Evidence map›Paper›PMID 9185514›Full record

ArticleThe Journal of clinical investigation1997

Regulation of the rat liver sodium-dependent bile acid cotransporter gene by prolactin. Mediation of transcriptional activation by Stat5.

T C Ganguly, M L O'Brien, S J Karpen, J F Hyde, F J Suchy, M Vore

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
12.4field-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

14 citing papers in PubMed, 104 citations in OpenAlex.

  1. The Culprit Behind HBV-Infected Hepatocytes: NTCP.Drug design, development and therapy · 2024
    Review
  2. Review
  3. Article
  4. Review
  5. Bile formation and secretion.Comprehensive Physiology · 2013
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Bile acid transporters.Journal of lipid research · 2009
    Review
  11. Bile acid transporters in health and disease.Xenobiotica; the fate of foreign compounds in biological systems · 2008
    Review
  12. Increased cholesterol 7alpha-hydroxylase expression and size of the bile acid pool in the lactating rat.American journal of physiology. Gastrointestinal and liver physiology · 2008
    Article
  13. Review
  14. Article
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

6 authors at 3 institutions in 1 country.

T C GangulyGraduate Center for Toxicology, University of Kentucky, Lexington, Kentucky 40536, USA.
M L O'Brien
S J Karpen
J F Hyde
F J Suchy
M Vore
University of Kentucky · USIcahn School of Medicine at Mount Sinai · USThe Graduate Center, CUNY · US

Funding

PROLACTIN AND BILE SECRETORY FUNCTIONR01DK046923 · NIDDK · UNIVERSITY OF KENTUCKY · PI VORE, MARY · 1994 to 2007
$1.4M
TRANSCRIPTIONAL REGULATION OF BILE ACID TRANSPORTK08DK002318 · NIDDK · YALE UNIVERSITY · PI KARPEN, SAUL JOSEPH · 1994 to 1998
–
NIDDK NIH HHS DK02318NIDDK NIH HHS DK46923NIGMS NIH HHS GM55343
6 · The paper itself

Abstract

The intracellular mechanism(s) underlying the upregulation of the hepatic Na+/taurocholate cotransporting polypeptide (ntcp) by prolactin (PRL) are unknown. In this report, we demonstrate a time-dependent increase in nuclear translocation of phosphorylated liver Stat5 (a member of the ignal ransducers and ctivators of ranscription family) that correlated with suckling-induced increases in serum PRL levels. In electrophoretic mobility gel shift assays, nuclear Stat5 exhibited specific DNA-binding ability towards IFN-gamma-activated sequence (GAS)-like elements (GLEs; 5'TTC/A-PyNPu-G/TAA-3') located in the -937 to -904 bp region of the ntcp promoter. Transient cotransfections in HepG2 cells revealed that PRL inducibility (2.5-3-fold) required coexpression of the long form of the PRL receptor (PRLRL) and Stat5. Deletion analysis mapped the PRLinducible region to -1237 to -758 bp of the ntcp promoter. Linking this 0.5-kb region to a heterologous thymidine kinase (tk) promoter, or linking multimerized ntcp GLEs either upstream of the ntcp minimal promoter (-158 to +47 bp) or the heterologous promoter conferred dose-dependent PRL responsiveness. The short form of the PRL receptor failed to transactivate ntcp GLEs. These results indicate that PRL acts via the PRLRL to facilitate Stat5 binding to ntcp-GLEs and to transcriptionally regulate ntcp.

Indexed as

Milk ProteinsOrganic Anion Transporters, Sodium-DependentSymportersAnimalsAnimals, SucklingBinding SitesCarrier ProteinsCell NucleusDNADNA-Binding ProteinsFemaleGene Expression RegulationInterferon-gammaKineticsLiverPhosphorylationCarrier ProteinsDNADNA-Binding ProteinsInterferon-gammaMilk ProteinsOrganic Anion Transporters, Sodium-DependentPhosphotyrosineProlactinReceptors, ProlactinSodiumsodium-bile acid cotransporterSTAT5 Transcription FactorSymportersTrans-Activators

Identifiers

PMID9185514
PMCPMC508142
OpenAlexW1979656599

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.