This work uncovers a mechanism by which T-cell antitumor responses are regulated by calnexin in tumor cells and suggests that calnexin might serve as a potential target for the improvement of antitumor immunotherapy.
Study discovered that calnexin is highly abundant in human brain endothelial cells of multiple sclerosis (MS) patients. Conversely mice lacking calnexin exhibited resistance to experimental autoimmune encephalomyelitis induction no evidence of immune cell infiltration into the CNS. These findings identify a link between calnexin expression in CNS endothelial cells and neuroinflammation.
In summary ER retention of pathogenic VLDLR mutants involves binding to calnexin elevated endoplasmic reticulum stress and delayed degradation which is dependent on SEL1L.
Charcot-Marie-Tooth disease-related PMP22 is trapped in the endoplasmic reticulum by calnexin-dependent retention and Rer1-mediated early Golgi retrieval systems and partly degraded by the Hrd1-mediated endoplasmic reticulum-associated degradation system.
H-ERG trafficking was impaired by H2O2 after 48 h treatment accompanied by reciprocal changes of expression between miR-17-5p seed miRNAs and several chaperones (Hsp70 Hsc70 CANX and Golga20)
These findings demonstrated that calnexin strictly monitors the maturation of S protein by its direct binding resulting in conferring infectivity on severe acute respiratory syndrome coronavirus., Pathway
Categories
Function, Interaction, Subcellular Location, Function
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