Common control of the heat shock gene and early adenovirus genes: evidence for a cellular E1A-like activity.

Imperiale, Michael J.; Kao, Hung‐Teh; Feldman, L T; Nevins, Joseph R.; Strickland, S

doi:10.1128/mcb.4.5.867

Cited by 291 publications

(199 citation statements)

References 28 publications

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“…The E1A-dependent E2A gene (9) is transcribed when EC stem cells are infected with dl312 (7). However, the E2A gene is not activated when infected into differentiated derivatives of EC stem cells (7). More recently, the presence of cellular factors responsible for the stimulation of E2A transcription was demonstrated in EC stem cells but not in differentiated cells (10,13).…”

mentioning

confidence: 98%

“…Adenovirus ElA gene products immortalize primary rodent cells and work as the trans-acting regulators which activate or repress transcription of other adenovirus genes and many cellular genes (12), such as heat shock proteins (7) and major histocompatibility complex antigen genes (14,19). Presence of the ElA-like activity in embryonal carcinoma (EC) stem cells was shown by infection of the stem cells with ElA-deleted an adenovirus type S (AdS) mutant (7), dl312, and by studies on regulation of virus gene expression, such as by polyomavirus and its mutants (5).…”

mentioning

confidence: 99%

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Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos.

Suemori¹,

Hashimoto²,

Nakatsuji³

1988

Mol. Cell. Biol.

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The presence of the adenovirus E1A-like activity in embryonal carcinoma stem cells has been reported. We now show that preimplantation stage mouse embryonic cells allow transcription of the E1A-dependent E2A gene when infected with E1A-deleted mutant dl312, indicating the presence of the E1A-like activity in morulae and blastocysts. Moreover, such activity seems to decrease or disappear at about the time of implantation.

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mentioning

confidence: 98%

mentioning

confidence: 99%

Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos.

Suemori¹,

Hashimoto²,

Nakatsuji³

1988

Mol. Cell. Biol.

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show abstract

“…This phenomenon has been reported before with the presence of IL-6 or papillomavirus E6 and E7 allowing replication of E1-deleted viruses. [60][61][62][63][64] In fact, it was demonstrated that factors produced by primary ovarian cancer cells allowed similar replication of an E1-deleted virus and a wild-type adenovirus. 60 While xenografts have traditionally been utilized for investigation of therapeutic efficacy, receptor levels on these cancer cell lines may not correspond well with primary tumors.…”

Section: Discussionmentioning

confidence: 99%

Replication of an integrin targeted conditionally replicating adenovirus on primary ovarian cancer spheroids

et al. 2003

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Replication competent viruses hold promise for treatment of advanced cancers resistant to available therapeutic modalities. Although preliminary clinical results have substantiated their efficacy, preclinical development of these novel approaches is limited by assay substrates. The evaluation of candidate agents could be confounded by differences between primary tumor cells and tumor cell lines, as discordance in the levels of surface receptors relevant for viral entry has been reported. Since primary tumor cells are difficult to analyze ex vivo for longitudinal observation of virus replication, we developed three-dimensional aggregates or spheroids of unpassaged and purified ovarian cancer cells as a means for prolonging primary tumor cell viability and as a threedimensional in vitro model for replicative viral infection. Ovarian cancer cells purified from ascites samples were sustained for 30 days while retaining the infection profile with tropism modified and unmodified adenoviruses (Ads). Cell line and primary cell spheroids were used to quantitate the replication and oncolytic potency of replicative Ads in preclinical testing for human ovarian cancer trials. Therefore, spheroids provide a method to sustain purified unpassaged primary ovarian cancer cells for extended periods and to allow evaluation of replicative viruses in a three-dimensional model.

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“…6b), suggesting a direct link between loss of PML-II and HSP70 expression. Ad5 infection also induces HSP70 expression (Nevins, 1982) and, since it inhibits many other host genes whose activity is detrimental to infection (Zhao et al, 2003) and pre-existing HSP70 levels correlate with permissivity to Ad infection (Imperiale et al, 1984), we inferred that HSP70 might be the relevant positive factor for Ad5 growth in HelaDII cells. To test this, hexon expression was compared in cells infected with or without HSP70 knockdown (Fig.…”

Section: Enhanced Growth Of Ad5 In Heladii Cells Reflects Overexpressmentioning

confidence: 99%

Promyelocytic leukemia protein isoform II inhibits infection by human adenovirus type 5 through effects on HSP70 and the interferon response

Atwan

Wright

Woodman

et al. 2016

Journal of General Virology

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Promyelocytic leukemia (PML) proteins have been implicated in antiviral responses but PML and associated proteins are also suggested to support virus replication. One isoform, PML-II, is required for efficient transcription of interferon and interferon-responsive genes. We therefore investigated the PML-II contribution to human adenovirus 5 (Ad5) infection, using shRNAmediated knockdown. HelaDII cells showed a 2-3-fold elevation in Ad5 yield, reflecting an increase in late gene expression. This increase was found to be due in part to the reduced innate immune response consequent upon PML-II depletion. However, the effect was minor because the viral E4 Orf3 protein targets and inactivates this PML-II function. The major benefit to Ad5 in HelaDII cells was exerted via an increase in HSP70; depletion of HSP70 completely reversed this replicative advantage. Increased Ad5 late gene expression was not due either to the previously described inhibition of inflammatory responses by HSP70 or to effects of HSP70 on major late promoter or L4 promoter activity, but might be linked to an observed increase in E1B 55K, as this protein is known to be required for efficient late gene expression. The induction of HSP70 by PML-II removal was specific for the HSPA1B gene among the HSP70 gene family and thus was not the consequence of a general stress response. Taken together, these data show that PML-II, through its various actions, has an overall negative effect on the Ad5 lifecycle.

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Common control of the heat shock gene and early adenovirus genes: evidence for a cellular E1A-like activity.

Abstract: We have employed an antiserum specific to the 70-kilodalton human heat shock protein and a cDNA clone specific to

Cited by 291 publications

References 28 publications

Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos.

Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos.

Replication of an integrin targeted conditionally replicating adenovirus on primary ovarian cancer spheroids

Promyelocytic leukemia protein isoform II inhibits infection by human adenovirus type 5 through effects on HSP70 and the interferon response

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