ArticlePloS one2019
The GalNAc-T Activation (GALA) Pathway: Drivers and markers.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- From Glycocode to Precision Oncology: Therapeutic Strategies Targeting Aberrant O-GalNAc Glycosylation in Cancer.Chemical reviews · 2026Review
- The Critical Role of GALNTs-Regulated O-GalNAc Glycosylation in Cancer Malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- GalNAc-Transferases in Cancer.Biomedicines · 2025Review
- ER O-glycosylation in synovial fibroblasts drives cartilage degradation.Nature communications · 2025Article
- SLC10A7 regulates O-GalNAc glycosylation and CaCellular and molecular life sciences : CMLS · 2025Article
- A Sweet Warning: Mucin-Type O-Glycans in Cancer.Cells · 2022Review
- Role of theFrontiers in cell and developmental biology · 2022Review
- Article
- miR-30b-5p inhibits proliferation, invasion, and migration of papillary thyroid cancer by targeting GALNT7 via the EGFR/PI3K/AKT pathway.Cancer cell international · 2021Article
- Global view of human protein glycosylation pathways and functions.Nature reviews. Molecular cell biology · 2020Review
- ER-resident oxidoreductases are glycosylated and trafficked to the cell surface to promote matrix degradation by tumour cells.Nature cell biology · 2020Article
- Point mutations that inactivate MGAT4D-L, an inhibitor of MGAT1 and complexThe Journal of biological chemistry · 2020Article
- miR-125a-5p post-transcriptionally suppresses GALNT7 to inhibit proliferation and invasion in cervical cancer cells via the EGFR/PI3K/AKT pathway.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The enzymes GALNTs add GalNAc sugar to Ser and Thr residues, forming the Tn glycan. GALNTs are activated by trafficking from Golgi to ER, a process driven by the Src kinase and negatively regulated by ERK8. This GALNTs activation (aka GALA) pathway induces high Tn levels and is a key driver of liver tumor growth. Recently, Tabak and colleagues have contested our previous data that EGF stimulation can induce GALNTs relocation. Here, we show that relocation induced by EGF is actually detectable in the very images acquired by Tabak et al. Furthermore, we show that over-expression of EGFR strongly enhances EGF-induced relocation and that EGFR appears required to drive relocation induced by ERK8 depletion. Direct co-localisation of GALNT with the ER marker Calnexin is observed after EGF stimulation. We furthermore propose that quantification of O-glycosylation of the ER resident protein PDIA4 provides a mean to quantify GALA independently of imaging. In sum, we demonstrate that the claimed non-reproducibility was due to experimental imaging conditions, that EGFR is indeed a driver of GALA and propose additional markers to facilitate the study of this pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.