Evidence map›Paper›PMID 18710943›Full record

ArticleMolecular and cellular biology2008

Epidermal growth factor receptor 1 (EGFR1) and its variant EGFRvIII regulate TATA-binding protein expression through distinct pathways.

Jody A Fromm, Sandra A S Johnson, Deborah L Johnson

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Biogenesis and functional implications of extracellular vesicles in cancer metastasis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  8. Article
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  10. CyclicOncotarget · 2018
    Article
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  15. Article
  16. Article
  17. Single-cell proteomic chip for profiling intracellular signaling pathways in single tumor cells.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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 1 country.

Jody A FrommDepartment of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Sandra A S Johnson
Deborah L Johnson
University of Southern California · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
TATA-binding protein, a novel target of EGFR signalingR01CA074138 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JOHNSON, DEBORAH L. · 1997 to 2015
$3.6M
NCI NIH HHS CA74138NCI NIH HHS R01 CA074138NIDDK NIH HHS P30 DK048522
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) family regulates essential biological processes. Various epithelial tumors are linked to EGFR overexpression or expression of variant forms, such as the EGFR1 variant, EGFRvIII. Perturbations in expression of the transcription initiation factor, TATA-binding protein (TBP), alter cellular growth properties. Here we demonstrate that EGFR1 and EGFRvIII, but not HER2, induce TBP expression at a transcriptional level through distinct mechanisms. EGFR1 enhances the phosphorylation and function of Elk-1, recruiting it to the TBP promoter. In contrast, EGFRvIII robustly induces c-jun expression, stimulating recruitment of c-fos/c-jun to an overlapping AP-1 site. Enhancing c-jun expression alone induces TBP promoter activity through the AP-1 site. To determine the underlying mechanism for differences in Elk-1 function and c-jun expression by these receptors, we inhibited the internalization of EGFR1. Persistent EGFR1 cell surface occupancy mimics EGFRvIII-mediated effects on Elk-1 and c-jun and switches the requirement of Elk-1 to AP-1 for TBP promoter induction. Together, these studies define a new molecular mechanism for the regulation of TBP expression. In addition, we identify distinct molecular targets of EGFR1 and EGFRvIII and demonstrate the importance of receptor internalization in distinguishing their specific functions.

Indexed as

Signal TransductionAnimalsCell LineClathrinEndocytosisEnzyme ActivationErb-b2 Receptor Tyrosine KinasesErbB Receptorsets-Domain Protein Elk-1HumansMiceMitogen-Activated Protein KinasesMolecular MimicryPromoter Regions, GeneticProto-Oncogene Proteins c-junTATA-Box Binding ProteinClathrinepidermal growth factor receptor VIIIErb-b2 Receptor Tyrosine KinasesErbB Receptorsets-Domain Protein Elk-1Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-junTATA-Box Binding ProteinTranscription Factor AP-1

Identifiers

PMID18710943
PMCPMC2577416
OpenAlexW2054504845

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.