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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.
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CNX has a specific role in cardiomyocyte viability and Ca(2+) cycling through its effects on endoplasmic reticulum stress, apoptosis and Ca(2+) channel expression.
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Calnexin discriminates between different conformational states of GlyT2 displaying a lectin-independent chaperone activity.
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calnexin and ERp57, but not calreticulin, play an important role in the biology of peripheral myelin proteins PMP22 and P0, and, consequently, these chaperones may contribute to the pathogenesis of peripheral neuropathies
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Enhanced clathrin-dependent endocytosis in the absence of calnexin may contribute to the neurological phenotype of calnexin-deficient mice
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Data show that the E351 mutation led to slightly enhanced ERp57 binding to calnexin, whereas W428 greatly enhanced binding of ERp57 to calnexin.
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Suggest that Adam7 functions in fertilization through the formation of a complex with heat shock protein 5, calnexin and Itm2b during capacitation in sperm.
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endoplasmic reticulum stress has effects on group VIA phospholipase A2 in beta cells that include tyrosine phosphorylation and increased association with calnexin
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Calnexin deficiency leads to dysmyelination
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Data give novel evidence that CyCAP regulates the post-translational modification of tissue transglutaminase through its colocalization with calnexin in endoplasmic reticulum.
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Association with mutant peripheral myelin protein-22 ex vivo: a basis for "gain-of-function" ER diseases.
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Calnexin is required for myelinated motor neuron function and postnatal survival in mice
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Data show that in calreticulin-deficient cells, calnexin-substrate association is severely reduced, leading to accumulation of unfolded proteins and a triggering of the unfolded protein response.
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caspase-3 or caspase-7 cleaves calnexin, whose cleaved product leads to the attenuation of apoptosis
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Data show that oculocutaneous albinism soluble tyrosinase is an endoplasmic reticulum-associated degradation substrate that, unlike other albino tyrosinases, associates with calreticulin and BiP/GRP78, but not calnexin.
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In mice, a calnexin-glycan interaction may be required to stabilize the weak association of MHC class I heavy chain with beta 2-microglobulin in the endoplasmic reticulum until peptide is bound.
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UGT1 activity might be required for a structural maturation needed for substrate dissociation from calnexin and export from the ER.
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Calnexin might stimulate the productive folding of WT CF transmembrane conductance regulator (CFTR), but not DeltaF508 CFTR, which has folding defects.
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Cnx (-/-) cells have significantly increased proteasomal activity, which may play a role in the adaptive mechanisms addressing the acute endoplasmic reticulum stress observed in the absence of calnexin.
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Mammalian rod opsin biogenesis does not appear to have an absolute requirement for Cnx.