Evidence map›Paper›PMID 12554749›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2003

A PIT-1 homeodomain mutant blocks the intranuclear recruitment of the CCAAT/enhancer binding protein alpha required for prolactin gene transcription.

John F Enwright, Margaret A Kawecki-Crook, Ty C Voss, Fred Schaufele, Richard N Day

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. The many faces of C/EBPδ and their relevance for inflammation and cancer.International journal of biological sciences · 2013
    Review
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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

5 authors at 2 institutions in 1 country.

John F EnwrightDepartment of Medicine, University of Virginia Health System, Charlottesville, Virginia 22908-0578, USA.
Margaret A Kawecki-Crook
Ty C Voss
Fred Schaufele
Richard N Day
University of Virginia Health System · USUniversity of California, San Francisco · US

Funding

SPECIFIC REPRESSION OF PROLACTIN GENE EXPRESSIONR01DK043701 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DAY, RICHARD N · 1994 to 2012
$3.4M
TRANSCRIPTION FACTOR INTERACTIONS AT THE GH PROMOTERR01DK054345 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SCHAUFELE, FRED J · 1999 to 2008
$2.0M
CEBPALPHA, Pit1and CBP interactons during GH regulationF32DK010093 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ENWRIGHT, JOHN F · 2001 to 2001
$15k
NIDDK NIH HHS DK-47301NIDDK NIH HHS F32 DK010093NIDDK NIH HHS F32DK-10093NIDDK NIH HHS R01 DK043701NIDDK NIH HHS R01 DK054345
6 · The paper itself

Abstract

The pituitary-specific homeodomain protein Pit-1 cooperates with other transcription factors, including CCAAT/enhancer binding protein alpha (C/EBPalpha), in the regulation of pituitary lactotrope gene transcription. Here, we correlate cooperative activation of prolactin (PRL) gene transcription by Pit-1 and C/EBPalpha with changes in the subnuclear localization of these factors in living pituitary cells. Transiently expressed C/EBPalpha induced PRL gene transcription in pituitary GHFT1-5 cells, whereas the coexpression of Pit-1 and C/EBPalpha in HeLa cells demonstrated their cooperativity at the PRL promoter. Individually expressed Pit-1 or C/EBPalpha, fused to color variants of fluorescent proteins, occupied different subnuclear compartments in living pituitary cells. When coexpressed, Pit-1 recruited C/EBPalpha from regions of transcriptionally quiescent centromeric heterochromatin to the nuclear regions occupied by Pit-1. The homeodomain region of Pit-1 was necessary for the recruitment of C/EBPalpha. A point mutation in the Pit-1 homeodomain associated with the syndrome of combined pituitary hormone deficiency in humans also failed to recruit C/EBPalpha. This Pit-1 mutant functioned as a dominant inhibitor of PRL gene transcription and, instead of recruiting C/EBPalpha, was itself recruited by C/EBPalpha to centromeric heterochromatin. Together our results suggest that the intranuclear positioning of these factors determines whether they activate or silence PRL promoter activity.

Indexed as

Transcription, GeneticActive Transport, Cell NucleusAnimalsCCAAT-Enhancer-Binding Protein-alphaCell NucleusCells, CulturedCentromereDNA-Binding ProteinsGene Expression RegulationGreen Fluorescent ProteinsHeterochromatinHomeodomain ProteinsHumansLuminescent ProteinsMiceMutationCCAAT-Enhancer-Binding Protein-alphaDNA-Binding ProteinsGreen Fluorescent ProteinsHeterochromatinHomeodomain ProteinsLuminescent ProteinsPOU1F1 protein, humanPou1f1 protein, mousePou1f1 protein, ratProlactinRecombinant Fusion ProteinsTranscription Factor Pit-1Transcription Factors

Identifiers

PMID12554749
PMCPMC2900764
OpenAlexW2056494482

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.