulates apoptosis. In addition, a negative interfering mutant blocks both target gene induction and apoptosis, demonstrating a requirement for gene expression by IRF-3/DRAF1 to promote apoptosis. IRF-3/DRAF1 target gene expression is also induced in response to a distinct apoptotic stimulus, the DNA damaging agent etoposide. The activity of the p53 tumor suppressor does not appear to be required for IRF-3/DRAF1-mediated apoptosis.

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Section: Plasmid Constructsmentioning

confidence: 99%

Apoptosis is promoted by the dsRNA‐activated factor (DRAF1) during viral infection independent of the action of interferon or p53

et al. 2001

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“…Adenovirus-infected cells require these two proteins to block apoptosis. E1B proteins help to block, apoptosis, which is caused by the E1A protein of the small adenovirus, which stabilizes the tumor suppressor p53 [10,11]. PML gene was overexpressed to investigate its antagonistic effect against the ability of Ad5 to transform cells [12].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of ABL1 Gene Expression Due to the Co-expression of PML-II and adenovirus Genome Transfection

2022

Basrah Researches Sciences

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Several promyelocytic leukemia proteins (PML) isoforms are involved in a wide range of cellular functions, including innate immune responses, gene transcription, and apoptosis. Adenoviridae are non-enveloped viruses that can disrupt cellular systems that control cell cycle progression and apoptosis,. The study analyzed the gene expression of ABL-1(Tyrosine Kinase gene), into cells transfected with adenovirus and PML-II expression plasmids. A human breast cancer cell line (MCF-7) cells were plated in 24 well plates in 500 microliters of Dulbecco's Modified Eagle Medium (DMEM) for each well, and after 24 hours, the cells were harvested and used for gene expression analysis. So, the aim was evaluate the effect of the effect of PML-II on ABL1 gene expression. The results showed that ABL1 gene expression was in transfected Ad5 and PML samples compared to the control.

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Human cytomegalovirus IE1 and IE2 proteins are mutagenic and mediate “hit-and-run” oncogenic transformation in cooperation with the adenovirus E1A proteins

Shen

Zhu²,

Shenk

1997

Proc. Natl. Acad. Sci. U.S.A.

162

109

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Some epidemiological studies have suggested a possible link between human cytomegalovirus (HCMV) infection and various malignancies, and HCMV has been shown to transform cultured cells. However, viral DNA is not detected in most transformants, and the mechanism by which HCMV might contribute to oncogenesis has remained obscure. Here we show that the HCMV immediate early 1 and 2 genes can cooperate with the adenovirus E1A gene to generate transformed foci of primary baby rat kidney cells. HCMV gene expression is transient and viral DNA is not present in clonal cell lines derived from the transformed foci. We find that the HCMV immediate early proteins are mutagenic, and we propose that HCMV has the potential to contribute to oncogenesis through a ''hit-and-run'' mechanism, by inducing mutations in cellular genes.Serological and molecular studies have suggested a possible association of human cytomegalovirus (HCMV) with the development of human malignancies, including cervical carcinoma, colon carcinoma, and prostate cancer (reviewed in refs. 1-5). A variety of laboratory observations demonstrate that HCMV has oncogenic potential, supporting the idea that HCMV might contribute to the induction of human tumors. HCMV has been shown to induce cervical neoplasia in mice (6), it can morphologically transform human (7,8) as well as other mammalian (9 -11) cells in culture, and HCMVtransformed cells can form tumors in experimental animals (6,8). In vitro assays have identified three regions on the HCMV genome with transforming activity (reviewed in ref. 5). However, if HCMV infection does contribute to tumor induction in humans, the mechanism underlying HCMV-induced oncogenesis is very likely different from that of DNA viruses that are known to play a role in human malignancies. Whereas specific viral genes are present and expressed in tumors induced by agents such as Epstein-Barr virus and the human papillomaviruses, no specific HCMV DNA sequence element is reliably present and often no viral DNA can be detected in cells transformed by HCMV (reviewed in refs. 4 and 12).We have previously reported (13) that the two most abundantly expressed immediate-early gene products of HCMV, IE1 and IE2 (reviewed in ref. 14), inhibit the induction of apoptosis by tumor necrosis factor ␣ (TNF-␣) or the adenovirus E1A oncoproteins. The fact that the IE1 and IE2 gene products are able to inhibit apoptosis raised the interesting possibility that they might cooperate with the adenovirus E1A oncoproteins to transform primary rodent cells, as do the adenovirus E1B 19-kDa (E1B) protein and the cellular Bcl-2 protein, each of which can block apoptosis (15,16). In this report, we show that the IE1 and IE2 gene products can, indeed, cooperate with E1A to transform primary baby rat kidney (BRK) cells. Unexpectedly, however, we find that expression of the IE1 and IE2 proteins is transient; HCMV proteins and DNA are not present in transformed cell lines derived from the foci. The IE1 and IE2 gene products are mutagenic, and we propose that...

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Role of Adenovirus E1B Proteins in Transformation: Altered Organization of Intermediate Filaments in Transformed Cells That Express the 19-Kilodalton Protein

Cited by 15 publications

References 60 publications

Apoptosis is promoted by the dsRNA‐activated factor (DRAF1) during viral infection independent of the action of interferon or p53

Apoptosis is promoted by the dsRNA‐activated factor (DRAF1) during viral infection independent of the action of interferon or p53

Upregulation of ABL1 Gene Expression Due to the Co-expression of PML-II and adenovirus Genome Transfection

Human cytomegalovirus IE1 and IE2 proteins are mutagenic and mediate “hit-and-run” oncogenic transformation in cooperation with the adenovirus E1A proteins

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