ArticleMolecular biology of the cell2014
Dab2 inhibits the cholesterol-dependent activation of JNK by TGF-β.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- HC-HA/PTX3 from amniotic membrane reprograms human corneal fibroblasts to neural crest progenitors by switching from canonical to noncanonical TGFβ signaling.Stem cell research & therapy · 2026Article
- Dual signaling pathways of TGF-β superfamily cytokines in hepatocytes: balancing liver homeostasis and disease progression.Frontiers in pharmacology · 2025Review
- Cholesterol modulates type I/II TGF-β receptor complexes and alters the balance between Smad and Akt signaling in hepatocytes.Communications biology · 2024Article
- Potential markers of cancer stem-like cells in ESCC: a review of the current knowledge.Frontiers in oncology · 2023Review
- Disabled-2 (International journal of molecular sciences · 2022Review
- Canonical TGFβ Signaling and Its Contribution to Endometrial Cancer Development and Progression-Underestimated Target of Anticancer Strategies.Journal of clinical medicine · 2021Review
- Emerging Roles of Disabled Homolog 2 (DAB2) in Immune Regulation.Frontiers in immunology · 2020Review
- Specificity, versatility, and control of TGF-β family signaling.Science signaling · 2019Review
- Cholesterol depletion enhances TGF-β Smad signaling by increasing c-Jun expression through a PKR-dependent mechanism.Molecular biology of the cell · 2018Article
- Non-Smad Signaling Pathways of the TGF-β Family.Cold Spring Harbor perspectives in biology · 2017Review
- TGF-β Signaling from Receptors to Smads.Cold Spring Harbor perspectives in biology · 2016Review
- Differential regulation of translation and endocytosis of alternatively spliced forms of the type II bone morphogenetic protein (BMP) receptor.Molecular biology of the cell · 2016Article
- ShcA Protects against Epithelial-Mesenchymal Transition through Compartmentalized Inhibition of TGF-β-Induced Smad Activation.PLoS biology · 2015Article
- Novel Molecular Insights into Classical and Alternative Activation States of Microglia as Revealed by Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC)-based Proteomics.Molecular & cellular proteomics : MCP · 2015Article
- Epigenetic modification and antibody-dependent expansion of memory-like NK cells in human cytomegalovirus-infected individuals.Immunity · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β (TGF-β) ligands activate Smad-mediated and noncanonical signaling pathways in a cell context-dependent manner. Localization of signaling receptors to distinct membrane domains is a potential source of signaling output diversity. The tumor suppressor/endocytic adaptor protein disabled-2 (Dab2) was proposed as a modulator of TGF-β signaling. However, the molecular mechanism(s) involved in the regulation of TGF-β signaling by Dab2 were not known. Here we investigate these issues by combining biophysical studies of the lateral mobility and endocytosis of the type I TGF-β receptor (TβRI) with TGF-β phosphoprotein signaling assays. Our findings demonstrate that Dab2 interacts with TβRI to restrict its lateral diffusion at the plasma membrane and enhance its clathrin-mediated endocytosis. Small interfering RNA-mediated knockdown of Dab2 or Dab2 overexpression shows that Dab2 negatively regulates TGF-β-induced c-Jun N-terminal kinase (JNK) activation, whereas activation of the Smad pathway is unaffected. Moreover, activation of JNK by TGF-β in the absence of Dab2 is disrupted by cholesterol depletion. These data support a model in which Dab2 regulates the domain localization of TβRI in the membrane, balancing TGF-β signaling via the Smad and JNK pathways.
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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.