ArticleDevelopmental biology2016
FGFR and PTEN signaling interact during lens development to regulate cell survival.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Phenotypic spectrum ofPeerJ · 2022Pooled it
- Downregulation of Pten Improves Huntington's Disease Phenotype by Reducing Htt Aggregates and Cell Death.Molecular neurobiology · 2025Article
- Combinatorial genetic manipulation of Cx50, PI3K and PTEN alters postnatal mouse lens growth and homeostasis.Frontiers in ophthalmology · 2025Article
- Altered Cell Clusters and Upregulated Aqp1 in Connexin 50 Knockout Lens Epithelium.Investigative ophthalmology & visual science · 2024Article
- Article
- Review
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- Changes in DNA methylation hallmark alterations in chromatin accessibility and gene expression for eye lens differentiation.Epigenetics & chromatin · 2022Article
- Jack of all trades, master of each: the diversity of fibroblast growth factor signalling in eye development.Open biology · 2022Review
- Physiological Mechanisms Regulating Lens Transport.Frontiers in physiology · 2021Review
- Lens fiber cell differentiation occurs independently of fibroblast growth factor receptor signaling in the absence of Pten.Developmental biology · 2020Article
- Lens Connexin Channels Show Differential Permeability to Signaling Molecules.International journal of molecular sciences · 2020Review
- High-throughput transcriptome analysis reveals that the loss of Pten activates a novel NKX6-1/RASGRP1 regulatory module to rescue microphthalmia caused by Fgfr2-deficient lenses.Human genetics · 2019Article
- Lens differentiation is controlled by the balance between PDGF and FGF signaling.PLoS biology · 2019Article
- Regulation of FGF10 Signaling in Development and Disease.Frontiers in genetics · 2018Review
- Signaling and Gene Regulatory Networks in Mammalian Lens Development.Trends in genetics : TIG · 2017Review
- Lens development requires DNMT1 but takes place normally in the absence of both DNMT3A and DNMT3B activity.Epigenetics · 2017Article
- Upregulation of multiple signaling pathways by Dock5 deletion in epithelial cells.Molecular vision · 2017Article
- FGFs: crucial factors that regulate tumour initiation and progression.Cell proliferation · 2016Review
- The Phosphoinosotide 3-Kinase Catalytic Subunit p110α is Required for Normal Lens Growth.Investigative ophthalmology & visual science · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Lens epithelial cells express many receptor tyrosine kinases (RTKs) that stimulate PI3K-AKT and RAS-RAF-MEK-ERK intracellular signaling pathways. These pathways ultimately activate the phosphorylation of key cellular transcription factors and other proteins that control proliferation, survival, metabolism, and differentiation in virtually all cells. Among RTKs in the lens, only stimulation of fibroblast growth factor receptors (FGFRs) elicits a lens epithelial cell to fiber cell differentiation response in mammals. Moreover, although the lens expresses three different Fgfr genes, the isolated removal of Fgfr2 at the lens placode stage inhibits both lens cell survival and fiber cell differentiation. Phosphatase and tensin homolog (PTEN), commonly known as a tumor suppressor, inhibits ERK and AKT activation and initiates both apoptotic pathways, and cell cycle arrest. Here, we show that the combined deletion of Fgfr2 and Pten rescues the cell death phenotype associated with Fgfr2 loss alone. Additionally, Pten removal increased AKT and ERK activation, above the levels of controls, in the presence or absence of Fgfr2. However, isolated deletion of Pten failed to stimulate ectopic fiber cell differentiation, and the combined deletion of Pten and Fgfr2 failed to restore differentiation-specific Aquaporin0 and DnaseIIβ expression in the lens fiber cells.
Indexed as
Identifiers
What Socratic 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 Socratic graph.