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We are analyzing https://link.springer.com/article/10.1007/s00441-014-1856-2.

Title:
Actin filament dynamics and endothelial cell junctions: the Ying and Yang between stabilization and motion | Cell and Tissue Research
Description:
The vascular endothelium is a cellular interface between the blood and the interstitial space of tissue, which controls the exchange of fluid, solutes and cells by both transcellular and paracellular means. To accomplish the demands on barrier function, the regulation of the endothelium requires quick and adaptive mechanisms. This is, among others, accomplished by actin dynamics that interdependently interact with both the VE-cadherin/catenin complex, the main components of the adherens type junctions in endothelium and the membrane cytoskeleton. Actin filaments in endothelium are components of super-structured protein assemblies that control a variety of dynamic processes such as endo- and exocytosis, shape change, cell–substrate along with cell–cell adhesion and cell motion. In endothelium, actin filaments are components of: (1) contractile actin bundles appearing as stress fibers and junction-associated circumferential actin filaments, (2) actin networks accompanied by endocytotic ruffles, lamellipodia at leading edges of migrating cells and junction-associated intermittent lamellipodia (JAIL) that dynamically maintain junction integrity, (3) cortical actin and (4) the membrane cytoskeleton. All these structures, most probably interact with cell junctions and cell–substrate adhesion sites. Due to the rapid growth in information, we aim to provide a bird’s eye view focusing on actin filaments in endothelium and its functional relevance for entire cell and junction integrity, rather than discussing the detailed molecular mechanism for control of actin dynamics.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
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Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,016 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

pubmed, google, scholar, cas, cell, endothelial, central, biol, actin, cells, physiol, junctions, schnittler, vascular, stress, endothelium, cytoskeleton, barrier, mol, complex, vecadherin, res, adhesion, molecular, regulation, control, sci, article, cellcell, fibers, human, function, dynamics, taha, protein, rho, role, rev, seebach, cellular, regulates, assembly, research, mechanisms, adherens, filaments, pcatenin, phosphorylation, permeability, dejana,

Topics {✒️}

binds e-cadherin-beta-catenin month download article/chapter nico lindemann & jochen seebach adherens type junctions endothelial ve-cadherin junctions ve-cadherin-mediated upregulation cadherin-dependent cell junctions ve-cadherin simultaneously stimulates ve-cadherin prevents binding myosin light-chain kinase e-cadherin forms oligomers ve-cadherin-p120 interaction ve-cadherin/catenin complex ve-cadherin/catenin complex cadherin-based cell adhesion regulates actin-filament assembly alphaii-spectrin-vasp complexes endothelial-specific membrane protein cadherin-catenin junctional complex e-cadherin physically associates mediated p120-catenin interaction super-structured protein assemblies cadherin-catenin-actin conundrum heal barrier micro-wounds cadherin-catenin-actin complex control force-dependent remodeling cadherin-directed actin assembly arp2/3-dependent actin assembly westfälische wilhelms-universität münster ifn-gamma-induced permeability tnf-alpha-induced reorganization cadherin-5/ve-cadherin endothelial cell-cell contacts injury-induced cell migration cell-cell junction formation cell–substrate adhesion sites actin stress fibers–assembly membrane adhesion complex disrupts vascular integrity endothelial cell junctions cadherin catenin complex bacterial protein toxins vascular endothelial cadherin ve-cadherin phosphorylation van hinsbergh vw actin filament dynamics mechano-signal transduction privacy choices/manage cookies cell-cell junctions related subjects

Schema {🗺️}

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         description:The vascular endothelium is a cellular interface between the blood and the interstitial space of tissue, which controls the exchange of fluid, solutes and cells by both transcellular and paracellular means. To accomplish the demands on barrier function, the regulation of the endothelium requires quick and adaptive mechanisms. This is, among others, accomplished by actin dynamics that interdependently interact with both the VE-cadherin/catenin complex, the main components of the adherens type junctions in endothelium and the membrane cytoskeleton. Actin filaments in endothelium are components of super-structured protein assemblies that control a variety of dynamic processes such as endo- and exocytosis, shape change, cell–substrate along with cell–cell adhesion and cell motion. In endothelium, actin filaments are components of: (1) contractile actin bundles appearing as stress fibers and junction-associated circumferential actin filaments, (2) actin networks accompanied by endocytotic ruffles, lamellipodia at leading edges of migrating cells and junction-associated intermittent lamellipodia (JAIL) that dynamically maintain junction integrity, (3) cortical actin and (4) the membrane cytoskeleton. All these structures, most probably interact with cell junctions and cell–substrate adhesion sites. Due to the rapid growth in information, we aim to provide a bird’s eye view focusing on actin filaments in endothelium and its functional relevance for entire cell and junction integrity, rather than discussing the detailed molecular mechanism for control of actin dynamics.
         datePublished:2014-03-19T00:00:00Z
         dateModified:2014-03-19T00:00:00Z
         pageStart:529
         pageEnd:543
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            Actin
            VE-cadherin
            Membrane cytoskeleton
            Adherens-type junctions
            Human Genetics
            Proteomics
            Molecular Medicine
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      headline:Actin filament dynamics and endothelial cell junctions: the Ying and Yang between stabilization and motion
      description:The vascular endothelium is a cellular interface between the blood and the interstitial space of tissue, which controls the exchange of fluid, solutes and cells by both transcellular and paracellular means. To accomplish the demands on barrier function, the regulation of the endothelium requires quick and adaptive mechanisms. This is, among others, accomplished by actin dynamics that interdependently interact with both the VE-cadherin/catenin complex, the main components of the adherens type junctions in endothelium and the membrane cytoskeleton. Actin filaments in endothelium are components of super-structured protein assemblies that control a variety of dynamic processes such as endo- and exocytosis, shape change, cell–substrate along with cell–cell adhesion and cell motion. In endothelium, actin filaments are components of: (1) contractile actin bundles appearing as stress fibers and junction-associated circumferential actin filaments, (2) actin networks accompanied by endocytotic ruffles, lamellipodia at leading edges of migrating cells and junction-associated intermittent lamellipodia (JAIL) that dynamically maintain junction integrity, (3) cortical actin and (4) the membrane cytoskeleton. All these structures, most probably interact with cell junctions and cell–substrate adhesion sites. Due to the rapid growth in information, we aim to provide a bird’s eye view focusing on actin filaments in endothelium and its functional relevance for entire cell and junction integrity, rather than discussing the detailed molecular mechanism for control of actin dynamics.
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         Actin
         VE-cadherin
         Membrane cytoskeleton
         Adherens-type junctions
         Human Genetics
         Proteomics
         Molecular Medicine
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      name:Abdallah Abu Taha
      affiliation:
            name:Westfälische Wilhelms-Universität MĂźnster
            address:
               name:Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität MĂźnster, MĂźnster, Germany
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            name:Westfälische Wilhelms-Universität MĂźnster
            address:
               name:Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität MĂźnster, MĂźnster, Germany
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      name:Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität MĂźnster, MĂźnster, Germany
      name:Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität MĂźnster, MĂźnster, Germany
      name:Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität MĂźnster, MĂźnster, Germany
      name:Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität MĂźnster, MĂźnster, Germany
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