ArticleScience advances2021
Lacrimal gland budding requires PI3K-dependent suppression of EGF signaling.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Bioelectric Reawakening by a Self-Powered Thermoelectric Hydrogel Accelerates Diabetic Ulcer Repair.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Chrysanthemum indicum L.-derived extracellular vesicles enhance the therapeutic efficacy of cyclosporine a against dry eye disease.Journal of nanobiotechnology · 2026Article
- Article
- FGF-induced phospholipase Cγ signaling regulates lacrimal gland branching by competing with PI3K in phosphoinositide metabolism.Cell reports · 2025Article
- Article
- Crk mediates Csk-Hippo signaling independently of Yap tyrosine phosphorylation to induce cell extrusion.bioRxiv : the preprint server for biology · 2024Article
- Duct ligation/de-ligation model: exploring mechanisms for salivary gland injury and regeneration.Frontiers in cell and developmental biology · 2024Review
- Jack of all trades, master of each: the diversity of fibroblast growth factor signalling in eye development.Open biology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The patterning of epithelial buds is determined by the underlying signaling network. Here, we study the cross-talk between phosphoinositide 3-kinase (PI3K) and Ras signaling during lacrimal gland budding morphogenesis. Our results show that PI3K is activated by both the p85-mediated insulin-like growth factor (IGF) and Ras-mediated fibroblast growth factor (FGF) signaling. On the other hand, PI3K also promotes extracellular signal-regulated kinase (ERK) signaling via a direct interaction with Ras. Both PI3K and ERK are upstream regulators of mammalian target of rapamycin (mTOR), and, together, they prevent expansion of epidermal growth factor (EGF) receptor expression from the lacrimal gland stalk to the bud region. We further show that this suppression of EGF signaling is necessary for induction of lacrimal gland buds. These results reveal that the interplay between PI3K, mitogen-activated protein kinase, and mTOR mediates the cross-talk among FGF, IGF, and EGF signaling in support of lacrimal gland development.
Identifiers
What OpenQuestion holds
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.