Evidence map›Paper›PMID 15121856›Full record

ArticleMolecular and cellular biology2004

Identification of PCIF1, a POZ domain protein that inhibits PDX-1 (MODY4) transcriptional activity.

Aihua Liu, Biva M Desai, Doris A Stoffers

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. The role of mFrontiers in endocrinology · 2023
    Review
  4. Review
  5. Review
  6. mCell discovery · 2022
    Article
  7. Article
  8. Association of SPOP Expression with the Immune Response toAnimals : an open access journal from MDPI · 2020
    Article
  9. SPOP and cancer: a systematic review.American journal of cancer research · 2020
    Review
  10. Article
  11. Article
  12. Review
  13. Functional analysis of Cullin 3 E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 2 countries.

Aihua LiuDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, and Penn Diabetes Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Biva M Desai
Doris A Stoffers
Diabetes Australia · AU

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
ZINC FINGER PROTEINS IN EARLY KIDNEY DEVELOPMENTP01DK049210 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI AHIMA, REXFORD S. · 1995 to 2016
$26.9M
NIDDK NIH HHS DK49210NIDDK NIH HHS P01 DK049210NIDDK NIH HHS P30 DK050306NIDDK NIH HHS P30 DK50306
6 · The paper itself

Abstract

Hox factors are evolutionarily conserved homeodomain-containing transcription factors that activate and repress gene expression in a precise temporally and spatially regulated manner during development and differentiation. Pancreatic-duodenal homeobox 1 (PDX-1) is a Hox-type protein that is a critical requirement for normal pancreas development and for proper differentiation of the endocrine pancreas. In humans, PDX-1 gene mutation causes pancreatic agenesis and early- and late-onset type 2 diabetes. PDX-1 consists of an N-terminal transactivation domain, a homeodomain responsible for DNA binding and nuclear localization, and a conserved C terminus that is mutated in human diabetes but whose function is poorly understood. We have identified a novel POZ domain protein, PDX-1 C terminus-interacting factor 1 (PCIF1)/SPOP, that interacts with PDX-1 both in vitro and in vivo. PCIF1 is localized to the nucleus in a speckled pattern, and coexpression of PDX-1 alters the subnuclear distribution of PCIF1. Functionally, PCIF1 inhibits PDX-1 transactivation of established target gene promoters in a specific and dose-dependent manner that requires critical amino acids in the PDX-1 C terminus. PCIF1 is expressed in adult pancreatic insulin-producing beta cells, and overexpression of PCIF1 inhibits the rat insulin 1 and rat insulin 2 promoters in the MIN6 insulinoma beta cell line. The coexpression of PCIF1 with PDX-1 in beta cells and the ability of PCIF1 to repress PDX-1 transactivation suggest that modulation of PDX-1 function by PCIF1 may regulate normal beta cell differentiation.

Indexed as

Homeodomain ProteinsAdaptor Proteins, Signal TransducingAmino Acid SequenceAnimalsBase SequenceDNAHeLa CellsHumansInsulinIn Vitro TechniquesIslets of LangerhansMiceMolecular Sequence DataNuclear ProteinsPromoter Regions, GeneticRatsAdaptor Proteins, Signal TransducingDNAHomeodomain ProteinsInsulinNuclear Proteinspancreatic and duodenal homeobox 1 proteinPCIF1 protein, humanTrans-Activators

Identifiers

PMID15121856
PMCPMC400448
OpenAlexW2030384642

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.