• exhibit
  • Calnexin-deficient mice exhibit no clinical symptoms of EAE or mononuclear cell infiltration of CNS. (jci.org)
  • cell
  • Conversely, mice lacking calnexin exhibited resistance to EAE induction, no evidence of immune cell infiltration into the CNS, and no induction of inflammation markers within the CNS. (jci.org)
  • Instead, the loss of calnexin led to a defect in brain endothelial cell function that resulted in reduced T cell trafficking across the blood-brain barrier. (jci.org)
  • cycle
  • This report identifies interactions of vIL-6 and VKORC1v2 with calnexin cycle enzymes GlucII and UGGT1, which are involved in glycan processing and nascent protein folding. (physiciansweekly.com)