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PaxillinFocal Adhesion Kinase 2Focal AdhesionsFocal Adhesion Protein-Tyrosine KinasesFocal Adhesion Kinase 1Crk-Associated Substrate ProteinProtein-Tyrosine KinasesCell AdhesionCell Adhesion MoleculesPhosphoproteinsVinculinPhosphorylationCytoskeletal ProteinsNeoplasm MetastasisCell MovementTissue AdhesionsIntegrinsIntercellular Adhesion Molecule-1ZyxinCytoskeletonActinsSignal TransductionTalinFibronectinsLymphatic MetastasisTyrosineAntigens, CD29Vascular Cell Adhesion Molecule-1Cells, Culturedsrc-Family KinasesRetinoblastoma-Like Protein p130Stress FibersActininExtracellular MatrixCell Line, TumorBacterial AdhesionLIM Domain ProteinsFibroblastsNeoplasm InvasivenessCell LineProtein BindingrhoA GTP-Binding Proteinrho GTP-Binding ProteinsPseudopodiaPhosphotyrosineEnzyme ActivationMicroscopy, FluorescenceProto-Oncogene Proteins pp60(c-src)Microfilament ProteinsTransfectionEndothelium, Vascular3T3 CellsCadherinsMolecular Sequence DataProto-Oncogene Proteins c-crkCell ShapeProtein Structure, TertiaryCell-Matrix JunctionsImmunohistochemistryAmino Acid SequenceRecombinant Fusion ProteinsBlotting, WesternLung NeoplasmsNeural Cell Adhesion Moleculesrac1 GTP-Binding ProteinActin CytoskeletonEndothelial CellsRNA, Small InterferingFluorescent Antibody TechniqueStress, MechanicalTumor Cells, CulturedMechanotransduction, CellularReceptors, VitronectinCell Surface Extensionsrho-Associated KinasesGTPase-Activating ProteinsLiver NeoplasmsAdaptor Proteins, Signal TransducingIntegrin alpha5beta1Integrin beta3LamininModels, BiologicalTime FactorsCell ProliferationCytochalasin DIntegrin alpha4beta1Syndecan-4Protein Tyrosine Phosphatase, Non-Receptor Type 12Breast NeoplasmsEpithelial CellsMutationPrecipitin TestsNIH 3T3 Cellssrc Homology DomainsCell Adhesion Molecules, NeuronalRNA InterferenceReceptors, FibronectinMelanomaIntegrin beta Chainsrac GTP-Binding Proteins

KinaseVinculinNascent adhesionsTumorPhosphorylationProteinsRegulatesComplexesFibersPathwayActin cytoskeletonExtracellularStructuresCarcinomaInvasionInhibitLamellipodiumCellActivationFormationCellsCancerTimeContributeRepresentShown

Kinase4

• Both vinY822F and vin −/− cells exhibit increased interaction between paxillin and focal adhesion kinase (FAK) and increased paxillin and FAK phosphorylation. (rupress.org)
• Focal adhesion kinase (FAK) and steroid receptor coactivator (c-Src) are signaling proteins that regulate cytoskeletal dynamics and cell motility by influencing actin polymerization and focal adhesion turn-over [ 11 , 12 ]. (biomedcentral.com)
• Podosomes are structurally divided into a core, which mainly contains proteins involved in actin polymerization (such as WASP, the Arp2/3 complex and cortactin ), and a surrounding ring populated by integrin receptors and adhesion proteins (for example, paxillin and focal adhesion kinase (FAK/Pyk2) ) [15] . (cellmigration.org)
• p21-activated kinase 4 (PAK4), a specific effector of the Rho GTPase Cdc42, is activated by HGF, and we have previously shown that activated PAK4 induces a loss of both actin stress fibres and focal adhesions. (silverchair.com)

Vinculin4

• A vinculin fragment (amino acids 811-1066) containing the paxillin binding site restored apoptosis and suppressed ERK activity in vin −/− cells. (rupress.org)
• Thus, vinculin regulates survival and motility via ERK by controlling the accessibility of paxillin for FAK interaction. (rupress.org)
• Vinculin expression in focal adhesions upon EL treatment was determined by immunocytochemistry. (biomedcentral.com)
• Although focal adhesions are similar, in terms of molecular composition, to nascent adhesions and focal complexes, several adhesion proteins appear to change as focal adhesions evolve in response to tension, e.g., zyxin and vinculin . (cellmigration.org)

Nascent adhesions5

• Newly formed nascent adhesions gradually grow and change their protein composition to mature into FAs. (life-science-alliance.org)
• Nascent adhesions are the first observable adhesive structures, emerging within the lamellipodium. (cellmigration.org)
• Nascent adhesions are small and highly transient - either maturing or disassembling ('turning over') - and are therefore not easily observed in every cell type [6] , [7] . (cellmigration.org)
• They are larger than nascent adhesions, depend on myosin II for their formation and maintenance, and reside at the boundary of the lamellum and lamellipodium [10] , [11] . (cellmigration.org)
• Like nascent adhesions, they also tend to either disassemble (turnover) or grow and elongate into focal adhesions. (cellmigration.org)

Tumor4

• Therefore, administration of EL may serve as a safe and complementary approach for inhibiting lung tumor cell motility, invasion, and metastasis. (biomedcentral.com)
• RCC tumors from patients showed downregulation of HSPA12A, which was associated with advanced tumor node metastasis stage. (thno.org)
• Our findings demonstrate that SPON2-driven M2-TAM infiltration plays an important role during CRC tumor growth and metastasis. (biomedcentral.com)
• The tumor microenvironment (TME) has been shown to play an essential role in CRC progression and metastasis [ 3 ]. (biomedcentral.com)

Phosphorylation2

• EL decreased phosphorylation of FAK and its downstream targets, Src, paxillin, and decreased mRNA expression of cell motility-related genes, RhoA, Rac1, and Cdc42 in lung cancer cells. (biomedcentral.com)
• Furthermore, we identified that phosphorylation of FAK and MOB1 is decreased in Rab40c knock-out cells, which may contribute to focal adhesion site regulation by Rab40c. (life-science-alliance.org)

Proteins2

• Adhesion complexes (i.e., focal adhesions and focal complexes) and cell-cell contacts are specialized structures that harbor a large number of cytoskeletal proteins and one of the highest concentrations of signaling molecules in cells ( Ruoslahti and Obrink, 1996 ). (rupress.org)
• Our data suggest that EL suppresses lung cancer cell motility and invasion by altering FAK activity and subsequent activation of downstream proteins needed for focal adhesion formation and cytoskeletal rearrangement. (biomedcentral.com)

Regulates2

• Here we showed that in migrating MDA-MB-231 cells Rab40c regulates focal adhesion's number, size, and distribution. (life-science-alliance.org)
• Thus, we propose a model where Rab40c/CRL5 regulates ANKRD28 ubiquitylation and degradation, leading to a decrease in PP6 activity, which ultimately affects FAK and Hippo pathway signaling to alter focal adhesion dynamics. (life-science-alliance.org)

Complexes2

• other signaling adaptors are also recruited to these complexes, including FAK and paxillin. (cellmigration.org)
• Focal complexes are adhesions in the early stages of maturation. (cellmigration.org)

Fibers2

• EL treatment reduced the density and number of F-actin fibers in lung cancer cell lines, and reduced the number and size of focal adhesions. (biomedcentral.com)
• The best-characterized molecules are Rho, which controls the stress fibers and focal adhesion formation, and Rac and Cdc42, which regulate membrane ruffling, and filopodium formation, respectively. (biomedcentral.com)

Pathway5

• Disease and disorder research has been conducted in relation to the Focal Adhesion Assembly Pathway and Tissue Adhesions, Malignant Neoplasms, Neoplasms, Cell Invasion, Carcinoma. (novusbio.com)
• The study of the Focal Adhesion Assembly Pathway has been mentioned in research publications which can be found using our bioinformatics tool below. (novusbio.com)
• The Focal Adhesion Assembly Pathway has been researched in relation to Cell Adhesion, Cell Migration, Cell Motility, Localization, Integrin Activation. (novusbio.com)
• The Focal Adhesion Assembly Pathway complements our catalog of research reagents including antibodies and ELISA kits against PTK2, PXN, VCL, FN1, PXDN. (novusbio.com)
• We have 2524 products for the study of the Focal Adhesion Assembly Pathway that can be applied to Chromatin Immunoprecipitation (ChIP), Flow Cytometry, Immunocytochemistry/Immunofluorescence, Immunohistochemistry, Western Blot from our catalog of antibodies and ELISA kits. (novusbio.com)

Actin cytoskeleton1

• Migration and invasion require coordinated reorganisation of the actin cytoskeleton and regulation of cell-adhesion dynamics. (silverchair.com)

Extracellular1

• Cell adhesion (the physical interaction of a cell with another cell or with the extracellular matrix (ECM)) is essential for cell migration and tissue integrity. (cellmigration.org)

Structures1

• Although their molecular composition is very similar to that of focal adhesions, their spatial distribution is radial, forming dot-like structures similar to 'suction cups' [14] . (cellmigration.org)

Carcinoma1

• Metastasis accounts for 90% of cancer-associated mortality in patients with renal cell carcinoma (RCC). (thno.org)

Invasion1

• Invasion and metastasis are controlled by the invadopodia, which delivers matrix-degrading enzymes to the invasion interface permitting cancer cell penetration and spread into healthy tissue. (nature.com)

Inhibit1

• This applies a tensile signal to the actin-binding domain (ABD) of α-catenin, which provides a clutch to promote lateral adhesion growth and inhibit the lamellipodial activity necessary for migration. (ibecbarcelona.eu)

Lamellipodium1

• These adhesions generate signals that activate Rac, promoting actin polymerization and preventing myosin II engagement in the lamellipodium. (cellmigration.org)

Cell9

• Cell migration is a fundamental cellular function that is involved in many important biological processes, including embryological development, tissue formation, wound healing, and cancer metastasis. (life-science-alliance.org)
• With nascent adhesion formation at the leading edge, the FAs at the cell rear need to be disassembled to promote rear end retraction and efficient cell migration. (life-science-alliance.org)
• These signals are also required for the dissolution of some adhesions (turnover) as the cell advances. (cellmigration.org)
• Cell-cell adhesion maintains epithelial tissues, supports functional contacts between specialized cells, and can facilitate directed migration (for example, radial glia can guide neuronal progenitor cells to specific layers of the brain). (cellmigration.org)
• Cell-matrix adhesion is the best-studied form of adhesion that mediates cell migration, and is the focus of this outline. (cellmigration.org)
• Owing to their highly localized nature, cell-matrix adhesions were initially called focal adhesions. (cellmigration.org)
• Over the years, several types of cell-matrix adhesion have been described. (cellmigration.org)
• In vitro migration assays, transendothelial migration assays (iTEM), and cell adhesion assays were used to investigate the effects of SPON2 on monocyte/macrophage migration. (biomedcentral.com)
• Moreover, these cells have a concomitant reduction in cell-adhesion turnover rates. (silverchair.com)

Activation2

• Transfection with paxillin Y31FY118F dominant-negative mutant in these cells inhibits ERK activation and restores apoptosis. (rupress.org)
• Rho activation is thought to generate focal adhesions and actin bundling due to increased myosin II activity. (cellmigration.org)

Formation2

• Whereas the formation of focal adhesions requires actomyosin-mediated contractile force mediated by RhoA , podosome formation is stimulated by a local loss of contractility and the recruitment of negative regulators of RhoA, such as p190RhoGAP [16] . (cellmigration.org)
• The transport of components along filopodial shafts is crucial to the continued growth of actin filaments and the formation of adhesions at the tips of filopodia. (mechanobio.info)

Cells4

• These adhesions are usually physically linked to large, readily visualized actomyosin bundles [13] , and their appearance correlates inversely with motility, such that they are conspicuously absent in cells migrating within a three-dimensional (3D) substrate. (cellmigration.org)
• Fibrillar adhesions represent an extreme in the maturation of adhesions and are not generally seen in migrating cells. (cellmigration.org)
• Podosomes are ring-shaped adhesions often found in fast-moving cells, such as macrophages. (cellmigration.org)
• We now report that DU145 human prostate cancer cells with reduced levels of PAK4 expression are unable to successfully migrate in response to HGF, have prominent actin stress fibres, and an increase in the size and number of focal adhesions. (silverchair.com)

Cancer2

• The prognosis of RCC is poor because approximately 25% of patients present with metastases at the time of diagnosis, and another 30-35% of patients underwent resection for localized or locally invasive kidney cancer will develop potentially fatal metachronous distant metastases [ 5 , 6 ]. (thno.org)
• Metastasis is the major cause of cancer morbidity and mortality in CRC. (biomedcentral.com)

Time1

• Focal adhesions: this term is currently reserved for mature adhesions that evolve slowly over time [12] . (cellmigration.org)

Contribute1

• and microtubule targeting, which may contribute to adhesion disassembly. (cellmigration.org)

Represent1

• Our results demonstrate that overexpression of HSPA12A might represent a viable strategy for managing RCC metastasis. (thno.org)

Shown1

• This increase is shown to result from vinculin's modulation of paxillin-FAK interactions. (rupress.org)