ArticleMolecular biology of the cell2012
Phosphorylation of threonine 1736 in the C-terminal tail of integrin β4 contributes to hemidesmosome disassembly.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Plectin: Dual Participation in Tumor Progression.Biomolecules · 2024Review
- Regulation of Kinase Signaling Pathways by α6β4-Integrins and Plectin in Prostate Cancer.Cancers · 2022Review
- Identification of biological pathways and processes regulated by NEK5 in breast epithelial cells via an integrated proteomic approach.Cell communication and signaling : CCS · 2022Article
- Integrin α6β4 requires plectin and vimentin for adhesion complex distribution and invasive growth.Journal of cell science · 2022Article
- BP180/Collagen XVII: A Molecular View.International journal of molecular sciences · 2021Review
- EGFR-dependent tyrosine phosphorylation of integrin β4 is not required for downstream signaling events in cancer cell lines.Scientific reports · 2021Article
- Integrin beta 4 (ITGB4) and its tyrosine-1510 phosphorylation promote pancreatic tumorigenesis and regulate the MEK1-ERK1/2 signaling pathway.Bosnian journal of basic medical sciences · 2020Article
- The plakin domain ofDevelopment (Cambridge, England) · 2019Article
- Chronic shisha exposure alters phosphoproteome of oral keratinocytes.Journal of cell communication and signaling · 2019Article
- Role of Integrins in Resistance to Therapies Targeting Growth Factor Receptors in Cancer.Cancers · 2019Review
- Plectin protects podocytes from adriamycin-induced apoptosis and F-actin cytoskeletal disruption through the integrin α6β4/FAK/p38 MAPK pathway.Journal of cellular and molecular medicine · 2018Article
- An Arf6- and caveolae-dependent pathway links hemidesmosome remodeling and mechanoresponse.Molecular biology of the cell · 2018Article
- Roles of Integrin α6β4 Glycosylation in Cancer.Cancers · 2017Review
- Syndecan-1 and Syndecan-4 Capture Epidermal Growth Factor Receptor Family Members and the α3β1 Integrin Via Binding Sites in Their Ectodomains: NOVEL SYNSTATINS PREVENT KINASE CAPTURE AND INHIBIT α6β4-INTEGRIN-DEPENDENT EPITHELIAL CELL MOTILITY.The Journal of biological chemistry · 2015Article
- Molecular architecture and function of the hemidesmosome.Cell and tissue research · 2015Review
- Keratins Stabilize Hemidesmosomes through Regulation of β4-Integrin Turnover.The Journal of investigative dermatology · 2015Article
- Molecular architecture and function of the hemidesmosome.Cell and tissue research · 2015Review
- Combination of X-ray crystallography, SAXS and DEER to obtain the structure of the FnIII-3,4 domains of integrin α6β4.Acta crystallographica. Section D, Biological crystallography · 2015Article
- Structural insights into Ca2+-calmodulin regulation of Plectin 1a-integrin β4 interaction in hemidesmosomes.Structure (London, England : 1993) · 2015Article
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Authors and funding
8 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During wound healing, hemidesmome disassembly enables keratinocyte migration and proliferation. Hemidesmosome dynamics are altered downstream of epidermal growth factor (EGF) receptor activation, following the phosphorylation of integrin β4 residues S1356 and S1364, which reduces the interaction with plectin; however, this event is insufficient to drive complete hemidesmome disassembly. In the studies reported here, we used a fluorescence resonance energy transfer-based assay to demonstrate that the connecting segment and carboxy-terminal tail of the β4 cytoplasmic domain interact, which facilitates the formation of a binding platform for plectin. In addition, analysis of a β4 mutant containing a phosphomimicking aspartic acid residue at T1736 in the C-tail suggests that phosphorylation of this residue regulates the interaction with the plectin plakin domain. The aspartic acid mutation of β4 T1736 impaired hemidesmosome formation in junctional epidermolysis associated with pyloric atresia/β4 keratinocytes. Furthermore, we show that T1736 is phosphorylated downstream of protein kinase C and EGF receptor activation and is a substrate for protein kinase D1 in vitro and in cells, which requires its translocation to the plasma membrane and subsequent activation. In conclusion, we identify T1736 as a novel phosphorylation site that contributes to the regulation of hemidesmome disassembly, a dynamically regulated process involving the concerted phosphorylation of multiple β4 residues.
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