Evidence map›Paper›PMID 15596821›Full record

ArticleJournal of virology2005

Mouse cytomegalovirus early M112/113 proteins control the repressive effect of IE3 on the major immediate-early promoter.

Qiyi Tang, Luge Li, Gerd G Maul

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Murine cytomegalovirus IE3 protein interacts with Ankrd17.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2011
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Qiyi TangThe Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
Luge Li
Gerd G Maul
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
EARLY INTERACTIONS OF DNA VIRUSES AND HOSTR01AI041136 · NIAID · WISTAR INSTITUTE · PI MAUL, GERD G · 1998 to 2005
$1.8M
Early interactions of DNA viruses and hostR56AI041136 · NIAID · WISTAR INSTITUTE · PI KAUFMAN, RUSSEL E. · 2008 to 2009
$828k
EARLY INTERACTIONS OF DNA VIRUSES AND HOSTR21AI041136 · NIAID · WISTAR INSTITUTE · PI MAUL, GERD G · 1997 to 1997
–
VIRUS DNA TARGETING MECHANISM--THE TARGETR21GM057599 · NIGMS · WISTAR INSTITUTE · PI MAUL, GERD G · 1998 to 1999
–
NCI NIH HHS CA-10815NCI NIH HHS P30 CA010815NIAID NIH HHS AI 41136NIAID NIH HHS R01 AI041136NIAID NIH HHS R56 AI041136NIGMS NIH HHS GM57599
6 · The paper itself

Abstract

The mouse cytomegalovirus major immediate-early (IE) transcript is differentially spliced to produce two IE proteins: IE1, which functions partly to maintain its own promoter, the major IE promoter (MIEP), free from repression, and IE3, which functions partly as a repressor of MIEP. Paradoxically, the site where transcription of the viral genome occurs is also the site where the greatest amounts of IE3 accumulate. This raises the question of how the repression capabilities of IE3 are controlled so soon after infection. We detected IE3, an activator of early proteins, contemporaneously with gene products of the early M112/113 locus. Both IE3 and the early M112/113 gene products colocalize and coimmunoprecipitate. Protein interaction most likely occurs between IE3 and the 87-kDa splice form of M112/113, because only the 87-kDa component coimmunoprecipitated with IE3. The complex also includes PML. Transiently expressed M112/113 can form large domains alone, even in the absence of full viral genomes or PML. Coexpression of M112/113 products and IE3 results in segregation of IE3 into newly formed M112/113-based domains. Importantly, coexpression eliminates the IE3-based repressive effect on MIEP, as determined by MIEP-driven reporter assays. The consequence of segregating IE3 into the M112/113-containing prereplication domains appears to make IE3 unavailable for binding and repressing MIEP during the earliest stages of infection. These findings establish a new feedback mechanism between IE and early proteins, a new mechanism of promoter control via segregation of the repressor, and a new function for proteins from the M112/113 locus.

Indexed as

Gene Expression Regulation, ViralAnimalsCell NucleusImmediate-Early ProteinsMiceMicroscopy, ConfocalMuromegalovirusNIH 3T3 CellsPromoter Regions, GeneticRepressor ProteinsTransfectionIE3 protein, cytomegalovirusImmediate-Early ProteinsRepressor Proteins

Identifiers

PMID15596821
PMCPMC538721
OpenAlexW2097402432

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.