Evidence map›Paper›PMID 9671466›Full record

ArticleMolecular and cellular biology1998

Regulation of cellular genes in a chromosomal context by the retinoblastoma tumor suppressor protein.

A M Buchmann, S Swaminathan, B Thimmapaya

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
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  5. Antisense-mediated depletion of p300 in human cells leads to premature G1 exit and up-regulation of c-MYC.Proceedings of the National Academy of Sciences of the United States of America · 2001
    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.

A M BuchmannRobert H. Lurie Cancer Center and Department of Microbiology and Immunology, Northwestern University Medical School, Chicago, Illinois 60611-3088, USA.
S Swaminathan
B Thimmapaya
Northwestern University · US

Funding

CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
FUNCTIONS OF AN EIA-ASSOCIATED CELLULAR PROTEINR01CA074403 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THIMMAPAYA, BAYAR · 1998 to 2010
$2.8M
ORGANIZATION AND EXPRESSION OF DNA TUMOR VIRUS GENOMESR01AI020156 · NIAID · NORTHWESTERN UNIVERSITY · PI THIMMAPAYA, BAYAR · 1985 to 1997
–
NCI NIH HHS CA74403NCI NIH HHS R01 CA074403NCI NIH HHS T32 CA009560NCI NIH HHS T32CA09560NIAID NIH HHS AI20156
6 · The paper itself

Abstract

The retinoblastoma tumor suppressor gene product (pRb) is involved in controlling cell cycle progression from G1 into S. pRb functions, in part, by regulating the activities of several transcription factors, making pRb involved in the transcriptional control of cellular genes. Transient-transfection assays have implicated pRb in the transcription of several genes, including c-fos, the interleukin-6 gene, c-myc, cdc-2, c-neu, and the transforming growth factor beta2 gene. However, these assays place the promoter in an artificial context and exclude the effects of far 5' upstream regions and chromosomal architecture on gene transcription. In these experiments, we have studied the role of pRb in the control of cell cycle-related genes within a chromosomal context and within the context of the G1 phase of the cell cycle. We have used adenovirus vectors to overexpress pRb in human osteosarcoma cells and breast cells synchronized in early G1. By RNase protection assays, we have assayed the effects of this virus-produced pRb on gene expression in these cells. These results indicate that pRb is involved in the transcriptional downregulation of the E2F-1, E2F-2, dihydrofolate reductase, thymidine kinase, c-myc, proliferating-cell nuclear antigen, p107, and p21/Cip1 genes. However, it has no effect on the transcription of the E2F-3, E2F-4, E2F-5, DP-1, DP-2, or p16/Ink4 genes. The results are consistent with the notion that pRb controls the transcription of genes involved in S-phase promotion. They also suggest that pRb negatively regulates the transcription of two of the transcription factors whose activity it also represses, E2F-1 and E2F-2, and that it plays a role in downregulating the immediate-early gene response to serum stimulation.

Indexed as

Carrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsTranscription, GeneticAdenoviruses, HumanBinding SitesCell DivisionCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsDown-RegulationE2F1 Transcription FactorE2F2 Transcription FactorE2F3 Transcription FactorE2F4 Transcription FactorE2F5 Transcription FactorCarrier ProteinsCDKN1A protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorE2F2 protein, humanE2F2 Transcription FactorE2F3 Transcription FactorE2F4 protein, humanE2F4 Transcription FactorE2F5 Transcription FactorE2F Transcription FactorsNuclear ProteinsProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-mycRBL1 protein, humanRetinoblastoma-Binding Protein 1Retinoblastoma-Like Protein p107Retinoblastoma ProteinTetrahydrofolate DehydrogenaseTFDP1 protein, humanThymidine KinaseTranscription Factor DP1Transcription Factors

Identifiers

PMID9671466
PMCPMC109042
OpenAlexW2111568069

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.