Evidence map›Paper›PMID 16024782›Full record

ArticleMolecular and cellular biology2005

hnRNP K binds a core polypyrimidine element in the eukaryotic translation initiation factor 4E (eIF4E) promoter, and its regulation of eIF4E contributes to neoplastic transformation.

Mary Lynch, Li Chen, Michael J Ravitz, Sapna Mehtani, Kevin Korenblat, Michael J Pazin, Emmett V Schmidt

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing 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

62 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
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  5. International journal of molecular sciences · 2021
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  7. Article
  8. Review
  9. Review
  10. Article
  11. Uncovering the Role of RNA-Binding Protein hnRNP K in B-Cell Lymphomas.Journal of the National Cancer Institute · 2020
    Article
  12. Article
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  14. Article
  15. Review
  16. Article
  17. Article
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  20. Article

2 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

7 authors at 4 institutions in 2 countries.

Mary LynchCancer Research Center at Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA.
Li Chen
Michael J Ravitz
Sapna Mehtani
Kevin Korenblat
Michael J Pazin
Emmett V Schmidt
Harvard University · USBoston Children's Hospital · USNeurological Institute of Athens · GRUniversity of Washington · US

Funding

RESEARCH TRAINING IN DIGESTIVE DISEASES AND NUTRITIONT32DK007191 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1986 to 2026
$14.6M
MOLECULAR IMMUNOLOGY AND TUMOR BIOLOGYT32CA009216 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI David Michael Langenau · 1985 to 2026
$10.6M
GENES REGULATED BY C-MYCR01CA063117 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SCHMIDT, EMMETT VANCE · 1994 to 2004
$1.9M
Chromatin Remodeling and Lymphocyte RegulationZIAAG000524 · NIA · NATIONAL INSTITUTE ON AGING · PI PAZIN, MICHAEL J · 2009 to 2012
$1.4M
Chromatin Remodeling and Lymphocyte RegulationZ01AG000524 · NIA · NATIONAL INSTITUTE ON AGING · PI PAZIN, MICHAEL J · 2005 to 2008
$999k
NCI NIH HHS 5T32 CA009216-24NCI NIH HHS R01 CA063117NCI NIH HHS R01-CA63117NCI NIH HHS T32 CA009216NIDDK NIH HHS T32 DK007191
6 · The paper itself

Abstract

Translation initiation factor eukaryotic translation initiation factor 4E (eIF4E) plays a key role in regulation of cellular proliferation. Its effects on the m7GpppN mRNA cap are critical because overexpression of eIF4E transforms cells, and eIF4E function is rate-limiting for G1 passage. Although we identified eIF4E as a c-Myc target, little else is known about its transcriptional regulation. Previously, we described an element at position -25 (TTACCCCCCCTT) that was critical for eIF4E promoter function. Here we report that this sequence (named 4EBE, for eIF4E basal element) functions as a basal promoter element that binds hnRNP K. The 4EBE is sufficient to replace TATA sequences in a heterologous reporter construct. Interactions between 4EBE and upstream activator sites are position, distance, and sequence dependent. Using DNA affinity chromatography, we identified hnRNP K as a 4EBE-binding protein. Chromatin immunoprecipitation, siRNA interference, and hnRNP K overexpression demonstrate that hnRNP K can regulate eIF4E mRNA. Moreover, hnRNP K increased translation initiation, increased cell division, and promoted neoplastic transformation in an eIF4E-dependent manner. hnRNP K binds the TATA-binding protein, explaining how the 4EBE might replace TATA in the eIF4E promoter. hnRNP K is an unusually diverse regulator of multiple steps in growth regulation because it also directly regulates c-myc transcription, mRNA export, splicing, and translation initiation.

Indexed as

AnimalsBase SequenceBinding SitesCell Transformation, NeoplasticEukaryotic Initiation Factor-4EGene Expression Regulation, NeoplasticHeLa CellsHeterogeneous-Nuclear Ribonucleoprotein KHumansMiceMolecular Sequence DataPromoter Regions, GeneticRatsTATA BoxTranscription, GeneticEukaryotic Initiation Factor-4EHeterogeneous-Nuclear Ribonucleoprotein K

Identifiers

PMID16024782
PMCPMC1190351
OpenAlexW2163930739

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.