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Related Experiment Video

Updated: Jun 2, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

TFG-1 function in protein secretion and oncogenesis.

Kristen Witte1, Amber L Schuh, Jan Hegermann

  • 1Department of Biomolecular Chemistry, University of Wisconsin-Madison Medical School, 1300 University Avenue, Madison, Wisconsin 53706, USA.

Nature Cell Biology
|April 12, 2011
PubMed
Summary
This summary is machine-generated.

Researchers discovered TFG-1, a protein regulating endoplasmic reticulum export. TFG-1

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09:18

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Published on: November 16, 2011

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncogenesis

Background:

  • Protein export from the endoplasmic reticulum (ER) is crucial for cellular function.
  • This process relies on COPII-coated vesicles forming at ER exit sites (ERES).
  • The scaffolding protein Sec16 is a key component of ERES.

Purpose of the Study:

  • To identify novel regulators of protein secretion.
  • To elucidate the role of TFG-1 in ER protein export.
  • To understand the link between TFG-1, ER export, and oncogenesis.

Main Methods:

  • Protein interaction studies.
  • Hydrodynamic studies to determine TFG-1 oligomerization.
  • Depletion studies using Caenorhabditis elegans to assess TFG-1 function.
  • Analysis of human TFG gene fusions in cancer.

Main Results:

  • TFG-1 directly interacts with Sec16 and regulates ER export.
  • TFG-1 forms hexamers that promote Sec16 and COPII subunit assembly.
  • TFG-1 depletion reduces Sec16 and COPII levels at ERES.
  • Human TFG fusions with kinases create oncogenes by mislocalizing kinase activity.

Conclusions:

  • TFG-1 is a conserved regulator of ER protein export.
  • TFG-1's function is essential for maintaining ERES integrity.
  • Aberrant TFG-1 interactions in cancer contribute to cellular transformation.