ArticleJournal of cell science2010
Plakoglobin regulates cell motility through Rho- and fibronectin-dependent Src signaling.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- PERK protein kinase facilitates keratinocyte collective cell migration by engagement with cell adhesion molecules, independent of its kinase activity.Molecular biology of the cell · 2025Article
- Plakoglobin does not participate in endothelial barrier stabilization mediated by cAMP.Scientific reports · 2025Article
- The desmosomal cadherin Desmoglein-2 controls extracellular matrix expression and remodeling via NF-κB signaling in keratinocytes.Frontiers in cell and developmental biology · 2025Article
- DPM1 modulates desmosomal adhesion and epidermal differentiation through SERPINB5.The Journal of cell biology · 2024Article
- KRT13 promotes stemness and drives metastasis in breast cancer through a plakoglobin/c-Myc signaling pathway.Breast cancer research : BCR · 2022Article
- Interplay of tRNA-Derived Fragments and T Cell Activation in Breast Cancer Patient Survival.Cancers · 2020Article
- Desmocollin-2 promotes intestinal mucosal repair by controlling integrin-dependent cell adhesion and migration.Molecular biology of the cell · 2020Article
- TOPK promotes metastasis of esophageal squamous cell carcinoma by activating the Src/GSK3β/STAT3 signaling pathway via γ-catenin.BMC cancer · 2019Article
- Up-regulated fibronectin in 3D culture facilitates spreading of triple negative breast cancer cells on 2D through integrin β-5 and Src.Scientific reports · 2019Article
- Fibronectin in Cancer: Friend or Foe.Cells · 2019Review
- Desmoplakin Harnesses Rho GTPase and p38 Mitogen-Activated Protein Kinase Signaling to Coordinate Cellular Migration.The Journal of investigative dermatology · 2019Article
- Desmoglein 1 Regulates Invadopodia by Suppressing EGFR/Erk Signaling in an Erbin-Dependent Manner.Molecular cancer research : MCR · 2019Article
- Lack of plakoglobin impairs integrity and wound healing in corneal epithelium in mice.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Adherens Junctions and Desmosomes Coordinate Mechanics and Signaling to Orchestrate Tissue Morphogenesis and Function: An Evolutionary Perspective.Cold Spring Harbor perspectives in biology · 2018Review
- Signaling by Small GTPases at Cell-Cell Junctions: Protein Interactions Building Control and Networks.Cold Spring Harbor perspectives in biology · 2018Review
- Immunohistochemical expression of NEDD9, E-cadherin and γ-catenin and their prognostic significance in pancreatic ductal adenocarcinoma (PDAC).Bosnian journal of basic medical sciences · 2018Article
- mTORC1 loss impairs epidermal adhesion via TGF-β/Rho kinase activation.The Journal of clinical investigation · 2017Article
- Beyond cell-cell adhesion: Plakoglobin and the regulation of tumorigenesis and metastasis.Oncotarget · 2017Review
- Intermediate Filaments at the Junction of Mechanotransduction, Migration, and Development.Frontiers in cell and developmental biology · 2017Review
- The physical interaction of p53 and plakoglobin is necessary for their synergistic inhibition of migration and invasion.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We previously showed that the cell-cell junction protein plakoglobin (PG) not only suppresses motility of keratinocytes in contact with each other, but also, unexpectedly, of single cells. Here we show that PG deficiency results in extracellular matrix (ECM)-dependent disruption of mature focal adhesions and cortical actin organization. Plating PG⁻/⁻ cells onto ECM deposited by PG+/⁻ cells partially restored normal cell morphology and inhibited PG⁻/⁻ cell motility. In over 70 adhesion molecules whose expression we previously showed to be altered in PG⁻/⁻ cells, a substantial decrease in fibronectin (FN) in PG⁻/⁻ cells stood out. Re-introduction of PG into PG⁻/⁻ cells restored FN expression, and keratinocyte motility was reversed by plating PG⁻/⁻ cells onto FN. Somewhat surprisingly, based on previously reported roles for PG in regulating gene transcription, PG-null cells exhibited an increase, not a decrease, in FN promoter activity. Instead, PG was required for maintenance of FN mRNA stability. PG⁻/⁻ cells exhibited an increase in activated Src, one of the kinases controlled by FN, a phenotype reversed by plating PG⁻/⁻ cells on ECM deposited by PG+/⁻ keratinocytes. PG⁻/⁻ cells also exhibited Src-independent activation of the small GTPases Rac1 and RhoA. Both Src and RhoA inhibition attenuated PG⁻/⁻ keratinocyte motility. We propose a novel role for PG in regulating cell motility through distinct ECM-Src and RhoGTPase-dependent pathways, influenced in part by PG-dependent regulation of FN mRNA stability.
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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.