ArticleScience signaling2009
Galpha(i1) and Galpha(i3) are required for epidermal growth factor-mediated activation of the Akt-mTORC1 pathway.
Article in Science signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 134 citations in OpenAlex.
- MYDGF promotes pathological and physiological retinal angiogenesis via the Gαi1/3-Gab1-Akt-mTOR signaling.Nature communications · 2026Article
- FSTL4 interaction with Gαi proteins activates the Akt-mTOR pathway to drive malignant phenotypes in non-small cell lung cancer.Cell communication and signaling : CCS · 2026Article
- Mechanistic study of TIMM44 mediating gastric carcinogenesis via the Gαi1-PI3K-AKT-mTOR signaling pathway.Scientific reports · 2026Article
- Gαi1 and Gαi3 mediate IL-11-induced signal transduction and are potential therapeutic targets for LUAD.Cell death & disease · 2026Article
- NLGN3 contributes to angiogenesis in myocardial infarction via activation of the Gαi1/3-Akt pathway.Basic research in cardiology · 2026Article
- Endothelial RAB5IF is required for pathological and developmental retinal angiogenesis.Nature communications · 2025Article
- Identification of Gαi1 as a key regulator of tumor progression in nasopharyngeal carcinoma.Discover oncology · 2025Article
- Gap junction protein beta 5 interacts with Gαi3 to promote Akt activation and cervical cancer cell growth.Cell death & disease · 2025Article
- Gαi3: a crucial biomarker and therapeutic target in bladder cancer.NPJ precision oncology · 2025Article
- Mitochondrial transcription elongation factor TEFM promotes malignant progression of gliomas.Cancer cell international · 2024Article
- The critical role of Gαi3 in oral squamous cell carcinoma cell growth.Cell death discovery · 2024Article
- Identification of Gαi3 as a promising molecular oncotarget of pancreatic cancer.Cell death & disease · 2024Article
- Increased expression of REG3A promotes tumorigenic behavior in triple negative breast cancer cells.Breast cancer research : BCR · 2024Article
- Targeting the mitochondrial protein YME1L to inhibit osteosarcoma cell growth in vitro and in vivo.Cell death & disease · 2024Article
- Targeting the postsynaptic scaffolding protein PSD-95 enhances BDNF signaling to mitigate depression-like behaviors in mice.Science signaling · 2024Article
- Expression and functional significance of phosphoenolpyruvate carboxykinase 1 in uveal melanoma.Cell death discovery · 2024Article
- miRNAs and related genetic biomarkers according to the WHO glioma classification: From diagnosis to future therapeutic targets.Non-coding RNA research · 2024Review
- Synaptic plasticity via receptor tyrosine kinase/G-protein-coupled receptor crosstalk.Cell reports · 2024Article
- G protein subunit alpha i2's pivotal role in angiogenesis.Theranostics · 2024Article
- Gαi1/3 signaling mediates IL-5-induced eosinophil activation and type 2 inflammation in eosinophilic chronic rhinosinusitis.Frontiers in immunology · 2024Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The precise mechanism whereby epidermal growth factor (EGF) activates the serine-threonine kinase Akt and the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) remains elusive. Here, we report that the alpha subunits of the heterotrimeric guanine nucleotide-binding proteins (G proteins) Galpha(i1) and Galpha(i3) are critical for this activation process. Both Galpha(i1) and Galpha(i3) formed complexes with growth factor receptor binding 2 (Grb2)-associated binding protein 1 (Gab1) and the EGF receptor (EGFR) and were required for the phosphorylation of Gab1 and its subsequent interaction with the p85 subunit of phosphatidylinositol 3-kinase in response to EGF. Loss of Galpha(i1) and Galpha(i3) severely impaired the activation of Akt and of p70 S6 kinase and 4E-BP1, downstream targets of mTORC1, in response to EGF, heparin-binding EGF-like growth factor, and transforming growth factor alpha, but not insulin, insulin-like growth factor, or platelet-derived growth factor. In addition, ablation of Galpha(i1) and Galpha(i3) largely inhibited EGF-induced cell growth, migration, and survival and the accumulation of cyclin D1. Overall, this study suggests that Galpha(i1) and Galpha(i3) lie downstream of EGFR, but upstream of Gab1-mediated activation of Akt and mTORC1, thus revealing a role for Galpha(i) proteins in mediating EGFR signaling.
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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.