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Article

Phosphorylation of Mig6 negatively regulates the ubiquitination and degradation of EGFR mutants in lung adenocarcinoma cell lines.

Cellular signalling - 1 Mar 2018

Boopathy Gandhi T K, Lynn Julia Lim Sze, Wee Sheena, Gunaratne Jayantha, Hong Wanjin

Abstract excerpt

Activating mutations in the kinase domain of epidermal growth factor receptor (EGFR) leads to the constitutively active kinase, improves the EGFR stability and promotes malignant transformation in lung adenocarcinoma. Despite the clinical significance, the mechanism by which the increased kinase activity stabilizes the receptor is not completely understood. Using SILAC phosphoproteomic approach, we identify that...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 29196224
DOI: 10.1016/j.cellsig.2017.11.006

Genes

EGFR

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Phosphorylation of Mig6 negatively regulates the ubiquitination and degradation of EGFR mutants in lung adenocarcinoma cell lines.PMID 29196224Read ↗

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Tyrosine phosphorylation of mig6 reduces its inhibition of the epidermal growth factor receptor.Semantic proximity Read ↗

Functional loss of ERBB receptor feedback inhibitor 1 ( MIG6 ) promotes glioblastoma tumorigenesis by aberrant activation of epidermal growth factor receptor ( EGFR )Semantic proximity Read ↗

Direct interaction of Cbl with pTyr 1045 of the EGF receptor (EGFR) is required to sort the EGFR to lysosomes for degradation.Semantic proximity Read ↗

Gefitinib-sensitive EGFR lacking residues 746-750 exhibits hypophosphorylation at tyrosine residue 1045, hypoubiquitination, and impaired endocytosis.Semantic proximity Read ↗

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