ArticleMolecular biology of the cell2011
DDR1 triggers epithelial cell differentiation by promoting cell adhesion through stabilization of E-cadherin.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 75 citations in OpenAlex.
- CRISPR and compound screens in a novel ex vivo tissue model identify DDR1 and ETA as regulators of cancer cell invasion.Cellular & molecular biology letters · 2026Article
- Chemical programming of kinase inhibitors in a modular chemputer-based system.Communications biology · 2026Article
- Evaluation of Discoidin domain receptor 1 (DDR1) in junctional epithelial permeability and wound healing.Journal of periodontology · 2026Article
- Differentiation in the human urothelia is defined by distinct alternative polyadenylation.Cell reports · 2026Article
- Single-dose cathepsin L CRISPR nanotherapy mitigates PASC-like lung damage in hamsters.Nano research · 2025Article
- Linking IFN-γ-Mediated Pathogenesis to ROCK-Targeted Therapy in a Scalable iPSCs-Based Vitiligo Model.International journal of molecular sciences · 2025Article
- Discoidin Domain Receptors in Tumor Biology and Immunology: Progression and Challenge.Biomolecules · 2025Review
- DDR1 Targeting HOXA6 Facilitates Bladder Cancer Progression via Inhibiting Ferroptosis.Journal of cellular and molecular medicine · 2025Article
- Clinical significance of immunohistochemical expression of DDR1 and β-catenin in colorectal carcinoma.World journal of surgical oncology · 2023Article
- Complex roles of discoidin domain receptor tyrosine kinases in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Review
- AR-dependent phosphorylation and phospho-proteome targets in prostate cancer.Endocrine-related cancer · 2020Review
- Discoidin Domain Receptors in Melanoma: Potential Therapeutic Targets to Overcome MAPK Inhibitor Resistance.Frontiers in oncology · 2020Review
- Collagen receptor cross-talk determines α-smooth muscle actin-dependent collagen gene expression in angiotensin II-stimulated cardiac fibroblasts.The Journal of biological chemistry · 2019Article
- Sex-biased differences in the correlation between epithelial-to-mesenchymal transition-associated genes in cancer cell lines.Oncology letters · 2019Article
- Discoidin domain receptor 1 deficiency in vascular smooth muscle cells leads to mislocalisation of N-cadherin contacts.Biology open · 2019Article
- Epithelial polarization in 3D matrix requires DDR1 signaling to regulate actomyosin contractility.Life science alliance · 2019Article
- Novel biomarkerCell death discovery · 2018Article
- The prognostic effects of somatic mutations in ER-positive breast cancer.Nature communications · 2018Article
- Essential Role of the a3 Isoform of V-ATPase in Secretory Lysosome Trafficking via Rab7 Recruitment.Scientific reports · 2018Article
- Discoidin domain receptor 1: New star in cancer-targeted therapy and its complex role in breast carcinoma.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Discoidin domain receptor 1 (DDR1) promotes E-cadherin-mediated adhesion. The underlying mechanism and its significance, however, have not been elucidated. Here we show that DDR1 overexpression augmented, whereas dominant negative mutant (DN-DDR1) or knockdown of DDR1 inhibited E-cadherin localized in cell-cell junctions in epithelial cells. DDR1 changed the localization and abundance of E-cadherin, as well as epithelial plasticity, as manifested by enhancement of microvilli formation and alteration of cytoskeletal organization. DDR1 also reduced protein abundance of mesenchymal markers, whereas DN-DDR1 and sh-DDR1 showed opposite effects. These results suggest that expression of DDR1 increases epithelial plasticity. Expression of DDR1 augmented E-cadherin protein levels by decreasing its degradation rate. Photobleaching and photoconversion of E-cadherin conjugated with Eos fluorescence protein demonstrated that DDR1 increased the stability of E-cadherin on the cell membrane, whereas sh-DDR1 decreased it. Pull-down assay and expression of constitutively active or dominant-negative Cdc42 showed that DDR1 stabilized E-cadherin through inactivation of Cdc42. Altogether, our results show that DDR1 promotes cell-cell adhesion and differentiation through stabilization of E-cadherin, which is mediated by Cdc42 inactivation.
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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.