Evidence map›Paper›PMID 8816482›Full record

ArticleMolecular and cellular biology1996

Deletion of the carboxyl-terminal transactivation domain of MGF-Stat5 results in sustained DNA binding and a dominant negative phenotype.

R Moriggl, V Gouilleux-Gruart, R Jähne, S Berchtold, C Gartmann, X Liu, L Hennighausen, A Sotiropoulos, B Groner, F Gouilleux

Open access · bronzeAbstract read
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 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
19.3field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 270 citations in OpenAlex.

  1. Article
  2. Review
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  4. Classical and novel GH receptor signaling pathways.Molecular and cellular endocrinology · 2020
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10 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

10 authors at 5 institutions in 4 countries.

R MorigglTumor Biology Center, Institute for Experimental Cancer Research, Freiburg, Germany.
V Gouilleux-Gruart
R Jähne
S Berchtold
C Gartmann
X Liu
L Hennighausen
A Sotiropoulos
B Groner
F Gouilleux
University of Freiburg · DENational Institute of Diabetes and Digestive and Kidney Diseases · USCentre Hospitalier Universitaire Amiens-Picardie · FRInserm · FRMax Planck Institute of Immunobiology and Epigenetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Stat (signal transducer and activator of transcription) factors transmit cytokine, growth factor, and hormone responses. Seven members of the Stat gene family are known. MGF-Stat5a has been discovered as a mediator of the prolactin response in mammary epithelial cells. Two closely related variants of Stat5, Stat5a and Stat5b, are encoded by distinct genes. We examined the functional properties of the carboxyl termini of these molecules. Wild-type Stat5a (794 amino acids) and the carboxyl-terminal deletion mutant Stat5a delta 772 supported prolactin-induced transcription of a beta-casein promoter-reporter construct in COS7 cells; Stat5a delta 750 did not. Upon prolactin activation, tyrosine phosphorylation and the specificity of DNA binding were indistinguishable among the three Stat5a variants. Tyrosine dephosphorylation and the downregulation of the DNA-binding activity were delayed in the Stat5a delta 750 mutant. The carboxyl-terminal transactivation domain of Stat5a, amino acids 722 to 794, can be conferred to the DNA-binding domain of the yeast transcription factor GAL4. Coexpression of Stat5a or Stat5b and of the carboxyl-terminal deletion mutants resulted in the suppression of transcriptional induction in COS or Ba/F3 cells. We propose that Stat5a delta 750 and Stat5b delta 754 are lacking functional transactivation domains and exert their dominant negative effects by blocking the DNA-binding site in Stat5-responsive gene promoters.

Indexed as

Milk ProteinsSaccharomyces cerevisiae ProteinsSequence DeletionTranscriptional ActivationTranscription FactorsTranscription, GeneticAmino Acid SequenceAnimalsBase SequenceCaseinsCattleCell NucleusCOS CellsDNADNA-Binding ProteinsFungal ProteinsCaseinsDNADNA-Binding ProteinsFungal ProteinsGAL4 protein, S cerevisiaeLuciferasesMilk ProteinsOligodeoxyribonucleotidesPhosphotyrosineSaccharomyces cerevisiae ProteinsSTAT5A protein, humanSTAT5B protein, humanSTAT5 Transcription FactorTrans-ActivatorsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID8816482
PMCPMC231569
OpenAlexW2096245547

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.