2013
DOI: 10.1074/jbc.r112.438978
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The O-Mannosylation Pathway: Glycosyltransferases and Proteins Implicated in Congenital Muscular Dystrophy

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Cited by 77 publications
(54 citation statements)
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References 79 publications
(79 reference statements)
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“…Stress-and nutrient-dependent changes in oligosaccharide levels can trigger the UPR (83)(84)(85)(86). Given that highly specific changes in glycosylation regulate diverse proteins like Notch (130), dystroglycan (131)(132)(133), amyloid precursor protein (134,135), and MUC1 (136), one can speculate that UPR regulates these proteins under some conditions. For example, in cancer cells, the global glycosylation of proteins is impacted (137,138), which includes MUC1, a major activator of the proliferative RAS-MEK-ERK MAPK pathway (9,139,140).…”
Section: Discussionmentioning
confidence: 99%
“…Stress-and nutrient-dependent changes in oligosaccharide levels can trigger the UPR (83)(84)(85)(86). Given that highly specific changes in glycosylation regulate diverse proteins like Notch (130), dystroglycan (131)(132)(133), amyloid precursor protein (134,135), and MUC1 (136), one can speculate that UPR regulates these proteins under some conditions. For example, in cancer cells, the global glycosylation of proteins is impacted (137,138), which includes MUC1, a major activator of the proliferative RAS-MEK-ERK MAPK pathway (9,139,140).…”
Section: Discussionmentioning
confidence: 99%
“…Given the known pathology of hypoglycosylated ␣DG resulting in a loss of laminin binding in a subset of muscular dystrophies, which can have associated cardiomyopathies (79,80), we examined the glycosylation of ␣DG specifically. We did not detect differences in ␣DG glycosylation or laminin binding between Pompe and control iPSC-CMs, suggesting that this specific glycosylation pathway is intact in Pompe disease and unlikely to be central to the pathophysiology.…”
Section: Discussionmentioning
confidence: 99%
“…In particular, Tmem2 may be relevant to the set of congenital muscular dystrophies known as dystroglycanopathies, which feature aberrant glycosylation of αDG (Muntoni et al, 2008;Wells, 2013). Mutations in 18 genes have been shown to cause dystroglycanopathies and several of these genes encode characterized or putative glycosyltransferases (Bouchet-Séraphin et al, 2015; Godfrey et al, 2011).…”
Section: Tmem2 Promotes Cell-matrix Interactions By Influencing Ecm Omentioning
confidence: 99%