Evidence map›Paper›PMID 11992002›Full record

ArticleJournal of virology2002

RelB-p50 NF-kappa B complexes are selectively induced by cytomegalovirus immediate-early protein 1: differential regulation of Bcl-x(L) promoter activity by NF-kappa B family members.

H Y Jiang, Constantinos Petrovas, Gail E Sonenshein

Open access · greenAbstract 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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Atypical IκB Bcl3 enhances the generation of the NF-κB p52 homodimer.Frontiers in cell and developmental biology · 2022
    Article
  2. PPE38-Secretion-Dependent Proteins ofFrontiers in immunology · 2021
    Article
  3. Review
  4. Article
  5. Noncanonical NF-κB in Cancer.Biomedicines · 2018
    Review
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  7. Article
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  11. Article
  12. Review
  13. Article
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  16. Article
  17. Article
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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.

H Y JiangDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118-2394, USA.
Constantinos Petrovas
Gail E Sonenshein
Boston University · US

Funding

TISSUE CULTURE FACILITY (MAMMALS) --COREP01HL013262 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SMITH, BARBARA A · 1985 to 2007
$12.5M
EXPRESSION OF ONCOGENES &IGA GENES IN TRANSFORMED CELLSR01CA036355 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SONENSHEIN, GAIL E · 1985 to 2007
$2.1M
NCI NIH HHS CA36355NCI NIH HHS R01 CA036355NHLBI NIH HHS HL13262NHLBI NIH HHS P01 HL013262
6 · The paper itself

Abstract

The NF-kappa B/Rel family has been implicated in control of transcription of the Bcl-x(L) gene, a target which mediates cell survival signals. The cytomegalovirus (CMV) immediate-early protein 1 (IE1) was previously shown to induce NF-kappa B activity. Here, we report that in both vascular smooth muscle cells (SMCs) and NIH 3T3 cells, surprisingly, IE1 failed to induce Bcl-x(L) promoter activity, although it induced activity of E8-CAT, a reporter construct driven by two copies of the NF-kappa B element upstream of the c-myc promoter (upstream regulatory element [URE]). Thus, the subunit nature of the NF-kappa B/Rel factors induced by IE1 was examined using immunofluorescence and immunoblotting. IE1 was found to selectively induce nuclear RelB and p50 in SMCs and NIH 3T3 cells. An increase in RelB protein mediated by IE1 could, in part, be related to an increase in steady-state relB mRNA levels. Consistent with this subunit identification, IE1 was unable to induce E8-CAT activity in relB(-/-) murine embryonic fibroblast cells. In cotransfection analysis of SMCs and NIH 3T3 cells, RelB and p50 proteins failed to induce Bcl-x(L) promoter activity while inducing E8-CAT. Furthermore, the NF-kappa B element of the Bcl-x(L) promoter only weakly bound RelB-p50 complexes compared to the URE NF-kappa B element. Overall, these findings demonstrate in SMCs and NIH 3T3 cells that the CMV IE1 protein selectively induces RelB and p50, which fail to activate the Bcl-x(L) promoter, indicating a strong specificity of binding and activity for the RelB member of the NF-kappa B family. Furthermore, our results implicate RelB in CMV infection of cells such as vascular SMCs.

Indexed as

Promoter Regions, GeneticTranscriptional ActivationViral Proteins3T3 CellsAnimalsbcl-X ProteinCattleCell NucleusCells, CulturedChloramphenicol O-AcetyltransferaseCytomegalovirusFemaleGenes, ReporterHumansImmediate-Early ProteinsMiceBCL2L1 protein, humanBcl2l1 protein, mousebcl-X ProteinChloramphenicol O-AcetyltransferaseIE1 protein, cytomegalovirusImmediate-Early ProteinsNF-kappa BNF-kappa B p50 SubunitProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2RELB protein, humanRelb protein, mouseTranscription Factor RelBTranscription FactorsViral Proteins

Identifiers

PMID11992002
PMCPMC137022
OpenAlexW2121712094

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.