Evidence map›Paper›PMID 12368334›Full record

ArticleJournal of virology2002

Modulation of the cell division cycle by human papillomavirus type 18 E4.

Tomomi Nakahara, Akiko Nishimura, Masakazu Tanaka, Takaharu Ueno, Akinori Ishimoto, Hiroyuki Sakai

Abstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

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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

6 authors.

Tomomi NakaharaLaboratory of Gene Analysis, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-Ku, Kyoto 606-8507, Japan.
Akiko Nishimura
Masakazu Tanaka
Takaharu Ueno
Akinori Ishimoto
Hiroyuki Sakai

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The life cycle of human papillomaviruses (HPVs) is tightly coupled to the differentiation program of their host epithelial cells. HPV E4 gene expression is first observed in the parabasal layers of squamous epithelia, suggesting that the E4 gene product contributes to the mechanism of differentiation-dependent virus replication, although its biological function remains unclear. We analyzed the effect of HPV type 18 E4 on cell proliferation and found that E4 expression induced cell cycle arrest at the G(2)/M boundary. The functional region of E4 necessary for the growth arrest activity was located in the central portion of the molecule, and this activity was independent of the E4-mediated collapse of cytokeratin intermediate filament structures.

Indexed as

AnimalsCell CycleCell DivisionCell LineChlorocebus aethiopsG2 PhaseHeLa CellsHumansKeratinsMitosisOncogene Proteins, ViralPapillomaviridaeKeratinsoncogene protein E1, Human papillomavirus type 18oncogene protein E4, Human papillomavirus type 18Oncogene Proteins, Viral

Identifiers

PMID12368334
PMCPMC136601

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.