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- W2140153012 abstract "ER O-glycosylation can be induced through relocalisation GalNAc-Transferases from the Golgi. This process markedly stimulates cell migration and is constitutively activated in more than 60% of breast carcinomas. How this activation is achieved remains unclear. Here, we screened 948 signalling genes using RNAi and imaging. We identified 12 negative regulators of O-glycosylation that all control GalNAc-T sub-cellular localisation. ERK8, an atypical MAPK with high basal kinase activity, is a strong hit and is partially localised at the Golgi. Its inhibition induces the relocation of GalNAc-Ts, but not of KDEL receptors, revealing the existence of two separate COPI-dependent pathways. ERK8 down-regulation, in turn, activates cell motility. In human breast and lung carcinomas, ERK8 expression is reduced while ER O-glycosylation initiation is hyperactivated. In sum, ERK8 appears as a constitutive brake on GalNAc-T relocalisation, and the loss of its expression could drive cancer aggressivity through increased cell motility. DOI: http://dx.doi.org/10.7554/eLife.01828.001." @default.
- W2140153012 created "2016-06-24" @default.
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- W2140153012 date "2014-03-11" @default.
- W2140153012 modified "2023-10-17" @default.
- W2140153012 title "ERK8 is a negative regulator of O-GalNAc glycosylation and cell migration" @default.
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- W2140153012 doi "https://doi.org/10.7554/elife.01828" @default.
- W2140153012 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3945522" @default.
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