The discovery of a reciprocal relationship between tyrosine-kinase signaling and cullin neddylation

PLoS One. 2013 Oct 4;8(10):e75200. doi: 10.1371/journal.pone.0075200. eCollection 2013.

Abstract

While neddylation is known to activate cullin (CUL)-RING ubiquitin ligases (CRLs), its role in regulating T cell signaling is poorly understood. Using the investigational NEDD8 activating enzyme (NAE) inhibitor, MLN4924, we found that neddylation negatively regulates T cell receptor (TCR) signaling, as its inhibition increases IL-2 production, T cell proliferation and Treg development in vitro. We also discovered that loss of CUL neddylation occurs upon TCR signaling, and CRLs negatively regulate IL-2 production. Additionally, we found that tyrosine kinase signaling leads to CUL deneddylation in multiple cell types. These studies indicate that CUL neddylation is a global regulatory mechanism for tyrosine kinase signaling.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death / physiology
  • Cells, Cultured
  • Cullin Proteins / genetics
  • Cullin Proteins / metabolism*
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Immunoblotting
  • Interleukin-2 / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • T-Lymphocytes, Regulatory / metabolism

Substances

  • Cullin Proteins
  • Interleukin-2
  • Protein-Tyrosine Kinases