Evidence map›Paper›PMID 21478858›Full record

ArticleNature cell biology2011

TFG-1 function in protein secretion and oncogenesis.

Kristen Witte, Amber L Schuh, Jan Hegermann, Ali Sarkeshik, Jonathan R Mayers, Katrin Schwarze, John R Yates, Stefan Eimer, Anjon Audhya

Abstract read
In one paragraph

Article in Nature cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 187 citations in OpenAlex.

  1. Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024
    Pooled it
  2. Inhibition of TFG function causes hereditary axon degeneration by impairing endoplasmic reticulum structure.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Trial
  3. Review
  4. Article
  5. JCO precision oncology · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. The life cycle of type IV collagen.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
  11. Article
  12. Cell type-specific gene therapy confers protection against motor neuron disease caused by a TFG variant.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

53 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Kristen WitteDepartment of Biomolecular Chemistry, University of Wisconsin-Madison Medical School, 1300 University Avenue, Madison, Wisconsin 53706, USA.
Amber L Schuh
Jan Hegermann
Ali Sarkeshik
Jonathan R Mayers
Katrin Schwarze
John R Yates
Stefan Eimer
Anjon Audhya
University of Wisconsin–Madison · USEuropean Neuroscience Institute Göttingen · DEScripps Research Institute · USBrain (Germany) · DE

Funding

ZDS2P REGULATES SWE1P-DEPENDENT POLARIZED CELL GROWTH IN S CEREVISIAEP41RR011823 · NCRR · UNIVERSITY OF WASHINGTON · PI DAVIS, TRACY · 1996 to 2011
$24.7M
Molecular Mechanisms that Regulate Lysosomal Protein TransportR01GM088151 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI AUDHYA, ANJON · 2010 to 2019
$3.0M
NCRR NIH HHS P41 RR011823NCRR NIH HHS P41RR011823NIGMS NIH HHS 1R01GM088151-01A1NIGMS NIH HHS R01 GM088151
6 · The paper itself

Abstract

Export of proteins from the endoplasmic reticulum in COPII-coated vesicles occurs at defined sites that contain the scaffolding protein Sec16. We identify TFG-1, a new conserved regulator of protein secretion that interacts directly with SEC-16 and controls the export of cargoes from the endoplasmic reticulum in Caenorhabditis elegans. Hydrodynamic studies indicate that TFG-1 forms hexamers that facilitate the co-assembly of SEC-16 with COPII subunits. Consistent with these findings, TFG-1 depletion leads to a marked decline in both SEC-16 and COPII levels at endoplasmic reticulum exit sites. The sequence encoding the amino terminus of human TFG has been previously identified in chromosome translocation events involving two protein kinases, which created a pair of oncogenes. We propose that fusion of these kinases to TFG relocalizes their activities to endoplasmic reticulum exit sites, where they prematurely phosphorylate substrates during endoplasmic reticulum export. Our findings provide a mechanism by which translocations involving TFG can result in cellular transformation and oncogenesis.

Indexed as

Cell Transformation, NeoplasticAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsEndoplasmic ReticulumHumansMembrane ProteinsCaenorhabditis elegans Proteinsdnj-29 protein, C elegansMembrane Proteins

Identifiers

PMID21478858
PMCPMC3311221
OpenAlexW2144487953

What OpenQuestion holds

Textmetadata
LicenceTDM
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.