ArticleScientific reports2016
N-Glycosylation of integrin α5 acts as a switch for EGFR-mediated complex formation of integrin α5β1 to α6β4.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Integrin α5β1 in pancreatic ductal adenocarcinoma: Tumour‒stroma crosstalk, hypoxia and therapeutic targeting.Clinical and translational medicine · 2026Review
- Characterizing the Effects of Protein Glycosylation Perturbation on Phosphorylation Signaling.Analytical chemistry · 2026Article
- Beyond Structure: The Dynamic Role of the Extracellular Matrix Components in Immune Evasion.Cancer communications (London, England) · 2026Review
- Characterizing the Effects of Protein Glycosylation Perturbation on Phosphorylation Signaling.bioRxiv : the preprint server for biology · 2025Article
- Discovering Glycosylation-Dependent Protein Function by Thermal Proteome Profiling.bioRxiv : the preprint server for biology · 2025Article
- Quantitative Glycan-Protein Cross-Linking Mass Spectrometry Using Enrichable Linkers Reveals Extensive Glycan-Mediated Protein Interaction Networks.Analytical chemistry · 2025Article
- Impact of CD151 overexpression on prognosis and therapy in non-small cell lung cancer patients lacking EGFR mutations.Cell proliferation · 2024Article
- TMTC1 promotes invasiveness of ovarian cancer cells through integrins β1 and β4.Cancer gene therapy · 2023Article
- SerumBiomolecules · 2023Article
- Roles of N-linked glycosylation and glycan-binding proteins in placentation: trophoblast infiltration, immunomodulation, angiogenesis, and pathophysiology.Biochemical Society transactions · 2023Review
- Non-canonical integrin signaling activates EGFR and RAS-MAPK-ERK signaling in small cell lung cancer.Theranostics · 2023Article
- The IRE1α-XBP1s Arm of the Unfolded Protein Response Activates N-Glycosylation to Remodel the Subepithelial Basement Membrane in Paramyxovirus Infection.International journal of molecular sciences · 2022Article
- TM4SF1 promotes esophageal squamous cell carcinoma metastasis by interacting with integrin α6.Cell death & disease · 2022Article
- Review
- Identification of distinct N-glycosylation patterns on extracellular vesicles from small-cell and non-small-cell lung cancer cells.The Journal of biological chemistry · 2022Article
- Quantification of Tumor Abnormal Proteins in the Diagnosis and Postoperative Prognostic Evaluation of Gastric Cancer.Clinical Medicine Insights. Oncology · 2022Article
- Cell surface integrin α5ß1 clustering negatively regulates receptor tyrosine kinase signaling in colorectal cancer cells via glycogen synthase kinase 3.Integrative biology : quantitative biosciences from nano to macro · 2021Article
- Review
- Essential Functions of Glycans in Human Epithelia Dissected by a CRISPR-Cas9-Engineered Human Organotypic Skin Model.Developmental cell · 2020Article
- Integrin Crosstalk Contributes to the Complexity of Signalling and Unpredictable Cancer Cell Fates.Cancers · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-Glycosylation of integrin α5β1 is involved in multiple cell behaviors. We previously reported that the N-glycosylations of the calf domain on integrin α5 (S3-5,10-14) are essential for its inhibitory effect on EGFR signaling in regulating cell proliferation. However, the importance of the individual N-glycosylation and the underlying mechanisms of inhibition remain unclear. Here, we characterize the S3-5,10-14 mutants in detail and found that the N-glycosylation of site-11 (Asn712) is key for cell growth. The restoration of site-11, unlike the other individual sites, significantly suppressed cell growth and EGFR signaling in a manner that was similar to that of wild-type (WT). Mechanistically, this N-glycosylation inhibited the response abilities upon EGF stimulation and EGFR dimerization. Interestingly, we found this N-glycosylation controlled the EGFR complex formation with integrin α5β1 or α6β4; i.e., the loss of site-11 switched EGFR-α5β1 to EGFR-α6β4, which is well known to promote cellular signaling for cell growth. Moreover, the site-11 N-glycan exhibited a more branching structure compared with other sites, which may be required for EGFR-α5β1 formation. Taken together, these data clearly demonstrate that the site-11 N-glycosylation on α5 is most important for its inhibitory effect on EGFR signaling, which may provide a novel regulatory mechanism for crosstalks between integrins and EGFR.
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