Evidence map›Paper›PMID 8754800›Full record

ArticleMolecular and cellular biology1996

Gfi-1 encodes a nuclear zinc finger protein that binds DNA and functions as a transcriptional repressor.

P A Zweidler-Mckay, H L Grimes, M M Flubacher, P N Tsichlis

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

137 citing papers in PubMed, 308 citations in OpenAlex.

  1. Review
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  10. Machine-guided design of synthetic cell type-specificbioRxiv : the preprint server for biology · 2023
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  20. Review

77 more citing papers are in PubMed but not listed here.

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.

P A Zweidler-MckayFox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA.
H L Grimes
M M Flubacher
P N Tsichlis
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
PROGRESSION OF T CELL LYMPHOMA LINE TO IL-2 INDEPENDENCER01CA056110 · NCI · THOMAS JEFFERSON UNIVERSITY · PI TSICHLIS, PHILIP N · 1992 to 2001
$696k
THE ROLE OF GFI-1 IN IL-2 SIGNALLING AND ONCOGENESISF32CA059302 · NCI · FOX CHASE CANCER CENTER · PI GRIMES, H LEIGHTON · 1993 to 1996
–
NCI NIH HHS CA06927NCI NIH HHS CA56110NCI NIH HHS CA59302
6 · The paper itself

Abstract

The Gfi-1 proto-oncogene encodes a zinc finger protein with six C2H2-type, C-terminal zinc finger motifs and is activated by provirus integration in T-cell lymphoma lines selected for interleukin-2 independence in culture and in primary retrovirus-induced thymomas. Gfi-1 expression in adult animals is restricted to the thymus, spleen, and testis and is enhanced in mitogen-stimulated splenocytes. In this report, we show that Gfi-1 is a 55-kDa nuclear protein that binds DNA in a sequence-specific manner. The Gfi-1 binding site, TAAATCAC(A/T)GCA, was defined via random oligonucleotide selection utilizing a bacterially expressed glutathione S-transferase-Gfi-1 fusion protein. Binding to this site was confirmed by electrophoretic mobility shift assays and DNase I footprinting. Methylation interference analysis and electrophoretic mobility shift assays with mutant oliginucleotides defined the relative importance of specific bases at the consensus binding site. Deletion of individual zinc fingers demonstrated that only zinc fingers 3, 4, and 5 are required for sequence-specific DNA binding. Potential Gfi-1 binding sites were detected in a large number of eukaryotic promoter-enhancers, including the enhancers of several proto-oncogenes and cytokine genes and the enhancer of the human cytomegalovirus (HCMV) major immediate-early promoter, which contains two such sites. HCMV major immediate-early-chloramphenicol acetyltransferase reporter constructs, transfected into NIH 3T3 fibroblasts, were repressed by Gfi-1, and the repression was abrogated by mutation of critical residues in the two Gfi-1 binding sites. These results suggest that Gfi-1 may play a role in HCMV biology and may contribute to oncogenesis and T-cell activation by repressing the expression of genes that inhibit these processes.

Indexed as

Promoter Regions, GeneticRepressor ProteinsTranscription Factors3T3 CellsAnimalsBase SequenceBinding SitesConsensus SequenceDNA-Binding ProteinsGene Expression RegulationHL-60 CellsHumansMethylationMiceMolecular Sequence DataNuclear ProteinsDNA-Binding ProteinsGFI1 protein, humanGfi1 protein, mouseMAS1 protein, humanNuclear ProteinsProto-Oncogene MasRepressor ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID8754800
PMCPMC231398
OpenAlexW2136317405

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.