Evidence map›Paper›PMID 15718298›Full record

ArticleNucleic acids research2005

Direct transcriptional repression of the genes encoding the zinc-finger proteins Gfi1b and Gfi1 by Gfi1b.

Lothar Vassen, Katharina Fiolka, Stefan Mahlmann, Tarik Möröy

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Lothar VassenInstitut für Zellbiologie (Tumorforschung), IFZ, Universitätsklinikum Essen Virchowstrasse 173, D-45122 Essen, Germany.
Katharina Fiolka
Stefan Mahlmann
Tarik Möröy
Institut für Medizinische Informatik, Biometrie und Epidemiologie · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gfi1b is a 37 kDa transcriptional repressor with six zinc-finger domains that is differentially expressed during hemato- and lymphopoiesis. We show here that transcription from the Gfi1b gene locus is silenced in the spleen but not in the bone marrow of transgenic mice that constitutively express Gfi1b under the control of the pan-hematopoietic vav promoter. Sequence analysis of the Gfi1b promoter showed the presence of potential Gfi1/Gfi1b-binding sites close to the mRNA start site. The expression of reporter gene constructs containing the Gfi1b core promoter appended to the luciferase gene were strongly repressed in the presence of exogenous Gfi1b. Moreover, analysis of combinatorial mutant mice that carry the vav-Gfi1b transgene and a green fluorescent protein-tagged Gfi1 gene locus demonstrated that the Gfi1 gene can be repressed by Gfi1b. Direct binding of Gfi1b and Gfi1 to the potential binding sites in the Gfi1b promoter could be demonstrated by gel-shift analyses in vitro. Chromatin-immunoprecipitation experiments showed that both the Gfi1b and the Gfi1 promoter are indeed occupied by Gfi1b in vivo. Hence, we conclude from our data that Gfi1b can auto-repress its own expression, but, in addition, is also able to cross-repress expression of the Gfi1 gene most likely in a cell type specific manner.

Indexed as

Gene SilencingAnimalsBase SequenceBinding SitesConserved SequenceDNA-Binding ProteinsHumansMiceMice, TransgenicMolecular Sequence DataPromoter Regions, GeneticProto-Oncogene ProteinsRepressor ProteinsTranscription FactorsTranscription, GeneticZinc FingersDNA-Binding ProteinsGFI1B protein, humanGfi1b protein, mouseGFI1 protein, humanGfi1 protein, mouseProto-Oncogene ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID15718298
PMCPMC549408
OpenAlexW2141478246

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.