Adherens Junctions: Anchoring points where the CYTOSKELETON of neighboring cells are connected to each other. They are composed of specialized areas of the plasma membrane where bundles of the ACTIN CYTOSKELETON attach to the membrane through the transmembrane linkers, CADHERINS, which in turn attach through their extracellular domains to cadherins in the neighboring cell membranes. In sheets of cells, they form into adhesion belts (zonula adherens) that go all the way around a cell.alpha Catenin: A catenin that binds F-ACTIN and links the CYTOSKELETON with BETA CATENIN and GAMMA CATENIN.beta Catenin: A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.Cadherins: Calcium-dependent cell adhesion proteins. They are important in the formation of ADHERENS JUNCTIONS between cells. Cadherins are classified by their distinct immunological and tissue specificities, either by letters (E- for epithelial, N- for neural, and P- for placental cadherins) or by numbers (cadherin-12 or N-cadherin 2 for brain-cadherin). Cadherins promote cell adhesion via a homophilic mechanism as in the construction of tissues and of the whole animal body.Catenins: A family of cytoskeletal proteins that play essential roles in CELL ADHESION at ADHERENS JUNCTIONS by linking CADHERINS to the ACTIN FILAMENTS of the CYTOSKELETON.Cell Adhesion: Adherence of cells to surfaces or to other cells.Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible.Cell Adhesion Molecules: Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.Intercellular Junctions: Direct contact of a cell with a neighboring cell. Most such junctions are too small to be resolved by light microscopy, but they can be visualized by conventional or freeze-fracture electron microscopy, both of which show that the interacting CELL MEMBRANE and often the underlying CYTOPLASM and the intervening EXTRACELLULAR SPACE are highly specialized in these regions. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p792)gamma Catenin: A multi-functional catenin that is highly homologous to BETA CATENIN. Gamma catenin binds CADHERINS and helps link their cytoplasmic tails to ACTIN in the CYTOSKELETON via ALPHA CATENIN. It is also found in DESMOSOMES where it mediates the link between DESMOSOMAL CADHERINS and DESMOPLAKIN.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)EncyclopediasTight Junctions: Cell-cell junctions that seal adjacent epithelial cells together, preventing the passage of most dissolved molecules from one side of the epithelial sheet to the other. (Alberts et al., Molecular Biology of the Cell, 2nd ed, p22)Dictionaries, MedicalDictionaries as Topic: Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.Cell Movement: The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.Desmoplakins: Desmoplakins are cytoskeletal linker proteins that anchor INTERMEDIATE FILAMENTS to the PLASMA MEMBRANE at DESMOSOMES.Stem Cell Research: Experimentation on STEM CELLS and on the use of stem cells.Hemangioma, Cavernous, Central Nervous System: A vascular anomaly composed of a collection of large, thin walled tortuous VEINS that can occur in any part of the central nervous system but lack intervening nervous tissue. Familial occurrence is common and has been associated with a number of genes mapped to 7q, 7p and 3q. Clinical features include SEIZURES; HEADACHE; STROKE; and progressive neurological deficit.Capillary Permeability: The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.Endothelial Cells: Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.Antigens, CD: Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.Morphogenesis: The development of anatomical structures to create the form of a single- or multi-cell organism. Morphogenesis provides form changes of a part, parts, or the whole organism.Molecular Biology: A discipline concerned with studying biological phenomena in terms of the chemical and physical interactions of molecules.Parasite Load: Measure of the number of the PARASITES present in a host organism.Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Body Patterning: The processes occurring in early development that direct morphogenesis. They specify the body plan ensuring that cells will proceed to differentiate, grow, and diversify in size and shape at the correct relative positions. Included are axial patterning, segmentation, compartment specification, limb position, organ boundary patterning, blood vessel patterning, etc.Epithelium: One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.Gene Expression Regulation, Developmental: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.Stress, Mechanical: A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.Shear Strength: The internal resistance of a material to moving some parts of it parallel to a fixed plane, in contrast to stretching (TENSILE STRENGTH) or compression (COMPRESSIVE STRENGTH). Ionic crystals are brittle because, when subjected to shear, ions of the same charge are brought next to each other, which causes repulsion.Hemorheology: The deformation and flow behavior of BLOOD and its elements i.e., PLASMA; ERYTHROCYTES; WHITE BLOOD CELLS; and BLOOD PLATELETS.Mechanotransduction, Cellular: The process by which cells convert mechanical stimuli into a chemical response. It can occur in both cells specialized for sensing mechanical cues such as MECHANORECEPTORS, and in parenchymal cells whose primary function is not mechanosensory.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Blood Vessels: Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).Lymphoid Enhancer-Binding Factor 1: A T-cell factor that plays an essential role in EMBRYONIC DEVELOPMENT.Drug Resistance, Neoplasm: Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.NM23 Nucleoside Diphosphate Kinases: A family of nucleotide diphosphate kinases that play a role in a variety of cellular signaling pathways that effect CELL DIFFERENTIATION; CELL PROLIFERATION; and APOPTOSIS. They are considered multifunctional proteins that interact with a variety of cellular proteins and have functions that are unrelated to their enzyme activity.Antigens, CD82: A widely expressed transmembrane glycoprotein that functions as a METASTASIS suppressor protein. It is underexpressed in a variety of human NEOPLASMS.Neoplasm Metastasis: The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Genes, Tumor Suppressor: Genes that inhibit expression of the tumorigenic phenotype. They are normally involved in holding cellular growth in check. When tumor suppressor genes are inactivated or lost, a barrier to normal proliferation is removed and unregulated growth is possible.Neoplasm Invasiveness: Ability of neoplasms to infiltrate and actively destroy surrounding tissue.Cell Line, Tumor: A cell line derived from cultured tumor cells.
(1/859) Cell confluence-dependent remodeling of endothelial membranes mediated by cholesterol.

The plasma membranes of endothelial cells reaching confluence undergo profound structural and functional modifications, including the formation of adherens junctions, crucial for the regulation of vascular permeability and angiogenesis. Adherens junction formation is accompanied by the tyrosine dephosphorylation of adherens junctions proteins, which has been correlated with the strength and stability of adherens junctions. Here we show that cholesterol is a critical determinant of plasma membrane remodeling in cultures of growing cow pulmonary aortic endothelial cells. Membrane cholesterol increased dramatically at an early stage in the formation of confluent cow pulmonary aortic endothelial cell monolayers, prior to formation of intercellular junctions. This increase was accompanied by the redistribution of caveolin from a high density to a low density membrane compartment, previously shown to require cholesterol, and increased binding of the annexin II-p11 complex to membranes, consistent with other studies indicating cholesterol-dependent binding of annexin II to membranes. Furthermore, partial depletion of cholesterol from confluent cells with methyl-beta-cyclodextrin both induced tyrosine phosphorylation of multiple membrane proteins, including adherens junctions proteins, and disrupted adherens junctions. Both effects were dramatically reduced by prior complexing of methyl-beta-cyclodextrin with cholesterol. Our results reveal a novel physiological role for cholesterol regulating the formation of adherens junctions and other plasma membrane remodeling events as endothelial cells reach confluence.  (+info)

(2/859) Cell volume-dependent phosphorylation of proteins of the cortical cytoskeleton and cell-cell contact sites. The role of Fyn and FER kinases.

Cell volume affects diverse functions including cytoskeletal organization, but the underlying signaling pathways remained undefined. We have shown previously that shrinkage induces Fyn-dependent tyrosine phosphorylation of the cortical actin-binding protein, cortactin. Because FER kinase was implicated in the direct phosphorylation of cortactin, we investigated the osmotic responsiveness of FER and its relationship to Fyn and cortactin. Shrinkage increased FER activity and tyrosine phosphorylation. These effects were abolished by the Src family inhibitor PP2 and strongly mitigated in Fyn-deficient but not in Src-deficient cells. FER overexpression caused cortactin phosphorylation that was further enhanced by hypertonicity. Exchange of tyrosine residues 421, 466, and 482 for phenylalanine prevented cortactin phosphorylation by hypertonicity and strongly decreased it upon FER overexpression, suggesting that FER targets primarily the same osmo-sensitive tyrosines. Because constituents of the cell-cell contacts are substrates of Fyn and FER, we investigated the effect of shrinkage on the adherens junctions. Hypertonicity provoked Fyn-dependent tyrosine phosphorylation in beta-catenin, alpha-catenin, and p120(Cas) and caused the dissociation of beta-catenin from the contacts. This process was delayed in Fyn-deficient or PP2-treated cells. Thus, FER is a volume-sensitive kinase downstream from Fyn, and the Fyn/FER pathway may contribute to the cell size-dependent reorganization of the cytoskeleton and the cell-cell contacts.  (+info)

(3/859) Myosin light chain kinase plays an essential role in S. flexneri dissemination.

Shigella flexneri, the causitive agent of bacillary dysentery, has been shown to disseminate in colonic epithelial cells via protrusions that extend from infected cells and are endocytosed by adjacent cells. This phenomenon occurs in the region of the eukaryotic cell's adherens junctions and is inhibited by pharmacological reagents or host cell mutations that completely disrupt the junctional complex. In this study, inhibitors of the myosin light chain kinase (MLCK) were shown to dramatically decrease intercellular spread of S. flexneri but to have no inhibitory effect on bacterial entry, multiplication or actin-based motility within the host cell. Furthermore, cell-to-cell spread of Listeria monocytogenes, another bacterial pathogen that uses an actin-based mechanism to move within the eukaryotic cytoplasm and to spread from cell to cell, was not affected by the MLCK inhibitors, indicating that (1) the inhibition of S. flexneri cell-to-cell spread in treated cells is not due to a complete break down of cell-cell contacts, which was subsequently confirmed by confocal microscopy, and (2) MLCK plays a role in a S. flexneri-specific mechanism of dissemination. Myosin has been shown to play a role in a variety of membrane-based phenomena. The work presented here suggests that activation of this molecule via phosphorylation by MLCK, at the very least participates in the formation of the bacteria-containing protrusion, and could also contribute to the endocytosis of this structure by neighboring cells.  (+info)

(4/859) The molecular organization of endothelial junctions and their functional role in vascular morphogenesis and permeability.

We review here our work on the molecular and functional organization of endothelial cell-to-cell junctions. The first part of the review is dedicated to VE-cadherin, characterized by our group few years ago. This protein is a member of the large family of transmembrane adhesion proteins called cadherins. It is endothelial cell specific and plays a major role in the organization of adherens junctions. Inactivation of VE-cadherin gene or in vivo truncation of its cytoplasmic tail leads to a lethal phenotype due to the lack of correct organization of the vasculature in the embryo. We found that the defect was due to apoptosis of endothelial cells, which became unresponsive to the survival signal induced by vascular endothelial cell growth factor. Our data indicate that VE-cadherin may act as a scaffolding protein able to associate vascular endothelial cell growth factor receptor and to promote its signaling. In the second part of the review we consider another protein more recently discovered by us and called junctional adhesion molecule (JAM). This protein is a small immunoglobulin which is located at tight junctions in the endothelium and in epithelial cells. Evidence is discussed indicating that JAM takes part in the organization of tight junctions and modulates leukocyte extravasation through endothelial intercellular junctions in vitro and in vivo. The general role of tight junctions in endothelial cells is also discussed.  (+info)

(5/859) Reversibility of increased microvessel permeability in response to VE-cadherin disassembly.

We determined the role of vascular endothelial (VE)-cadherin complex in regulating the permeability of pulmonary microvessels. Studies were made in mouse lungs perfused with albumin-Krebs containing EDTA, a Ca(2+) chelator, added to study the VE-cadherin junctional disassembly. We then repleted the perfusate with Ca(2+) to restore VE-cadherin integrity. Confocal microscopy showed a disappearance of VE-cadherin immunostaining in a time- and dose-dependent manner after Ca(2+) chelation and reassembly of the VE-cadherin complex within 5 min after Ca(2+) repletion. We determined the (125)I-labeled albumin permeability-surface area product and capillary filtration coefficient (K(fc)) to quantify alterations in the pulmonary microvessel barrier. The addition of EDTA increased (125)I-albumin permeability-surface area product and K(fc) in a concentration-dependent manner within 5 min. The permeability response was reversed within 5 min after repletion of Ca(2+). An anti-VE-cadherin monoclonal antibody against epitopes responsible for homotypic adhesion augmented the increase in K(fc) induced by Ca(2+) chelation and prevented reversal of the response. We conclude that the disassembled VE-cadherins in endothelial cells are mobilized at the junctional plasmalemmal membrane such that VE-cadherins can rapidly form adhesive contact and restore microvessel permeability by reannealing the adherens junctions.  (+info)

(6/859) Actin-dependent membrane association of a Drosophila epithelial APC protein and its effect on junctional Armadillo.

BACKGROUND: The adenomatous polyposis coli (APC) protein is an important tumour suppressor in the colon. It promotes the destabilisation of free cytoplasmic beta-catenin (the vertebrate homologue of the Drosophila protein Armadillo), a critical effector of the Wnt signalling pathway. The beta-catenin protein is also a component of adherens junctions, linking these to the actin cytoskeleton. In Drosophila epithelial cells, the ubiquitous form of APC, known as E-APC, is associated with adherens junctions. This association appears to be necessary for E-APC to function in destabilising Armadillo. RESULTS: Using actin-depolymerising drugs, we established that an intact actin cytoskeleton is required for the association of E-APC with adherens junctions in the Drosophila embryo. From an analysis of profilin mutants, whose actin cytoskeleton is disrupted, we found that E-APC also requires actin filaments to associate with adhesive cell membranes in the ovary. Notably, conditions that delocalised E-APC from membranes, including a mutation in E-APC itself, caused partial detachment of Armadillo from adhesive membranes. CONCLUSIONS: Actin filaments are continuously required for E-APC to be associated with junctional membranes. These filaments may serve as tracks for E-APC to reach the adherens junctions. The failure of E-APC to do so appears to affect the integrity of junctional complexes.  (+info)

(7/859) Reversal of the Ras-induced transformed phenotype by HR12, a novel ras farnesylation inhibitor, is mediated by the Mek/Erk pathway.

We have used the selective farnesylation inhibitor HR12 [cysteine-N(methyl)valine-N(cyclohexyl) glycine-methionine-O-methyl-ester] to study the role of oncogenic Ras in cytoskeletal reorganization in Ha-ras(V12)-transformed Rat1 cells (Rat1/ras). Application of HR12 resulted in complete restoration of the cytoskeleton and associated cell adhesions disrupted by oncogenic Ras. This included an increase in the number and size of focal adhesions, accompanied by massive stress fiber formation and enhanced tyrosine phosphorylation. Furthermore, HR12 induced assembly of adherens junctions and dramatically elevated the level of the junctional components, cadherin and beta-catenin. HR12 was unable to restore the nontransformed phenotype in cells expressing farnesylation-independent, myristylated Ras. Examination of the main Ras-regulated signaling pathways revealed that HR12 induced a dose- and time-dependent decline in Erk1&2 activation (t(1/2) approximately 6 h), which correlated with the accumulation of nonfarnesylated oncogenic-Ras. Inhibition of the Mek/Erk pathway in Rat1/ras cells, using the Mek inhibitor, PD98059, resulted in complete cytoskeletal recovery, indistinguishable from that induced by HR12. Moreover, a constitutively active Mek mimicked the effect of ras transformation in Rat1 cells, and prevented HR12-induced cytoskeletal effects in Rat1/ras cells. No such effects were observed after treatment of Rat1/ras cells with the phosphatidylinositol 3-kinase inhibitor LY294002. These findings establish the Mek/Erk pathway as the dominant pathway involved in conferring the cytoskeletal and junctional manifestations of the Ras-induced transformed phenotype.  (+info)

(8/859) Endothelial adherens junctions.

The principle of the molecular organization of adherens junctions follows a uniform pattern, which is found in epithelial, muscular, neuroneal as well as in endothelial cells and is highly conserved among species. Transmembrane molecules of the cadherin family link to catenins, which anchor the adhesion plaque to the cytoskeleton. The kind of cadherin used in adherens junctions is cell-type specific, vascular endothelial (VE)-cadherin is specific for endothelial cells. The assembly and disassembly of the cadherin/catenin complex is dynamic and regulated by growth factors. The functional status of adherens junctions controls endothelial cell-to-cell adhesion, cell scattering, vessel morphogenesis and has intracellular signaling properties, thereby playing an important role in vasculogenesis and angiogenesis.  (+info)

*  Adherens junction
MBInfo - Adherens Junction MBInfo - Adherens Junction Assembly Adherens Junctions at the US National Library of Medicine ... Adherens junctions (or zonula adherens, intermediate junction, or "belt desmosome") are protein complexes that occur at cell- ... cell junctions in epithelial and endothelial tissues, usually more basal than tight junctions. An adherens junction is defined ... "Signaling to and through the Endothelial Adherens Junction". In LaFlamme SE, Kowalczyck AP. Cell Junctions: Adhesion, ...
*  MYH10
It appears that NM-IIB plays an essential role in maintaining normal adherens junction integrity and structure. A cardiac ... widened adherens junctions; and progressive hypertrophic cardiomyopathy at 6 months. These data indicate that NM-IIB functions ... where it localizes to adherens junctions within intercalated discs. NM-IIB is essential for normal development of cardiac ...
*  Keith Burridge
Geiger, B; Volk, T; Volberg, T (1985). "Molecular heterogeneity of adherens junctions". The Journal of Cell Biology. 101 (4): ...
*  Cadherin
Volk, T.; Cohen, O.; Geiger, B. (1987). "Formation of heterotypic adherens-type junctions between L-CAM containing liver cells ... Harris, T. J.; Tepass, U (2010). "Adherens junctions: From molecules to morphogenesis". Nature Reviews Molecular Cell Biology. ... adherens junctions can then be made when protein complexes, usually composed of α-, β-, and γ-catenins, bind to the actin ... that is important in the formation of adherens junctions to bind cells with each other. Cadherins are a class of type-1 ...
*  Homeobox
"HoxA5 stabilizes adherens junctions via increased Akt1". Cell Adhesion & Migration. 1 (4): 185-95. doi:10.4161/cam.1.4.5448. ... and stabilizing adherens junctions by upregulating TIMP1/downregulating uPAR and MMP14, and by upregulating Tsp2/downregulating ...
*  VEZT
... adherens junctions transmembrane protein". Blaschuk OW, Rowlands TM (2003). "Plasma membrane components of adherens junctions ( ... The protein is documented as an adherens junction component in a number of cell types. VEZT has been shown to interact with ... a protein associated to adherens junctions, is required for mouse blastocyst morphogenesis". Developmental Biology. 287 (1): ...
*  HOXA5
"HoxA5 stabilizes adherens junctions via increased Akt1". Cell Adhesion & Migration. 1 (4): 185-95. doi:10.4161/cam.1.4.5448. ...
*  Stress fiber
... such as the formation of adherens junctions, tight junctions and focal adhesions. Adherens junctions are a type of cell-cell ... This may serve as a mechanism for how actin is recruited to adherens junctions. Tight junctions, or zona occludens, are the ... α-catenin and β-catenin are integral components of adherens junctions, which bind together to produce cadherin-α-catenin-β- ... Hartsock, Andrea; Nelson, W. James (March 2008). "Adherens and tight junctions: Structure, function and connections to the ...
*  MARCKSL1
The encoded protein affects the formation of adherens junction. Alternative splicing results in multiple transcript variants. ...
*  PLEKHA7
... is an adherens junction (AJ) protein, involved in the junction's integrity and stability. The protein was discovered in ... Knock-out of PLEKHA7 results in the loss of PDZD11 from epithelial adherens junctions, and this is rescued by the introduction ... Pulimeno P, Bauer C, Stutz J, Citi S (Aug 2010). "PLEKHA7 is an adherens junction protein with a tissue distribution and ... The first identified function of PLEKHA7 was is to contribute to integrity and stability of the zonula adherens junctions by ...
*  Marilyn Farquhar
Together Farquhar and Palade named tight junctions and adherens junctions. Since then, Farquhar has continued to study ... Cell junction-associated proteins IQGAP1, MAGI-2, CASK, spectrins, and alpha-actinin are components of the nephrin multiprotein ... junctions in the podocytes. After leaving Rockefeller in 1962, she established her own laboratory at the University of ...
*  Adhesome
"Jack of all trades: functional modularity in the adherens junction". Current Opinion in Cell Biology. 36: 32-40. doi:10.1016/j. ... they localize to a cell adhesion structure such as focal adhesion or adherens junction. 2. they directly interact with one of ...
*  Cadherin-catenin complex in learning and memory
"Endocytosis is required for E-cadherin redistribution at mature adherens junctions". PNAS. 106 (17): 7010-15. doi:10.1073/pnas. ... of cadherins into the adhesive junctions at the synapse. P120 ctn proteins are thought to either inhibit endocytosis of neural ...
*  Intercalated disc
Three types of cell junction make up an intercalated disc - fascia adherens, desmosomes and gap junctions. Fascia adherens are ... Thus cardiomyocyte adherens junctions differ from epithelial adherens junctions and desmosomes. Franke, Werner W.; Borrmann, ... Desmosomes are also known as macula adherens. Gap junctions allow action potentials to spread between cardiac cells by ... and comprehensive studies have shown that intercalated discs consist for the most part of mixed type adherens junctions, termed ...
*  Epidermis
The junctions between the epidermal cells is adherens junction type. These junctions are formed by transmembrane proteins ... Because of the proximity of the neighboring cells and tightness of the junctions, the actin immunofluorescence appears as a ... Characteristics Physical barrier through keratinocytes attached together via cell-cell junctions and associated to cytoskeletal ...
*  Stem cell
Song X, Zhu CH, Doan C, Xie T (2002). "Germline stem cells anchored by adherens junctions in the Drosophila ovary niches". ... Studies in Drosophila germarium have identified the signals decapentaplegic and adherens junctions that prevent germarium stem ...
*  DIAPH1
Sahai E, Marshall CJ (June 2002). "ROCK and Dia have opposing effects on adherens junctions downstream of Rho". Nature Cell ...
*  Poliovirus receptor-related 2
This protein is one of the plasma membrane components of adherens junctions. It also serves as an entry for certain mutant ... 1999). "Nectin/PRR: An Immunoglobulin-like Cell Adhesion Molecule Recruited to Cadherin-based Adherens Junctions through ... a Component of Cell-Cell Adherens Junctions". Mol. Cell. Biol. 20 (8): 2865-73. doi:10.1128/MCB.20.8.2865-2873.2000. PMC 85510 ...
*  Stem-cell niche
Song, Xiaoqing; Zhu, Chun-Hong; Doan, Chuong; Xie, Ting (2002). "Germline Stem Cells Anchored by Adherens Junctions in the ... adherens junctions and if this physical attachment is lost GSCs will differentiate and lose their identity as a stem cell. The ... whereby differentiating spermatocytes must traverse the tight junctions. These tight junctions form the blood testis barrier ( ... The bulge area at the junction of arrector pili muscle to the hair follicle sheath has been shown to host the skin stem cells ...
*  Janus kinase 3
Compromise in adherens junctions (AJs) is associated with several chronic inflammatory diseases. Functional characterization ... Mishra, Jayshree; Das, Jugal Kishore; Kumar, Narendra (2017). "Janus kinase 3 regulates adherens junctions and epithelial ... Jak3 redistributed to basolateral surfaces and interacted with adherens junction (AJ) protein β-catenin. Jak3 expression in ...
*  Actin
Principal interactions of structural proteins are at cadherin-based adherens junction. Actin filaments are linked to α-actinin ... and the establishment and maintenance of cell junctions and cell shape. Many of these processes are mediated by extensive and ...
*  Catenin
The exact mechanisms by which α-catenin acts in adherens junctions is still unclear; however, it is likely that α-catenin acts ... For instance, when an epithelial layer is complete and the adherens junctions indicate that the cell is surrounded, β-catenin ... α-catenin participates in the formation and stabilization of adherens junctions by binding to β-catenin-cadherin complexes in ... Tripathi V, Popescu NC, Zimonjic DB (April 2012). "DLC1 interaction with α-catenin stabilizes adherens junctions and enhances ...
*  Plakoglobin
... is a major cytoplasmic component of both desmosomes and adherens junctions, and is the only known constituent ... Shasby DM, Ries DR, Shasby SS, Winter MC (Jun 2002). "Histamine stimulates phosphorylation of adherens junction proteins and ... Plakoglobin is a cytoplasmic component of desmosomes and adherens junctions structures located within intercalated discs of ... "Plakoglobin is essential for myocardial compliance but dispensable for myofibril insertion into adherens junctions". Journal of ...
*  VE-cadherin
Shasby DM, Ries DR, Shasby SS, Winter MC (Jun 2002). "Histamine stimulates phosphorylation of adherens junction proteins and ... and the VE-cadherin-based adherens junction is thought to be particularly important. VE-cadherin is known to be required for ... "Alteration of interendothelial adherens junctions following tumor cell-endothelial cell interaction in vitro". Exp. Cell Res. ... "Alteration of interendothelial adherens junctions following tumor cell-endothelial cell interaction in vitro". Exp. Cell Res. ...
*  CRB1
2002). "Drosophila Crumbs is a positional cue in photoreceptor adherens junctions and rhabdomeres". Nature. 416 (6877): 178-83 ...
*  Signet ring cell carcinoma
Highly differentiated adenocarcinomas form SRCCs via a loss of adherens and tight junctions that typically separate MUC4, a ...
Adherens junctions have an important role in the control of vascular permeability. These structures are located at cell-to-cell contacts, mediate cell adhesion and transfer intracellular signals. Adhesion is mediated by cadherins, which interact homophilically in trans and form lateral interactions in cis. VE-cadherin (also known as CDH5 and CD144) is the major component of endothelial adherens junctions and is specific to endothelial cells. Endothelial cells from different types of vessels, such as lymphatic vessels, arteries and veins, show differences in junction composition and organization. Vascular permeability is increased by modifications in the expression and function of adherens junction components. In some cases these defects might be cause of pathology. In this Cell Science at a Glance article, we present the example of the so-called cerebral cavernous malformation (CCM), where adherens junctions are dismantled in the vessels contributing to brain microcirculation. This causes the ...
The Mouse Adherens Junctions RT Profiler PCR Array profiles the expression of 84 key genes encoding components, interactors, and regulators of adherens junctions and desmosomes involved in cell cell contacts mediated by cadherins. Adherens junctions occur at adhesion belts linking adjacent epithelial cells or the focal contacts on the lower surface of cultured fibroblasts. Desmosomes are anchoring cell cell junctions, usually formed between 2 epithelial cells and characterized by dense protein plaques. Adherens junctions connect cadherins to actin filaments internally, while desmosomes connect cadherins to intermediate filaments such as keratin and desmin filaments. Besides cadherins, cell surface receptor components of adherens junctions also include desmocollins, desmogleins, nectins, and Notch proteins. Adherens-junction associated proteins, especially the catenins, recruit protein kinases that regulate the cytoskeleton via phosphorylation cascades and G-proteins that directly recruit ...
Dynamic regulation of cell-cell adhesion by the coordinated formation and dissolution of E-cadherin-based adherens junctions is crucial for tissue homeostasis. The actin-binding protein cortactin interacts with E-cadherin and enables F-actin accumulation at adherens junctions. Here, we were interested to study the broader functional interactions of cortactin in adhesion complexes. In line with literature, we demonstrate that cortactin binds to E-cadherin, and that a posttranslational modification of cortactin, RhoA-induced phosphorylation by protein kinase D1 (PKD1;also known as PRKD1) at S298, impairs adherens junction assembly and supports their dissolution. Two new S298-phosphorylation-dependent interactions were also identified, namely, that phosphorylation of cortactin decreases its interaction with beta-catenin and the actin-binding protein vinculin. In addition, binding of vinculin to beta-catenin, as well as linkage of vinculin to F-actin, are also significantly compromised upon ...
The structure and physiology of the endothelial cells that line the mammalian vasculature are greatly influenced by the shear stresses that are continuously imposed on them by blood flow. The most obvious structural responses of endothelium to shear stress are changes in cell shape and orientation; in areas of low or inconsistent shear stress in vivo, or when cells are maintained in static culture, endothelial cells assume a cuboidal, cobblestone morphology, whereas they elongate and align in the direction of flow when shear stress is moderate or high.1 2 These morphological changes are adaptive in that they reduce the spatial fluctuations in shear stress and the maximum shears to which the cells are exposed.3 Shape change of cells within monolayers probably necessitate changes in the interaction of individual cells with their neighbors at cell-cell junctions; however, changes in endothelial cell-cell contacts during responses to altered shear stress have not been examined. Endothelial cells ...
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Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
VE-PTP stabilizes endothelial adherens junctions (AJs) through constitutive dephosphorylation of VE-cadherin. Here we investigated the role of STIM1 activation of store-operated Ca2+ entry (SOCE) in regulating adherens junction assembly. We observed that SOCE induced by STIM1 activated Pyk2 in human lung microvascular endothelial cells (ECs) and induced tyrosine phosphorylation of VE-PTP at Y1981. Pyk2-induced tyrosine phosphorylation of VE-PTP promoted Src binding to VE-PTP, Src activation, and subsequent VE-cadherin phosphorylation, and thereby increased the endothelial permeability response. The increase in permeability was secondary to disassembly of AJs. Pyk2-mediated responses were blocked in EC-restricted Stim1 knockout mice indicating the requirement for STIM1 in initiating the signaling cascade. A peptide derived from the Pyk2 phosphorylation site on VE-PTP abolished the STIM1/SOCE-activated the permeability response. Thus, Pyk2 activation secondary to STIM1-induced SOCE causes tyrosine ...
Looking for online definition of zona adherens in the Medical Dictionary? zona adherens explanation free. What is zona adherens? Meaning of zona adherens medical term. What does zona adherens mean?
Muramidase-released protein (MRP) is as an important virulence marker of Streptococcus suis (S. suis) serotype 2. Our previous works have shown that MRP can bind human fibrinogen (hFg); however, the function of this interaction in S.suis meningitis is not known. In this study, we found that the deletion of mrp significantly impairs the hFg-mediated adherence and traversal ability of S. suis across human cerebral microvascular endothelial cells (hCMEC/D3). Measurement of the permeability to Lucifer yellow in vitro and Evans blue extravasation in vivo show that the MRP-hFg interaction significantly increases the permeability of the blood-brain barrier (BBB). In the mouse meningitis model, wild type S. suis caused higher bacterial loads in the brain and more severe histopathological signs of meningitis than the mrp mutant at day 3 post-infection. Western blot analysis and immunofluorescence observations reveal that the MRP-hFg interaction can destroy the cell adherens junction protein p120-catenin of hCMEC
Poly-ADP-ribose (PAR) is a polymer of up to 400 ADP-ribose units synthesized by poly-ADP-ribose-polymerases (PARPs) and degraded by poly-ADP-ribose-glycohydrolase (PARG). Nuclear PAR modulates chromatin compaction, affecting nuclear functions (gene expression, DNA repair). Diverse defined PARP cytoplasmic allocation patterns contrast with the yet still imprecise PAR distribution and still unclear functions. Based on previous evidence from other models, we hypothesized that PAR could be present in epithelial cells where cadherin-based adherens junctions are linked with the actin cytoskeleton (constituting the adhesion belt). In the present work, we have examined through immunofluorescence and confocal microscopy, the subcellular localization of PAR in an epithelial monkey kidney cell line (VERO). PAR was distinguished colocalizing with actin and vinculin in the epithelial belt, a location that has not been previously reported. Actin filaments disruption with cytochalasin D was paralleled by PAR belt
Background: - Protein S-glutathionylation (Pr-SSG) is a prevalent form of oxidative modification of reactive cysteines and serves as an important mode of redox signaling. Vascular redox dysregulation and impaired barrier function have long been recognized as early vascular alterations in diabetes, a major risk factor for atherosclerotic cardiovascular diseases, but the mechanistic link of Pr-SSG to the metabolic stress-induced endothelial cell (EC) hyper-permeability is not established and being investigated in the present study.. Methods and Results: - elevated Pr-SSG was observed in ECs isolated from patients with type-2 diabetes and atherosclerotic lesions of ApoE deficient (ApoE-/-) mice, concurring with a decrease in glutaredoxin-1 (Glrx-1), a specific deglutathionylation enzyme. Exposure of human aortic ECs to diabetic conditions increased the formation of Pr-SSG and permeability that was associated with the disassembly of cell adherens junctions and cortical actin structures, all of which ...
Ukropec, Jon A., "Fluid shear stress-induced reorganization of adherens junctions in human endothelial cells" (1999). Theses. 24 ...
TY - JOUR. T1 - Glutamine supplementation attenuates ethanol-induced disruption of apical junctional complexes in colonic epithelium and ameliorates gut barrier dysfunction and fatty liver in mice. AU - Chaudhry, Kamaljit K.. AU - Shukla, Pradeep Kumar. AU - Mir, Hina. AU - Manda, Bhargavi. AU - Gangwar, Ruchika. AU - Yadav, Nikki. AU - McMullen, Megan. AU - Nagy, Laura E.. AU - Rao, Radhakrishna. PY - 2016/1/1. Y1 - 2016/1/1. N2 - Previous in vitro studies showed that glutamine (Gln) prevents acetaldehyde-induced disruption of tight junctions and adherens junctions in Caco-2 cell monolayers and human colonic mucosa. In the present study, we evaluated the effect of Gln supplementation on ethanol-induced gut barrier dysfunction and liver injury in mice in vivo. Ethanol feeding caused a significant increase in inulin permeability in distal colon. Elevated permeability was associated with a redistribution of tight junction and adherens junction proteins and depletion of detergent-insoluble ...
Epithelial cells contain a variety of junctions that are essential for the maintenance of tissue integrity, barrier function and regulation of tissue growth. Some of these cellular junctions exhibit a strict polarised distribution in epithelial cells. Whereas intercellular junctions, such as adherens junctions and tight junctions, exhibit apicolateral localisation, focal adhesions and hemidesmosomes are localised basally to mediate cell-matrix adhesion. The formation and positioning of adherens and tight junctions (or septate junctions in invertebrates) are dependent on the activity of genes involved in the establishment and maintenance of cell polarity (reviewed by Bryant, 1997; Knust and Bossinger, 2002; Humbert et al., 2003; Shin et al., 2006; Suzuki and Ohno, 2006).. The balanced activities of the Crumbs, Par3 (Bazooka, Pard3)-atypical Protein kinase C (aPKC) and Lgl-Scrib-Dlg pathways are essential for the formation of adherens junctions or tight junctions in epithelia. Whereas the ...
Relative or absolute hypoxia activates signaling pathways that alter gene expression and stabilize the pulmonary microvasculature. Alveolar hypoxia occurs in disorders ranging from altitude sickness to airway obstruction, apnea, and atelectasis. Here, we report that the phospholipid-binding protein, annexin A2 (ANXA2) functions to maintain vascular integrity in the face of alveolar hypoxia. We demonstrate that microvascular endothelial cells (ECs) from Anxa2−/− mice display reduced barrier function and excessive Src-related tyrosine phosphorylation of the adherens junction protein vascular endothelial cadherin (VEC). Moreover, unlike Anxa2+/+ controls, Anxa2−/− mice develop pulmonary edema and neutrophil infiltration in the lung parenchyma in response to subacute alveolar hypoxia. Mice deficient in the ANXA2-binding partner, S100A10, failed to demonstrate hypoxia-induced pulmonary edema under the same conditions. Further analyses reveal that ANXA2 forms a complex with VEC and its ...
RV infection decreased mRNA levels of ZO-1, occludin, claudin-1, and E-cadherin to 64.2%, 51.8%, 56.2%, and 56.3%, respectively, of those in controls (P , .05). Decreases in ZO-1, occludin, claudin-1, and E-cadherin protein levels in RV-infected cells were evident in immunofluorescent confocal microscopic images. Expression levels of these proteins were also lower in the RV-infected group in Western blot analyses. RV infection reduced the mean TER from 143.1 Ω/cm2 (controls) to 122.6 Ω/cm2. ...
Costa, M., et al. (1998). A putative catenin-cadherin system mediates morphogenesis of the Caenorhabditis elegans embryo. J. Cell Biol. 141(1): 297-308 Coste, A. L., et al. (1998). Somatic mutations of the beta-catenin gene are frequent in mouse and human hepatocellular carcinomas. Proc. Natl. Acad. Sci. 95(15): 8847-8851 Cox, R. T., Kirkpatrick, C. and Peifer, M. (1996), Armadillo is required for adherens junction assembly, cell polarity and morphogenesis during Drosophila embryogenesis. J. Cell Biol. 134: 133-148 Cox, R. T., et al. (1999). Membrane-tethered Drosophila Armadillo cannot transduce Wingless signal on its own. Development 126: 1327-1335 Cox, R. T., et al. (2000). A screen for mutations that suppress the phenotype of Drosophila armadillo, the ß-catenin homolog. Genetics 155: 1725-1740 Daniels, D. L. and Weis, W. I. (2002). ICAT inhibits ß-Catenin binding to Tcf/Lef-family transcription factors and the general coactivator p300 using independent structural modules. Molec. Cell 10: ...
Abstract Measles virus is an aerosol-transmitted virus that affects more than 10 million children each year and accounts for approximately 120,000 deaths. Although it was long beli..
Classical cadherins mediate Ca2+-dependent intercellular adhesion and are essential for tissue morphogenesis and maintenance. They are key components of adherens junctions (AJs). In vitro studies in simple epithelial cells indicated an essential role for E-cadherin not only in the formation of AJs but also other intercellular contacts, such as desmosomes and tight junctions. In contrast, in vivo tissue specific knockout studies did not reveal a necessity of E-cadherin in the formation of intercellular junctions, raising the question if classical cadherins are necessary or if other classical cadherins can compensate for the loss of E-cadherin. Therefore, the aim of this thesis was to ask how E-cadherin regulates tight junctions and if E-cadherin has a specific function in the formation of tight junctions. In addition, the question was asked if classical cadherin function is necessary for the formation of other intercellular contacts, such as desmosomes. Using primary keratinocytes as a model for ...
Cadherin 2, also known as N-cadherin, is a member of the cadherin superfamily of predominantly Ca2+-dependent cell surface adhesion proteins.30 In the heart, cadherin 2 is located at the intercalated disc, a complex and highly organized intercellular structure that ensures structural integrity and functional synchronization across the myocardium through the tight electromechanical coupling of cardiomyocytes.30,31 In the intercalated disc, intercellular communication and adhesion are achieved through 3 main junctional structures forming functional zones, the gap junctions, the fascia adherens junctions, and the desmosomes, with the latter 2 being the main contributors to cell-cell adhesion.30-32 In desmosomes, desmosomal cadherins (desmocollin and desmoglein) are mainly anchored to the intermediate filaments of the cytoskeleton through many intracellular protein partners, whereas in fascia adherens junctions, the classical cadherin, N-cadherin, is primarily anchored to the actin microfilaments of ...
How stem cells are recruited to and maintained in their niches is crucial to understanding their regulation and use in regenerative medicine. Here, we demonstrate that DE-cadherin-mediated cell adhesion is required for anchoring germline stem cells (GSCs) in their niches in the Drosophila ovary. Two major components of this adhesion process, DE-cadherin and Armadillo/β-catenin, accumulate at high levels in the junctions between GSCs and cap cells, one of the niche components. Removal of these proteins from GSCs results in stem cell loss. Furthermore, DE-cadherin is required for recruiting GSCs to their niche. Our study demonstrates that anchorage of GSCs in their niche by DE-cadherin-mediated adhesion is important for stem cell maintenance and function. |P /|
The movement of developing germ cells across the seminiferous epithelium during spermatogenesis involves extensive adherens junction (AJ) restructuring between Sertoli cells, as well as between Sertoli and germ cells. In this report, we show that the intricate interactions between Cdc42 (a Rho family protein of Mr approximately 23 kDa originally identified in membranes of human platelets and placenta, and is the homolog of CDC42Sc, which is known to regulate of bud-site assembly in Saccharomyces cerevisiae) and its effector, IQ motif containing GTPase activating protein (IQGAP1, Mr approximately 189 kDa, it is also an actin-binding protein known to interact with Cdc42 and Rac1 GTPases), regulate Sertoli-germ cell, but not Sertoli-Sertoli cell, AJ dynamics. Using testis lysates for immunoprecipitation (IP), IQGAP1 was shown to associate with E-cadherin, N-cadherin, and beta-catenin (but not beta1-integrin and nectin-2), as well as with actin and vimentin (but not alpha-tubulin). Moreover, IQGAP1 ...
Rab GTPases define the vesicle trafficking pathways underpinning cell polarization and migration. Here, we find that Rab4, Rab11, and Rab14 and the candidate Rab GDP-GTP exchange factors (GEFs) FAM116A and AVL9 are required for cell migration. Rab14 and its GEF FAM116A localize to and act on an intermediate compartment of the transferrin-recycling pathway prior to Rab11 and after Rab5 and Rab4. This Rab14 intermediate recycling compartment has specific functions in migrating cells discrete from early and recycling endosomes. Rab14-depleted cells show increased N-cadherin levels at junctional complexes and cannot resolve cell-cell junctions. This is due to decreased shedding of cell-surface N-cadherin by the ADAM family protease ADAM10/Kuzbanian. In FAM116A- and Rab14-depleted cells, ADAM10 accumulates in a transferrin-positive endocytic compartment, and the cell-surface level of ADAM10 is correspondingly reduced. FAM116 and Rab14 therefore define an endocytic recycling pathway needed for ADAM protease
An increasing body of evidence indicates that cellular polyamines play a critical role in maintenance of the intestinal epithelial integrity, but few specific functions of polyamines at cellular and molecular levels are defined. We (18) have recently reported that polyamines are implicated in regulation of the intestinal epithelial barrier function and that depletion of cellular polyamines increases epithelial paracellular permeability at least partially by inhibiting expression of adherens junctions in undifferentiated parental IEC-6 cells. The present studies further confirm our previous observations by demonstrating that polyamines are crucial for expression of adherens junctions in differentiated IEC-Cdx2L1 cells. The most significant of the new findings reported in this study, however, is that polyamines are required for normal function of tight junctions and that polyamines regulate expression of various tight junction proteins through different mechanisms. Polyamines regulate occludin ...
Here, we isolated a novel F-actin-binding protein with a molecular mass of ∼205 kD (p205). This protein was copurified with another protein with a molecular mass of 190 kD (p190) that lacked the F-actin-binding activity on various column chromatographies. The molecular cloning of the cDNAs of these two proteins revealed that the nucleotide sequence of the p190 cDNA was identical to that of the p205 cDNA, except for the two splicing regions. FISH analysis revealed that the genes of these two proteins were localized at the same locus. These results suggest that p205 and p190 are splicing variants derived from the same gene. Because a computer homology search revealed that the aa sequence of p190 was almost identical to that of human AF-6 protein, we theorize that p190 may be a rat counterpart of human AF-6 protein. We named p205 and p190 l- and s-afadins, respectively. Further purification steps of l-afadin, including Mono S column and Superdex 200 column chromatographies, did not separate l- ...
The development of cell-cell junctions was a fundamental step in metazoan evolution and human health depends on the formation and function of cell junctions. the apical junction and an apically-directed actin flow generated by NMII contraction.45 As a major force generator and component of adherens junctions NMII may also have yet to be discovered roles at the junction. Myo1e at Specialized Glomerular Junctional Complexes Class I myosins are single-headed motors with short tails that bind to lipid membranes.46 They are phylogenetically ancient and are found in amoebae fungi and animals. Many organisms express several class I myosins; the slime mold expresses seven46 and humans express eight class I myosins.3 Myo1a one of the best known class I myosins forms a link between the plasma membrane and the actin filaments of intestinal microvilli.47 Myo1e (initially called human myosin-1c or myr3) has a longer tail that contains both a membrane-binding domain and an SH3 domain48 (Fig.?1). Myo1e is ...
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Arm and Abl proteins function cooperatively at adherens junctions in both the CNS and epidermis; critical for embryonic epithelial morphogenesis regulating cell shape changes and cell migration. Plays a critical role in transducing embryonic midline repulsive cues; may regulate cytoskeletal dynamics underlying a growth cones response to midline cues. The ability of pCC/MP2 axons to correctly interpret midline repulsive cues and stay on the ipsilateral side is dependent on the strength of both Slit/robo and Abl-dependent signaling pathways.
Diseases culminating in photoreceptor loss are a major cause of untreatable blindness. Transplantation of rod photoreceptors is feasible, provided donor cells are at an appropriate stage of development when transplanted. Nevertheless, the proportion of cells that integrate into the recipient outer nuclear layer (ONL) is low. The outer limiting membrane (OLM), formed by adherens junctions between Müller glia and photoreceptors, may impede transplanted cells from migrating into the recipient ONL. Adaptor proteins such as Crumbs homologue 1 (Crb1) and zona occludins (ZO-1) are essential for localization of the OLM adherens junctions. We investigated whether targeted disruption of these proteins enhances donor cell integration. Transplantation of rod precursors in wild-type mice achieved 949 +/- 141 integrated cells. By contrast, integration is significantly higher when rod precursors are transplanted into Crb1(rd8/rd8) mice, a model of retinitis pigmentosa and Lebers congenital amaurosis that lacks
To better treat breast cancer patients, it is imperative to be able to predict breast cancer relapse and metastasis. Here, we identified the cluster of differentiation 177 (CD177) expression is positively correlated with relapse-free and metastasis-free survival of breast cancer patients. CD177 protein is highly expressed in normal breast epithelial cells and is significantly reduced in invasive cancers. Using mouse models, we found that CD177 suppresses breast cancer, primarily by forming a complex with E-Cadherin and b-Catenin at adherens junctions. The physical interaction prevents the activation of b-Catenin-mediated transcription by the canonical WNT signaling as demonstrated by a TOP-flash dual luciferase assay. In conclusion, we have identified CD177 as a novel breast cancer suppressor and uncovered a new regulatory mechanism for the canonical WNT/b-Catenin-mediated oncogenic signaling transduction.. Citation Format: Paige N. Kluz, Ryan Kolb, Qing Xie, Nicholas Borcherding, Linna Wang, ...
Cytoskeletal signaling complexes include G-protein complexes, focal adhesions, and adherens junctions. Focal adhesions and adherens junctions link the cell exterior to the plasma membrane and the actin cytoskeleton, acting as key initiators of signaling pathways in response to cell adhesion.
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Purpose.: Toelucidate the influences of light exposure on the retinal pigment epithelium (RPE) in vivo that may be involved in the pathogenesis of AMD. Methods.: Six- to 7-week-old BALB/c mice were exposed to light at 2000 lux for 3 hours. Flat-mount RPE samples were immunostained with anti-ZO-1 antibody for evaluating tight junction, anti-N-cadherin, and anti-β-catenin antibodies for adherens junction, and stained with phalloidin for actin cytoskeleton. The reactive oxygen species (ROS) level was measured using DCFH-DA; Rho-associated coiled-coil forming kinase (ROCK) activity was by ELISA. Cytokine expression was analyzed by real-time RT-PCR and/or ELISA in the RPE-choroid, and macrophage recruitment was by real-time RT-PCR and immunohistochemistry. Either an antioxidant, N-Acetyl-L-cysteine (NAC), or a ROCK inhibitor, Y-27632, were administered to analyze the roles of ROS and ROCK activation, respectively. Results.: Light exposure disrupted staining patterns of tight junctions, adherens ...
In multi-cellular organisms, cell-cell contacts that are mediated by classical cadherins have essential roles in many fundamental processes, such as morphogenesis, maintenance of tissue integrity, wound healing and cell polarity. Furthermore, there is overwhelming evidence that the adherens junctions (AJs) are also an important tumor and/or invasion suppressor. Alpha-catenin is the protein that connects E-cadherin-beta-catenin complexes with the actin cytoskeleton. Although it was previously considered to be a solely structural protein, it has become increasingly clear that alpha-catenin has a central role in both assembling the actin cytoskeleton and regulating its dynamics at cell-cell junctions thus regulating cell polarity. Cell-polarity mechanisms are responsible not only for the diversification of cell shapes but also for regulation of the asymmetric cell divisions of stem cells that are crucial for their correct self-renewal and differentiation. Disruption of cell polarity is a hallmark ...
SELECTED PUBLICATIONS. Li X, McDermott B , Yuan B, Goff SP. Homomeric interactions between transmembrane proteins of Moloney murine leukemia virus. J Virol. 1996 Feb; 70(2): 1266-70 Belnap DM, McDermott BM Jr. , Filman DJ, Cheng N, Trus BL, Zuccola HJ, Racaniello VR, Hogle JM, Steven AC. Three-dimensional structure of poliovirus receptor bound to poliovirus. Proc Natl Acad Sci U S A. 2000 Jan 4; 97(1): 73-8 Bouchard MJ, Dong Y, McDermott BM Jr. , Lam DH, Brown KR, Shelanski M, Bellve AR, Racaniello VR. Defects in nuclear and cytoskeletal morphology and mitochondrial localization in spermatozoa of mice lacking nectin-2, a component of cell-cell adherens junctions. Mol Cell Biol. 2000 Apr; 20(8): 2865-73 McDermott BM Jr. , Rux AH, Eisenberg RJ, Cohen GH, Racaniello VR. Two distinct binding affinities of poliovirus for its cellular receptor. J Biol Chem. 2000 Jul 28; 275(30): 23089-96. Tsang SK , McDermott BM Jr., Racaniello VR, Hogle JM. A Kinetic Analysis of the Effect of Poliovirus Receptor on ...
Malignant glioma is a formidable disease that commonly leads to death, mainly due to the invasion of tumor cells into neighboring tissues. Therefore, inhibition of tumor cell invasion may provide an effective therapy for malignant glioma. Here we report that nicotinic acid (NA), an essential vitamin, inhibits glioma cell invasion in vitro and in vivo. Treatment of the U251 glioma cells with NA in vitro results in reduced invasion, which is accompanied by a loss of mesenchymal phenotype and an increase in cell-cell adhesion. At the molecular level, transcription of the adherens junction protein E-cadherin is upregulated, leading to accumulation of E-cadherin protein at the cell-cell boundary. This can be attributed to NAs ability to facilitate the ubiquitination and degradation of Snail1, a transcription factor that represses E-cadherin expression. Similarly, NA transiently inhibits neural crest migration in Xenopus embryos in a Snail1-dependent manner, indicating that the mechanism of action ...
In metazoan adherens junctions, β-catenin links the cytoplasmic tail of classical cadherins to the F-actin-binding protein α-catenin. Phosphorylation of a Ser/Thr-rich region in the cadherin tail dramatically enhances affinity for β-catenin and promotes cell-cell adhesion in cell culture systems, but its importance has not been demonstrated in vivo. In this paper, we identify a critical phosphorylated serine in the C. elegans cadherin HMR-1 required for strong binding to the β-catenin homolog HMP-2. Ablation of this phosphoserine interaction produces developmental defects that resemble full loss-of-function (Hammerhead and Humpback) phenotypes. Most metazoans possess a single gene for β-catenin, which is also a transcriptional coactivator in Wnt signaling. Nematodes and planaria, however, have a set of paralogous β-catenins; for example, C. elegans HMP-2 functions only in cell-cell adhesion, whereas SYS-1 mediates transcriptional activation through interactions with POP-1/Tcf. Finally, our ...
Impairment of the BBB is a critical event in the development and progression of several diseases that affect the CNS. We demonstrated here that increased BBB permeability with downregulation of TJ and AJ proteins was involved in T2DM-induced cognitive impairment. TJs present between cerebral endothelial cells perform diffusion barrier functions of the BBB and consist of many proteins, such as claudin 3, claudin 5, occludin, and ZO-1. On the other hand, AJs are required for the correct organization of TJs and are largely composed of VE-cadherin in endothelial cells.1 Therefore, alteration of the interaction between these TJ proteins and VE-cadherin plays an essential role in modulating BBB function. Our results are consistent with these ideas and previous observations, suggesting that reduced ZO-1 and occludin expression, for example, might contribute to enhanced BBB permeability in diabetes mellitus.10 However, further alterations of BBB ultrastructure in diabetic patients or animal models are a ...
Lu, Q*, Jankowich, MD*, Newton, J, Harrington, EO, and S. Rounds. Alterations in molecular chaperones and eIF2a during lung endothelial cell apoptosis. Am J Physiol:Lung Cell Molec Physiol. 298:501-508, 2010. *shared first authorship. Lu, Q, Harrington, EO, Newton, J, Casserly, B, Radin, G, Warburton,R, Zhou, Y, Blackburn MR, and Rounds, S. Adenosine protected against pulmonary edema through transporter- and receptor2-mediated endothelial barrier enhancement. Am J Physiol:Lung Cell Molec Physiol, 298:L755-767, 2010.. Lu, Q, Patel, B, Harrington, EO, and Rounds, S. Transforming Growth Factor-β1 Causes Pulmonary Microvascular Endothelial Cell Apoptosis via ALK5. Am J Physiol:Lung Cell Molec Physiol. 296:L825-L838, 2009.. Lu, Q, Harrington, EO, Newton, J, Jankowich, M, and S. Rounds. Inhibition of ICMT induces endothelial cell apoptosis through GRP94. Am J Resp Cell Mol Biol. 37:20-30, 2007. An illustration from this paper was Cover Image for the journal.. Lu, Q, Harrington, EO, Jackson, H, Morin, ...
Integrin-linked kinase (ILK) is a β integrin adaptor protein that translates extracellular stimuli to intracellular signaling events. ILK plays a role in actin cytoskeleton dynamics and cell adhesion. The structure and function of the epidermis is highly dependent on cell-cell adhesion and cell-basement membrane interactions. The mechanisms whereby ILK contributes to epidermal integrity are poorly understood. Using a mouse model of epidermis-restricted Ilk gene inactivation, I observed that ILK loss causes abnormal morphology and presence of intra-epidermal and epidermal-dermal microblisters in embryos as early as E17.5. ILK-deficient epidermis is also characterized by abnormal localization or/and absence of adherens junctions, tight junctions and desmosomes. These are structures that maintain the barrier properties of the epidermis. Ca2+ is an important inducer of cell-cell junctions and differentiation in epidermal keratinocytes. In the absence of ILK, cultured keratinocytes are unable to properly
Understanding the factors that regulate endothelial cell-cell junctions is important for many pathophysiological processes in which functional vascular integrity is compromised, such as development of neovasculature during angiogenesis and chronic inflammatory disorders. The present study shows that IQGAP1 colocalizes and forms a complex with VE-cadherin at the site of cell-cell contacts in unstimulated confluent HUVECs, and VEGF stimulation reduces their localization at the cell margin without affecting their complex formation. Knockdown of IQGAP1 using siRNA inhibits localization of VE-cadherin at cell-cell contacts as well as the following VEGF-stimulated events: (1) recruitment of VEGF2 to and the dissociation of α-catenin from the VE-cadherin/β-catenin complex; (2) ROS-dependent tyrosine phosphorylation of VE-cadherin, which is required for loss of cell-cell contacts8,9; and (3) capillary tube formation in 3-dimensional collagen gels. We also found that IQGAP1 expression is markedly ...
Cell-cell adhesion is critical for the control of tissue organization and homeostasis. A family of proteins that regulate cell-cell adhesions is the FERM (4.1 protein, Ezrin, Radixin, Moesin) domain-containing proteins.One FERM domain protein, the non-receptor tyrosine phosphatase PTPN14, is mutated or deleted in several human cancers suggesting that it may be involved in tumor development and/or progression. Additionally, the loss of the FERM domain protein Merlin is associated with tumor development and metastasis.Both PTPN14 and Merlin have been shown to localize and possibly regulate adherens junction (AJ) functions. This work sought to determine if PTPN14 is required for the establishment of epithelial adhesion and polarity. Using mammalian epithelial cells as a model to test these hypotheses, we down-regulated the tyrosine phosphatase, PTPN14. Decreased levels of PTPN14 increased E-cadherin membrane movement at cell contacts, disrupting cell contacts and abolishing E-cadherin localization during
Small intestine villus (human), coloured transmission electron micrograph (TEM). Two columnar epithelial cells with microvilli on surface and epithelial glycocalyx. Note the junctional complexes where the cells are connected (terminal bar). Starting from the base of the microvilli the regions are - outer region: Zonula occludens (tight junction) - middle region: Zonula adherens - inner region: macula adherens (desmosome). The small intestine is the part of the gastrointestinal tract between the stomach and the large intestine. It is where most of the digestion and absorption of food takes place, via the villi, which increase its surface area. The villi have an outer epithelial cell layer (columnar epithelial cells) that possess many tiny microvilli. Microvilli are tiny finger-like projections, which increase the surface area available for absorption of nutrients such as lipids, proteins and fat-soluble vitamins. Magnification: x6,480 when shortest - Stock Image C032/0780
The pathogen Bacillus anthracis secretes two potent toxins during anthrax infection, known as lethal factor (LF) and oedema factor (EF). Using transgenic Drosophila as a model system for the identification of pathways that might be involved in anthrax pathogenesis, Ethan Bier and colleagues show that these two toxins interact synergistically to block Rab11/Sec15 exocyst-dependent endocytic recycling, resulting in reduced Notch signalling and cadherin-dependent adhesion at the adherens junction. Tests in human endothelial cells indicate that the toxins have a similar effect on Rab11/Sec15 activity and Notch signalling. During infection, Bacillus anthracis secretes two potent toxins called lethal factor and oedema factor. Using Drosophila melanogaster as a model system, these authors show that these toxins interact with the Rab11/Sec15 exocyst, which is involved in endocytic recycling. This interaction may explain vascular leakage during infection. Bacillus anthracis is the causative agent of anthrax in
OBJECTIVE: E-cadherin is a potent adherens junction molecule implicated in tissue morphogenesis, epithelial functioning, and immune regulation. Serum levels of soluble E-cadherin (sE-cadherin), an end product of proteolytic cleavage of E-cadherin, is increased in patients with cancer, infections, and inflammation-related diseases. The aim of our study was to measure serum levels of sE-cadherin in systemic lupus erythematosus (SLE) and to determine associations between serum levels of sE-cadherin and markers of inflammation and organ damage in female patients with SLE.. METHODS: Serum levels of sE-cadherin were analyzed by ELISA in 150 female patients with SLE and 31 healthy women. Simple and multiple regression analyses between sE-cadherin levels and disease-related variables were performed in patients with SLE.. RESULTS: Serum levels of sE-cadherin were elevated in patients with SLE compared with levels in healthy controls. sE-cadherin levels correlated positively with age, disease duration, ...
β-Catenin, the downstream effector of the Wnt signaling, plays important roles in hepatic development, regeneration and tumorigenesis. However, its role at hepatocyte adherens junctions (AJ) is relatively poorly understood, chiefly due to spontaneous compensation by γ-catenin. Here, we simultaneously ablate β- and γ-catenin expression in mouse liver by interbreeding β-catenin-γ-catenin double-floxed mice and albumin-cre transgenic mice. Double knockout mice (DKO) show failure to thrive, impaired hepatocyte differentiation, cholemia, ductular reaction, progressive cholestasis, inflammation, fibrosis and tumorigenesis, which was associated with deregulation of tight junctions (TJ) and bile acid transporters, leading to early morbidity and mortality, a phenotype reminiscent of Progressive Familial Intrahepatic Cholestasis (PFIC ...
3.0.CO;2-R. PMID 8806074. Sheikh F, Chen Y, Chen Y, Liang X, Hirschy A, Stenbit AE, Gu Y, Dalton ND, Yajima T, Lu Y, Knowlton KU, Peterson KL, Perriard JC, Chen J (Sep 2006). "alpha-E-catenin inactivation disrupts the cardiomyocyte adherens junction, resulting in cardiomyopathy and susceptibility to wall rupture". Circulation. 114 (10): 1046-55. doi:10.1161/CIRCULATIONAHA.106.634469. PMID 16923756. Su LK, Vogelstein B, Kinzler KW (December 1993). "Association of the APC tumor suppressor protein with catenins". Science. 262 (5140): 1734-7. doi:10.1126/science.8259519. PMID 8259519. Daniel JM, Reynolds AB (September 1995). "The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha-catenin". Mol. Cell. Biol. 15 (9): 4819-24. doi:10.1128/mcb.15.9.4819. PMC 230726 . PMID 7651399. Oyama T, Kanai Y, Ochiai A, Akimoto S, Oda T, Yanagihara K, Nagafuchi A, Tsukita S, Shibamoto S, Ito F (December 1994). "A truncated beta-catenin disrupts ...
E-cadherin-mediated cell-cell interactions in the zonula adherens play an important role in the formation of the intercellular tight junctions found in the blood-brain barrier. However, it is also responsible for the low permeation of drugs into the brain. In this study, HAV6 peptide derived from the EC1 domain of E-cadherin was found to enhance the permeation of 14C-mannitol and [3H(G)]-daunomycin through the blood brain barrier of the in situ rat brain perfusion model. In addition, HAV6 peptide and verapamil have a synergistic effect in enhancing the BBB permeation of daunomycin. A new intercellular-junction resealing assay was also developed using Caco-2 monolayers to evaluate new peptides (BLG2, BLG3, and BLG4) derived from the bulge regions of the EC2, EC3, and EC4 domains of E-cadherin. BLG2 and BLG4 peptides but not BLG3 peptides were found to be effective in blocking the resealing of the intercellular junctions. The positive control peptides (ADT10, ADT6, and HAV10) block the resealing ...
Rap1 plays an important role in cell migration and morphogenesis in both vertebrates and invertebrates. In Drosophila, embryos lacking both zygotic and maternal Rap1 display strong defects in diverse morphological aspects of embryogenesis, such as ventral invagination, migration of mesodermal precursors, head involution, and DC. A key question is which effector pathways mediate the morphogenetic functions of Rap1. We used the YTH system to identify Drosophila Rap1-specific effector molecules from an embryonic library and retrieved several cDNAs encoding Cno. We found that both N-terminal Ras-binding domains (RA1 and RA2) possess Rap1-binding potential and that they interact only with a constitutively active Rap1 mutant, Rap1V12, but not with a dominant negative version of Rap1, Rap1N17, suggesting that Cno may act as an effector for Rap1.. We have provided several lines of evidence confirming this hypothesis. Rap1 and Cno partially colocalize at the adherens junction in the two tissues that are ...
Given the function and stability of clustered cell-cell adhesions is tightly coupled to the formation and function of the actin cytoskeleton, it is not surprising that many of the components that regulate actin filament dynamics, also localize to adhesions sites, and have been implicated in their regulation. This has been highlighted for the Arp2/3 complex, formins and various nucleation promotion factors (NPFs), where, depending on the experimental conditions and cell types used, their presence was required for stability and function of the adhesion complex [1][2][3][4][5]. For example, down-regulation of Dia1 in human MCF7 cells by shRNA reportedly disrupted both E-cadherin localization to adhesion sites, and AJ integrity [2]. Likewise, it was found that knockdown of N-WASP diminished the integrity of zonula adherens [3]. This was manifested in the fragmentation of the apical actin ring structure and was attributed to the role of the WIP-family protein WIRE; which is normally recruited to the ...
Plakophilin 1 (PKP1) is an essential component of desmosomes and a member of the armadillo adhesion protein family. Other armadillo proteins, like β-catenin and p120ctn, have additional functions outside of holding cells together: β-catenin is a transcription factor as well as a constituent of adherens junctions, for example. Wolf et al. performed a yeast two-hybrid screen using PKP1 as bait, to see if the desmosomal protein was also capable of moonlighting.. The researchers found that PKP1 binds an ATPase called eIF4A1, a subunit of a cytoplasmic translation initiation complex that recruits ribosomes to the 5′ end of mRNAs. PKP1 overexpression promoted eIF4A1s association with its fellow initiating factors and boosted the translation of mRNAs that depend on this complex. In vitro, PKP1 stimulated eIF4A1s enzymatic activity, which is used to unwind mRNAs and make them accessible to ribosomes. PKP1 isnt essential for translation, but its depletion resulted in small, slowly proliferating ...
Identify an antibody against an adhesion junction protein that is commercially available. Add a link to the original data sheet page and identify the type of adhesion junction. Include the following information: type of antibody (polyclonal, monoclonal), species raised in, species reacts against, types of application uses, and if available any reference using that antibody. Tight Junction Protein 1 Antibody Original Data Sheer for Tight Junction Protein 1 Antibody Type of adhesion junction: human zona occludens 1, specifically ZO-1 alpha-minus found both in endothelial cells and the highly specialized epithelial junctions of renal glomeruli and Sertoli cells of the seminiferous tubules. Type of antibody: Polyclonal Species raised in: Guinea Pig Species reactivity: Human, Mouse, Rat, and Canine Types of application uses: Immunohistology, immunofluorescence and Western blotting References that uses this antibody: 1. ,pubmed,22314269,/pubmed,[3] 2. ,pubmed,22162948,/pubmed,[4] ...
Abbott RD, Raja WK, Wang RY, Stinson JA, Glettig DL, Burke KA, Kaplan DL. 2015. Long term perfusion system supporting adipogenesis. Methods. Epub ahead of print.. Algarrahi K, Franck D, Ghezzi CE, Cristofaro V, Yang X, Sullivan MP, Chung YG, Affas S, Jennings R, Kaplan DL, Estrada CR Jr, Mauney JR. 2015. Acellular bi-layer silk fibroin scaffolds support functional tissue regeneration in a rat model of onlay esophagoplasty. Biomaterials 53: 149-159.. Asrat S, Davis KM, Isberg RR. 2015. Modulation of the host innate immune and inflammatory response by translocated bacterial proteins. Cell Microbiol. Epub ahead of print.. Cilla R, Mechery V, Hernandez de Madrid B, Del Signore S, Dotu I, Hatini V. 2015. Segmentation and tracking of adherens junctions in 3D for the analysis of epithelial tissue morphogenesis. PLoS Comput Biol. 11: e1004124.. Dokukin ME, Guz NV, Woodworth CD, Sokolov I. 2015. Emerging of fractal geometry on surface of human cervical epithelial cells during progression towards cancer. ...
Exhibits actin filament binding activity and identical protein binding activity. Involved in several processes, including actin filament polymerization; magnesium ion homeostasis; and renal system development. Localizes to the adherens junction and cytoplasm. Used to study non-Hodgkin lymphoma. Orthologous to human MTSS1 (MTSS I-BAR domain containing 1 ...
exhibited decreased VE-PTP expression and increased VE-cadherin phosphorylation, resulting in defective AJs. Mice lacking HIF2α in ECs had increased lung vascular permeability and water content, both of which were further exacerbated by endotoxin-mediated injury. Treatment of these mice with Fg4497, a prolyl hydroxylase domain 2 (PHD2) inhibitor, activated HIF2α-mediated transcription in a hypoxia-independent manner. HIF2α activation increased VE-PTP expression, decreased VE-cadherin phosphorylation, promoted AJ integrity, and prevented the loss of endothelial barrier function. These findings demonstrate that HIF2α enhances endothelial barrier integrity, in part through VE-PTP expression and the resultant VE-cadherin dephosphorylation-mediated assembly of AJs. Moreover, activation of HIF2α/VE-PTP signaling via PHD2 inhibition has the potential to prevent the formation of leaky vessels and edema in inflammatory diseases such as ARDS.. ...
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Poly (I:C)-treatment increases tight junction function in keratinocytesTransepithelial electrical resistance (TEER) was measured in confluent differentiated pri
Define alloyed junction. alloyed junction synonyms, alloyed junction pronunciation, alloyed junction translation, English dictionary definition of alloyed junction. n a semiconductor junction used in some junction transistors and formed by alloying metal contacts, functioning as emitter and collector regions, to a wafer...
Component: reverse biased pn junction Semiconductors Electrical Properties Of Materials Part 3 Reverse Biased Pn Junction Capacitance Tmp reverse biased pn junction capacitance reverse biased pn junction reverse biased pn junction animation reverse bias pn junction leakage current reverse bias pn junction band diagram
As a result of the track modifications at Clark Junction, a temporary change was made in the operation of Brown Line shuttle trains effective April 10, 2006. Still berthing at Belmont on Track #1, rather than being routed to Track #3 then onto the northbound Ravenswood branch track at Clark Junction the trains operate against traffic northbound on Track #1 and onto the branch, then are switched onto the northbound track at Lakewood-Seminary Interlocking, essentially operating in a tower-protected single-track mode.. In April 2006, a new relay house was installed at Clark Junction immediately north of the tower. While the tower was being rehabilitated, control of Clark Junction was temporary transferred to a local panel in the relay house. Control of the junction was slowly cut over to the relay house over the course of the summer of 2006. Because each track was cut over one at a time, control of the junction was actually split between the tower and the relay house for approximately one month, ...
The cadherin-catenin complex (CCC) is crucial for successful completion of morphogenesis during embryonic development, and for suppression of metastatic phenoty...
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Diagram showing a tight junction. Tight junctions seal adjacent epithelial cells in a narrow band just beneath their apical surface ...
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Catenin Beta 1, CTNNB are cell adhesion molecules called (p120*␠-catenin) cadherins (the (CDH1) E-cadherin/catenin complex) include the beta-catenins a multifunctional molecule Locus: 3p22.1 [§§; ^]. Neurons also exhibited a higher CTNNB/TCF pathway association (concentration versus accumulation) with cadherins; CAS-chromosome segregation 1-like (yeast) binds with E-cadherin but not with beta-catenin. Which interacts with (Tcf-T-cell factor where a…
Complete information for CTNNA1 gene (Protein Coding), Catenin Alpha 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Expression of CTNNA2 (CAP-R, CT114) in cancer tissue. The cancer tissue page shows antibody staining of the protein in 20 different cancers.
Human CTNNA2 qPCR primer pairs, confirmed in positive organizations; screened the primer with high specificity and high sensitivity.
Background: Approximately one third of the hereditary diffuse gastric cancer (HDGC) families carry germline mutations in the E-cadherin gene (CDH1). Risk prediction in members of families with this rare but deadly cancer could be improved by the identification of additional HDGC genes in non-CDH1 families.. Methods: Affected individuals from 22 CDH1 mutation-negative families were screened for germline mutations in four catenin genes: CTNNA1, CTNNB1, JUP, and CTNND1. Catenins interact closely with E-cadherin molecules in cells, and are therefore logical candidate genes for mutation screening in HDGC families.. Results: No nonsynonymous variants were seen in CTNNA1, CTNNB1, or CTNND1; only JUP contained nonsynonymous variants, of which only two rare variants were predicted to be deleterious.. Conclusion: Catenin genes are not commonly mutated in non-CDH1 HDGC families.. Impact: Germline mutations in CTNNA1, CTNNB1, JUP, or CTNND1 are unlikely to play a major role in HDGC. Cancer Epidemiol ...
BACKGROUND: Approximately one third of the hereditary diffuse gastric cancer (HDGC) families carry germline mutations in the E-cadherin gene (CDH1). Risk prediction in members of families with this rare but deadly cancer could be improved by the identification of additional HDGC genes in non-CDH1 families.METHODS: Affected individuals from 22 CDH1 mutation-negative families were screened for germline mutations in four catenin genes: CTNNA1, CTNNB1, JUP, and CTNND1. Catenins interact closely with E-cadherin molecules in cells, and are therefore logical candidate genes for mutation screening in HDGC families.RESULTS: No nonsynonymous variants were seen in CTNNA1, CTNNB1, or CTNND1; only JUP contained nonsynonymous variants, of which only two rare variants were predicted to be deleterious.CONCLUSION: Catenin genes are not commonly mutated in non-CDH1 HDGC families.Impact: Germline mutations in CTNNA1, CTNNB1, JUP, or CTNND1 are unlikely to play a major role in HDGC. Cancer Epidemiol Biomarkers Prev; 1-3.
BACKGROUND. To the authors knowledge, little is known regarding the role of E-cadherin/β-catenin system dysregulation in pulmonary neuroendocrine tumors. METHODS. E-cadherin and β-catenin immunoreactivity was evaluated in 10 hyperplastic neuroendocrine tumorlets and 210 neuroendocrine tumors, including 96 typical carcinoids (CTs), 35 atypical carcinoids (ACTs), 49 large cell neuroendocrine carcinomas (LCNECs), and 30 small cell lung carcinomas (SCLCs). RESULTS. Normal and hyperplastic bronchial neuroendocrine cells expressed E-cadherin/β-catenin with an orderly distribution along the cell membrane. Neuroendocrine tumors retained β-catenin expression in all tumors and E-cadherin in most tumors, with the exception of 2% of LCNECs, 3% of SCLCs and 9% of ACTs. E-cadherin showed a prevalent membrane-associated, linear immunoreactivity in CTs, whereas membrane-disarrayed and cytoplasmic staining was seen in most ACTs, LCNECs, and SCLCs (P , 0.001). β-Catenin exhibited similar immunoreactivity ...
A key component of the Wnt pathway, beta-catenin combines with alpha-catenin and regulates cell-cell adhesion. It also interacts with alpha-catenin in the nucleus.. The alpha-catenin component of this beta-catenin/alpha-catenin complex has an inhibitory effect on beta-catenin that helps keep tumor cell migration and invasion in check. This inhibition is lost, however, when the EGFR pathway is activated. Upon activation, beta-catenin becomes untethered from alpha-catenin and translocates to the cell nucleus, where it increases expression of key target genes involved in tumor cell invasion and metastasis.. New Pathway Regulates Beta-Catenin Transactivation. The M. D. Anderson-led team made a surprising discovery: Beta-catenin also can travel to the nucleus via activation of the EGFR pathway-and it does so independently of Wnt signaling or mutations. The newly described pathway disrupts the beta-catenin/alpha catenin complex through an EGFR-extracellular receptor kinase (ERK)-protein kinase CK2- ...
Polyclonal antibody for ALPHA 1 CATENIN/CTNNA1 detection. Host: Rabbit.Size: 100μg/vial. Tested applications: IHC-P. Reactive species: Human. ALPHA 1 CATENIN/CTNNA1 information: Molecular Weight: 100071 MW; Subcellular Localization: Isoform 1: Cytoplasm,
Cadherins are calcium-dependent, cell surface glycoproteins involved in cell-cell adhesion. To function in cell-cell adhesion, the transmembrane cadherin molecule must be associated with the cytoskeleton via cytoplasmic proteins known as catenins. Three catenins, alpha-catenin, beta-catenin, and gamma-catenin (also known as plakoglobin), have been identified. The domain of the cadherin molecule important for its interaction with the catenins has been mapped to the COOH-terminal 70 amino acids, but less is known about regions of the catenins that allow them to associate with one another or with the cadherin molecule. In this study we have transfected carboxyl-terminal deletions of plakoglobin into the human fibrosarcoma HT-1080 and used immunofluorescence localization and co-immunoprecipitation to map the regions of plakoglobin that allow it to associate with N-cadherin and with alpha-catenin. Plakoglobin is an armadillo family member containing 13 weakly similar internal repeats. These data show ...
It has been posited that aspirin treatment may reduce risk for colorectal cancer through inhibition of WNT/cadherin-associated protein β1 (CTNNB1, or β-catenin) signaling. In a study reported recently in the Journal of the National Cancer Institute, Nan et al investigated the potential role of the single nucleotide polymorphism rs6983267 (chromosome 8q24) in the protective effect of aspirin.1 This colorectal cancer susceptibility locus affects binding activity of transcription factor 7 like-2 (TCF7L2) to CTNNB1 and alters expression of target oncogenes, including MYC. The study showed that the T allele of rs6983267 was associated with a protective effect in regular aspirin users and was associated with reduced MYC expression.. The study involved investigation of regular aspirin use and colorectal cancer risk according to genotypes of rs6983267 and CTNNB1 expression in two prospective case-control studies within the Nurses Health Study (women) and the Health Professionals Follow-up Study ...
Thymic epithelial tumors (TET) are rare. Wingless and INT (WNT), NOTCH and sonic hedgehog pathway interactions between thymocytes and thymic stroma are important to thymus and T-cell development. We analyzed a thymoma tissue microarray (TMA) for glioma associated oncogene homolog 1 (GLI1), NOTCH1 and catenin (cadherin-associated protein, beta 1) (CTNNB1) expression as surrogate markers of sonic hedgehog, NOTCH and WNT pathway activity.GLI1, NOTCH1 and CTNNB1 expression were assayed in a tissue microarray of 68 TET and eight benign thymus by fluorescent immunohistochemistry (AQUA) as surrogates for activity of the sonic hedgehog, NOTCH and WNT pathways respectively.No difference in tumor GLI1 (mean 201 vs. 211, p=0.31), CTNNB1 (mean 222 vs. 306, p=0.66) or NOTCH1 expression (mean 317 vs. 325, p=0.82) was noted between thymic tumor and benign thymus.No evidence for preferential expression of GLI1, NOTCH1 or CTNNB1 was noted. High-throughput immunofluorescence using AQUA technology can help ...
Several studies have shown that β‐catenin levels increase upon Wg/Wnt signaling (Miller and Moon, 1996; Yost et al., 1996; Young et al., 1998). Here, we have investigated whether this increased half‐life sets the threshold for signaling. Using ALLN and ts20 cells, we demonstrate that signaling by β‐catenin/TCF is not a direct consequence of the increased β‐catenin half‐life that occurs upon Wnt signaling. Rather, the data suggest that changes in the phosphorylation status of the N‐terminus of β‐catenin that occur upon Wnt signaling independently affect the signaling properties and half‐life of β‐catenin. Using a monoclonal antibody (αABC) directed against dephosphorylated β‐catenin, we show that only bona fide Wnt signals lead to an increase in unphosphorylated β‐catenin.. We noticed that the increase in TCF‐mediated transcription for LiCl treatment is far greater than the increase in the active form of β‐catenin, whereas Wnt1 transfection results in a modest ...
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We review evidence concerning the basis for tissue segregation during embryonic development. This compartmentalization is shown to be an immiscibility phenomenon caused by changes in the strengths of adhesions between mobile cells which accompany their differentiation and generate interfacial tensions at cell population boundaries. The mobile cells exchange neighbors in response to these adhesion-generated forces which impel the system toward the configuration of maximal binding. Cadherins dominate these intercellular adhesions, but integrin-fibronectin-based adhesions also contribute to them as well as to cell-matrix adhesions. At the interface between two segregating cell populations are three kinds of cell-cell interfaces: a-a, b-b and a-b. Tissue immiscibility (segregation) results when the cross-adhesion is weaker than the mean value of the two kinds of self-adhesions, does not require (although it permits) qualitative changes in cell adhesion molecules and is easily generated even by
Androgen receptor (AR) is the major therapeutic target in aggressive prostate cancer. However, targeting AR alone can result in drug resistance and disease recurrence. Therefore, simultaneous targeting of multiple pathways could in principle be an effective approach to treating prostate cancer. Here we provide proof-of-concept that a small-molecule inhibitor of nuclear β-catenin activity (called C3) can inhibit both the AR and β-catenin-signaling pathways that are often misregulated in prostate cancer. Treatment with C3 ablated prostate cancer cell growth by disruption of both β-catenin/T-cell factor and β-catenin/AR protein interaction, reflecting the fact that T-cell factor and AR have overlapping binding sites on β-catenin. Given that AR interacts with, and is transcriptionally regulated by β-catenin, C3 treatment also resulted in decreased occupancy of β-catenin on the AR promoter and diminished AR and AR/β-catenin target gene expression. Interestingly, C3 treatment resulted in ...
In addition to its crucial role in cell adhesion, β-catenin is also known to augment gene expression by forming a complex with lymphoid enhancer factor/T-cell factor in the nucleus. Unregulated β-catenin expression and/or its increased nuclear presence can lead to abnormal cell proliferation, tumour invasion and metastasis. Pertinent is the fact that the actin cytoskeleton is central to the translocation of several nuclear proteins. This study investigated whether the actin cytoskeleton influences the nuclear translocation of β-catenin in human oesophageal squamous cell carcinoma (HOSCC), a metastatic disease of common occurrence in South Africa. Disruption of the actin cytoskeleton of five moderately differentiated HOSCC cell lines, with cytochalasin D (cytoD), showed that the nuclear β-catenin level was unaltered in SNO, WHCO1 and WHCO5, but decreased in WHCO3 and WHCO6. CytoD treatment did not affect the cytoplasmic/membrane β-catenin level in these cell lines. Further examination of the ...
The natural agent rhein is an ananthraquinone derivative of rhubarb, which has anticancer effects. To determine the mechanisms underlying the anticancer effects of rhein, we detected the effect of rhein on several oncoproteins. Here, we show that rhein induces β-catenin degradation in both hepatoma cell HepG2 and cervical cancer cell Hela. Treatment of HepG2 and Hela cells with rhein shortens the half-life of β-catenin. The proteasome inhibitor MG132 blunts the downregulation of β-catenin by rhein. The induction of β-catenin degradation by rhein is dependent on GSK3 but independent of Akt. Treatment of HepG2 and Hela cells with GSK3 inhibitor or GSK3β knockdown abrogates the effect of rhein on β-catenin. GSK3β knockdown compromises the inhibition of HepG2 and Hela cell growth by rhein. Furthermore, rhein dose not downregulate β-catenin mutant that is deficient of phosphorylation at multiple residues including Ser33, Ser37, Thr41 and Ser45. Moreover, rhein induces cell cycle arrest at S ...
Beginning at Leu 1029, the APC‐rA peptide adopts a conformation strikingly different from that of XTcf3 or E‐cadherin (Figure 3B). The C‐terminal half of the peptide, from Leu1029 to Glu1034, bulges out of the β‐catenin groove, away from the paths of XTcf3 and E‐cadherin (Figures 2B and 3B). This difference in conformation is probably due to the presence of a lysine residue at amino acid 1030 of APC‐rA. In XTcf3 and E‐cadherin this position is occupied by an acidic residue (Glu24 of XTcf3, Glu682 of E‐cadherin), which forms a salt bridge with β‐catenin Lys312 to form the second charged button of the extended region (Figure 3B). The lysine at this position in APC‐rA probably causes charge repulsion with β‐catenin Lys312, leading to a deviation from the conformations of the other two ligands. The conformation of the backbone at Lys1030 suggests that the side chain of this residue is in the vicinity of β‐catenin Glu462 and several other acidic residues. Although APC‐rA ...
E-cadherin-mediated cell-cell adhesion is critical for naive pluripotency of cultured mouse embryonic stem cells (mESCs). E-cadherin-depleted mESC fail to downregulate their pluripotency program and are unable to initiate lineage commitment. To further explore the roles of cell adhesion molecules during mESC differentiation, we focused on p120 catenin (p120ctn). Although one key function of p120ctn is to stabilize and regulate cadherin-mediated cell-cell adhesion, it has many additional functions, including regulation of transcription and Rho GTPase activity. Here, we investigated the role of mouse p120ctn in early embryogenesis, mESC pluripotency and early fate determination. In contrast to the E-cadherin-null phenotype, p120ctn-null mESCs remained pluripotent, but their in vitro differentiation was incomplete. In particular, they failed to form cystic embryoid bodies and showed defects in primitive endoderm formation. To pinpoint the underlying mechanism, we undertook a structure-function approach.
How does cadherin-mediated cell-cell adhesion lead to the formation of a new membrane domain? Two mechanisms will be discussed. First, changes in the actin cytoskeleton at sites of cell-cell adhesion induce formation of the membrane cytoskeleton and the recruitment of a subset of membrane proteins. Second, cell-cell adhesion results in recruitment of specific docking sites for vesicles containing basolateral membrane proteins presorted in the Golgi complex.. Localized assembly of the membrane-associated cytoskeleton and recruitment of membrane proteins. E-cadherin-mediated cell-cell contact between MDCK cells leads to formation of the (baso-) lateral membrane domain. Some membrane proteins (e.g., Na+-K+-ATPase) become localized to cell-cell contacts through integration into the actin membrane cytoskeleton, although most proteins must be delivered there in transport vesicles from the Golgi complex or endosomes (14).. Changes in the local organization of the actin cytoskeleton as a consequence of ...
ARMc8 (armadillo-repeat-containing protein 8) is a key component of the CTLH (C-terminal to lissencephaly type-1-like homology motif) complex in mammalian cells. This complex is well conserved in Saccharomyces cerevisiae and has been characterized as a FBPase (fructose-1, 6-bisphosphatase)-degrading complex. The yeast homologue of ARMc8, Gid (glucose-induced degradation) 5p, plays an essential role in the ubiquitin- and proteasome-dependent degradation of FBPase. To elucidate the function of ARMc8, we used a yeast two-hybrid system to screen a human skeletal muscle cDNA library. α-Catenin was isolated as a binding protein of ARMc8α. This association was confirmed by co-immunoprecipitation assay using MDCK (Madin-Darby canine kidney) cells in which exogenous α-catenin and ARMc8α were overexpressed. The association was also confirmed by co-immunoprecipitation assay using endogenous proteins in untransfected MDCK cells. We then used immunofluorescence microscopy of MDCK cells and C2C12 cells to ...
Leukemia stem cells (LSCs) are capable of limitless self-renewal and are responsible for the maintenance of leukemia. Because selective eradication of LSCs could offer substantial therapeutic benefit, there is interest in identifying the signaling pathways that control their development. We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpression of the Hoxa9 and Meis1a oncogenes or by the fusion oncoprotein MLL-AF9. We show that the Wnt/β-catenin signaling pathway is required for self-renewal of LSCs that are derived from either hematopoietic stem cells (HSC) or more differentiated granulocyte-macrophage progenitors (GMP). Because the Wnt/β-catenin pathway is normally active in HSCs but not in GMP, these results suggest that reactivation of β-catenin signaling is required for the transformation of progenitor cells by certain oncogenes. β-catenin is not absolutely required for self-renewal of adult HSCs; thus, targeting the Wnt/β-catenin pathway may ...
Anti-tumor necrosis factor (anti-TNF) drugs are effective against psoriasis, although 20-30% of patients are nonresponders. Few pharmacogenomic studies have been performed to predict the response to anti-TNF drugs in psoriasis. We studied 173 polymorphisms to establish an association with the response to anti-TNF drugs in patients with moderate-to-severe plaque psoriasis (N=144). We evaluated the response using PASI75 at 3, 6 and 12 months. The results of the multivariate analysis showed an association between polymorphisms in PGLYR4, ZNF816A, CTNNA2, IL12B, MAP3K1 and HLA-C genes and the response at 3 months. Besides, the results for polymorphisms in IL12B and MAP3K1 were replicated at 6 months. We also obtained significant results for IL12B polymorphism at 1 year. Moreover, polymorphisms in FCGR2A, HTR2A and CDKAL1 were significant at 6 months. This is the first study to show an association with these polymorphisms. However, these biomarkers should be validated in large-scale studies before ...
In embryonic development in vertebrates, β-catenin signaling promotes polarization of the embryo to establish the dorsoventral axis and it is this process that is highlighted by the Xenopus Egg Wnt/β-catenin Pathway. In the amphibian Xenopus, fertilization of the egg results in the establishment of a parallel array of microtubules with the plus end pointing away from the sperm entry point. Concurrent with a process of cortical rotation, in which the cortex of the egg utilizes these microtubules to rotate relative to the inner cytoplasm, there is a movement of small vesicles toward the plus end of the microtubules. Cells inheriting these vesicles are destined to give rise to dorsal and anterior structures of the embryo. Two components of the Wnt/β-catenin pathway, Dishevelled and β-catenin, accumulate on the side of the egg and early embryo that receive these small vesicles. It is likely that Dishevelled is associated with the vesicles that move along the microtubules, and that it promotes ...
Differential adhesion between cadherin subtypes expressed on cell surfaces is postulated to direct cell segregation during tissue morphogenesis. The studies described here used magnetic twisting cytometry and traction force microscopy to test the impact of cadherin binding selectivity on mechanotransduction and substrate rigidity sensing at cadherin-based adhesions. Micropipette measurements in turn quantified the binding affinities of different cadherin subtypes. Here we present evidence that …
Canine Formin-1 (FMN1) ELISA Kit,KTE20173,,,,FMN1 (Formin 1) is a Protein Coding gene. Diseases associated with FMN1 include Thoracic Outlet Syndrome and Renal Hypoplasia. Among its related pathways are Cell adhesion_Cadherin-mediated cell adhesion and E-cadherin signaling in keratinocytes. This gene belongs to the formin homology family and encodes a protein that has a role in the formation of adherens junction and the polymerization of linear actin cables. The homologous gene in mouse is associated with limb deformity.
Wnt signaling is important for T-cell differentiation at the early CD4(-)CD8(-) stage and is subsequently downregulated with maturation. To assess the importance of this downregulation, we generated a mouse line (R26-βcat) in which high levels of active β-catenin are maintained throughout T-cell development. Young R26-βcat mice show a differentiation block at the CD4(+)CD8(+) double-positive (DP) stage. These DP cells exhibit impaired apoptosis upon irradiation or dexamethasone treatment. All R26-βcat mice develop T-cell leukemias at 5 to 6 months of age. R26-βcat leukemias remain dependent on β-catenin function but lack Notch pathway activation. They exhibit recurrent secondary genomic rearrangements that lead to Myc overexpression and loss of Pten activity. Because β-catenin activation and Myc translocations were previously found in murine T-cell acute lymphoblastic leukemias (T-ALLs) deficient for Pten, our results suggest that activation of the canonical Wnt pathway is associated with a
Cell-matrix and cell-cell adhesions are often characterized as functionally distinct adhesion systems within the cell that mediate different proliferative outcomes. In contrast to the widely accepted pro-proliferative effect of cell-matrix adhesion, the proliferative effect of cadherin-dependent cell-cell adhesion remains unresolved. While the majority of studies demonstrate that cadherins mediate contact inhibition of proliferation, there have also been compelling reports of cadherins stimulating cell cycling. Here, we show that matrix stiffness is the mechanistic basis for crosstalk between N-cadherin at cell-cell junctions and focal adhesion kinase (FAK) at cell-matrix adhesions, and that this interplay between adhesive systems modulates the proliferative role of N-cadherin. We demonstrate that N-cadherin is induced in smooth muscle cells (SMCs) following vascular injury, an in vivo model of tissue stiffening and proliferation. Complementary experiments on deformable polyacrylamide hydrogels
The Wnt/ß-catenin signaling pathway controls important cellular events during development and often contributes to disease when dysregulated. Using high throughput screening we have identified a new small molecule inhibitor of Wnt/ß-catenin signaling, WIKI4. WIKI4 inhibits expression of ß-catenin target genes and cellular responses to Wnt/ß-catenin signaling in cancer cell lines as well as in human embryonic stem cells. Furthermore, we demonstrate that WIKI4 mediates its effects on Wnt/ß-catenin signaling by inhibiting the enzymatic activity of TNKS2, a regulator of AXIN ubiquitylation and degradation. While TNKS has previously been shown to be the target of small molecule inhibitors of Wnt/ß-catenin signaling, WIKI4 is structurally distinct from previously identified TNKS inhibitors.
Synovial sarcoma (SS) is an aggressive soft tissue malignancy of children and young adults, with no effective systemic therapies. Its specific oncogene, SYT-SSX (SS18-SSX), drives sarcoma initiation and development. The exact mechanism of SYT-SSX oncogenic function remains unknown. In a SYT-SSX2 transgenic model, we show that a constitutive Wnt/β-catenin signal is aberrantly activated by SYT-SSX2, and inhibition of Wnt signaling through the genetic loss of β-catenin blocks SS tumor formation. In a combination of cell-based and SS tumor xenograft models, we show that inhibition of the Wnt cascade through co-receptor blockade and the use of small molecule CK1α activators arrests SS tumor growth. We find that upregulation of the Wnt/β-catenin cascade by SYT-SSX2 correlates with its nuclear reprogramming function. These studies reveal the central role of Wnt/β-catenin signaling in SYT-SSX2-induced sarcoma genesis, and open new venues for the development of effective SS curative agents. ...
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IQGAP1 is a master cytoskeletal regulatory protein that connects extracellular signaling to changes in cell polarity, motility, and adhesion with adjacent cells. IQGAP1 achieves these fundamental outcomes by acting as a scaffolding protein that coordinates a wide variety of signaling cascades in a highly spatially-dependent manner. This dissertation details the use of multiple imaging modalities to characterize localized, highly-dynamic IQGAP1-related processes in epithelial MCF-10A cells. This led to the discovery of a novel multi-vesicular compartment that is surrounded by an outer layer of IQGAP1-associated actin filaments. Further studies showed that this compartment shares many common identifiers with traditional multi-vesicular bodies and participates in the internalization of cell-cell adhesion proteins via endocytic and recycling pathways. Live-cell imaging studies were conducted to correlate local cytoskeletal remodeling of this outer layer to various dynamic behaviors of the ...
In the developing nervous system, synapse formation becomes possible when outgrowing axons and dendrites come into contact with one another. In order for functional synaptic connections to be established, however, both presynaptic and postsynaptic protein complexes must be recruited and stabilized at appropriate points of cell-cell contact (McAllister, 2007). Synaptic proteins are thought to mobilize within developing axons and dendrites long before synaptogenesis occurs, with the recruitment of synaptic vesicles occurring within minutes to hours after the initiation of axodendritic contact. This process is thought to be regulated at least in part by adhesion molecules and their intracellular binding partners.. Transsynaptic adhesion molecules forming the cadherin/β-catenin/scribble complex regulate clustering of synaptic vesicles (SVs) in axons (Bamji et al., 2003; Sun et al., 2009). SV clustering also depends on filamentous actin, which is enriched at synapses (Colicos et al., 2001; Zhang and ...
Rabbit polyclonal antibody raised against recombinant ARMC7. Recombinant protein corresponding to amino acids of human ARMC7. (PAB21666) - Products - Abnova
Sigma-Aldrich offers abstracts and full-text articles by [Tzu-Rong Su, Jen-Jie Lin, Chi-Chu Tsai, Tsu-Kei Huang, Zih-Yan Yang, Ming-O Wu, Yu-Qing Zheng, Ching-Chyuan Su, Yu-Jen Wu].
ARMC6 Full-Length MS Protein Standard (NP_219483), Labeled with [U- 13C6, 15N4]-L-Arginine and [U- 13C6, 15N2]-L-Lysine, was produced in human 293 cells (HEK293) with fully chemically defined cell culture medium to obtain incorporation efficiency at Creative-Proteomics. The function of this genes protein product has not been determined. A related protein in mouse suggests that this protein has a conserved function. Two transcript variants encoding different isoforms have been found for this gene.
Scientists at the Mechanobiology Institute (MBI) at the National University of Singapore (NUS) have discovered the molecular mechanisms responsible for the formation of the adherens junction at the nanoscale level. This research ...
Abcams E Cadherin ELISA Kit (ab100678) suitable for Cell culture supernatant, Serum, Plasma in mouse. Reliably quantify 6 pg/ml of E Cadherin.
KEGG PATHWAY: Adherens junction - Homo sapiens (human)  KEGG PATHWAY: Adherens junction - Homo sapiens (human)
Adherens junction - Homo sapiens (human) [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show description , ... Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue ...
more infohttp://www.genome.jp/kegg-bin/show_pathway?133837803022751/hsa04520.args
KEGG PATHWAY: Adherens junction - Homo sapiens (human)  KEGG PATHWAY: Adherens junction - Homo sapiens (human)
Adherens junction - Homo sapiens (human) [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show description , ... Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue ...
more infohttp://www.genome.jp/kegg-bin/show_pathway?131081650219559/hsa04520.args
adherens junction facts, information, pictures | Encyclopedia.com articles about adherens junction  adherens junction facts, information, pictures | Encyclopedia.com articles about adherens junction
Make research projects and school reports about adherens junction easy with credible articles from our FREE, online ... and pictures about adherens junction at Encyclopedia.com. ... adherens junction (zonula adherens) A type of cell junction, ... adherens junction A cell junction that is commonly observed in epithelial (see EPITHELIUM) cells (e.g. those lining the ... adherens junction A Dictionary of Zoology © A Dictionary of Zoology 1999, originally published by Oxford University Press 1999. ...
more infohttps://www.encyclopedia.com/plants-and-animals/zoology-and-veterinary-medicine/zoology-general/adherens-junction
Adherens junction - Wikipedia  Adherens junction - Wikipedia
MBInfo - Adherens Junction MBInfo - Adherens Junction Assembly Adherens Junctions at the US National Library of Medicine ... Adherens junctions (or zonula adherens, intermediate junction, or "belt desmosome") are protein complexes that occur at cell- ... cell junctions in epithelial and endothelial tissues, usually more basal than tight junctions. An adherens junction is defined ... "Signaling to and through the Endothelial Adherens Junction". In LaFlamme SE, Kowalczyck AP. Cell Junctions: Adhesion, ...
more infohttps://en.wikipedia.org/wiki/Adherens_junction
AFDN (afadin, adherens junction formation factor )  AFDN (afadin, adherens junction formation factor )
... adherens junction formation factor ) , Authors: Jean-Loup Huret. Published in: Atlas Genet Cytogenet Oncol Haematol. ... protein binding nucleoplasm cytosol cytosol plasma membrane cell-cell junction cell-cell adherens junction cell adhesion signal ... protein binding nucleoplasm cytosol cytosol plasma membrane cell-cell junction cell-cell adherens junction cell adhesion signal ... AFDN (afadin, adherens junction formation factor ) Written. 1997-12. Jean-Loup Huret. ...
more infohttp://atlasgeneticsoncology.org/Genes/AF6ID6.html
Pathway Central: Remodeling of Adherens Junctions  Pathway Central: Remodeling of Adherens Junctions
The Adherens Junctions have a crucial role both as sensors of extracellular stimuli and in regulating the dynamics of ... The intercellular Adherens Junctions (AJs) are specialized sub-apical structures that function as principle mediators of cell- ... Disassembling adherens junctions: breaking up is hard to do.. Trends Cell Biol. 2005 Jan;15(1):19-26. ... Ctnn-Alpha (Catenin-Alpha) binds to Ctnn-Beta and links components of the Adherens Junctions to the Actin cytoskeleton. It also ...
more infohttp://www.sabiosciences.com/pathway.php?sn=Remodeling_of_Adherens_Junctions
NIOSHTIC-2  Publications Search - 20030033 - Reduction of IQGAP1 increases insoluble VE-cadherin at endothelial adherens...  NIOSHTIC-2 Publications Search - 20030033 - Reduction of IQGAP1 increases insoluble VE-cadherin at endothelial adherens...
The objectives of the present study were to determine if IQGAP1 associates with components of the endothelial adherens junction ... The objectives of the present study were to determine if IQGAP1 associates with components of the endothelial adherens junction ... Furthermore, more insoluble (actin-associated) VE-cadherin was localized at intercellular junctions and less insoluble N- ...
more infohttps://www.cdc.gov/niosh/nioshtic-2/20030033.html
Drosophila Crumbs is a positional cue in photoreceptor adherens junctions and rhabdomeres.  - PubMed - NCBI  Drosophila Crumbs is a positional cue in photoreceptor adherens junctions and rhabdomeres. - PubMed - NCBI
In contrast to normal photoreceptor adherens junctions and rhabdomeres, which span the depth of the retina, adherens junctions ... Drosophila Crumbs is a positional cue in photoreceptor adherens junctions and rhabdomeres.. Izaddoost S1, Nam SC, Bhat MA, ... Here, we describe properties of Crb that control the position and integrity of the photoreceptor adherens junction and ... We show that Crb controls localization of the adherens junction through its intracellular domain containing a putative binding ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/11850624
Endothelial adherens junctions at a glance | Journal of Cell Science  Endothelial adherens junctions at a glance | Journal of Cell Science
Adherens junctions have an important role in the control of vascular permeability. These structures are located at cell-to-cell ... VE-cadherin (also known as CDH5 and CD144) is the major component of endothelial adherens junctions and is specific to ... Vascular permeability is increased by modifications in the expression and function of adherens junction components. In some ... where adherens junctions are dismantled in the vessels contributing to brain microcirculation. This causes the loss of ...
more infohttp://jcs.biologists.org/content/early/2013/06/11/jcs.124529
KEGG PATHWAY: Adherens junction - Homo sapiens (human)  KEGG PATHWAY: Adherens junction - Homo sapiens (human)
Adherens junction - Homo sapiens (human) [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show description , ... Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue ...
more infohttp://www.kegg.jp/kegg-bin/show_pathway?hsa04520+6934
KEGG PATHWAY: Adherens junction - Homo sapiens (human)  KEGG PATHWAY: Adherens junction - Homo sapiens (human)
Adherens junction - Homo sapiens (human) [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show description , ... Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue ...
more infohttp://www.kegg.jp/kegg-bin/highlight_pathway?scale=1.0&map=hsa04520
Overexpression of EPHA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism | Development  Overexpression of EPHA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism | Development
Overexpression of EPHA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism ... Overexpression of EPHA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism ... Overexpression of EPHA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism ... Overexpression of EPHA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism ...
more infohttp://dev.biologists.org/content/135/4/e1.1
The Role of Tight and Adherens Junctions in Cervical Neoplasia by Ciaran Cunniffe  "The Role of Tight and Adherens Junctions in Cervical Neoplasia" by Ciaran Cunniffe
Adherens (AJ) and tight junctions (TJ) play a key role in maintaining the apical-basolateral polarity and cohesive structure of ... These junctions are maintained by the interaction of several key proteins including, claudins, catenins, cadherins and SNAIL. ... Cunniffe, C. The Role of Tight and Adherens Junctions in Cervical Neoplasia.. Doctoral Thesis. Dublin Institute of Technology. ... Adherens (AJ) and tight junctions (TJ) play a key role in maintaining the apical-basolateral polarity and cohesive structure of ...
more infohttps://arrow.dit.ie/sciendoc/154/
AJAP1 (adherens junction associated protein 1) - KOMP (Knockout Mouse Project)  AJAP1 (adherens junction associated protein 1) - KOMP (Knockout Mouse Project)
Vega: OTTMUSG10367 (Ajap1, adherens junction associated protein 1)*CCDS: 23976.1, 38987*OMIM: ADHERENS JUNCTION-ASSOCIATED ... adherens junction associated protein 1. Synonyms: LOC230959. Gene nomenclature, locus information, and GO, OMIM, and PMID ...
more infohttps://www.komp.org/geneinfo.php?geneid=22564
Vang-like protein 2 and Rac1 interact to regulate adherens junctions | Journal of Cell Science  Vang-like protein 2 and Rac1 interact to regulate adherens junctions | Journal of Cell Science
Caudal of this, adherens junctions displayed aberrant distribution of cytoskeletal components. Ring-like adherens junctions ... over the adherens junctions. Rac1 in loop-tail embryos (L, arrowhead) is not focused to adherens junctions but evenly ... which is located at adherens junctions (Fig. 1O′), is required for the proper recruitment of Rac1 to the adherens junction. ... displayed a reduced level of Rac1 labeling over the adherens junctions (Fig. 7D, arrowhead). Apart from the adherens junctions ...
more infohttp://jcs.biologists.org/content/123/3/472
Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis | Development  Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis | Development
Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis ... Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis ... Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis ... Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis ...
more infohttp://dev.biologists.org/content/early/2008/02/27/dev.015982
Fluid shear stress-induced reorganization of adherens junctions in hum by Jon A. Ukropec  "Fluid shear stress-induced reorganization of adherens junctions in hum" by Jon A. Ukropec
Ukropec, Jon A., "Fluid shear stress-induced reorganization of adherens junctions in human endothelial cells" (1999). Theses. ... Fluid shear stress-induced reorganization of adherens junctions in human endothelial cells ...
more infohttp://jdc.jefferson.edu/theses/24/
Transient and Steady-State Effects of Shear Stress on Endothelial Cell Adherens Junctions | Circulation Research  Transient and Steady-State Effects of Shear Stress on Endothelial Cell Adherens Junctions | Circulation Research
... and probably other members of the adherens junction complex, regulates the disassembly of adherens junctions.19 20 21 In ... because the status of the adherens junctions is important to the physiology of the endothelium. For example, adherens junctions ... Thus, both linear adherens junctions and some adherens plaques characterized cell-cell adhesion under static conditions. ... In static cultures, both F-actin and adherens junction proteins are distributed continuously around the cell-cell junction, as ...
more infohttp://circres.ahajournals.org/content/85/6/504
Molecular Vision: Adherens junction proteins are expressed in collagen corneal equivalents produced in vitro with human cells  Molecular Vision: Adherens junction proteins are expressed in collagen corneal equivalents produced in vitro with human cells
Adherens junction proteins are expressed in collagen corneal equivalents produced in vitro with human cells. Claude J. Giasson, ... The comparative histology and immunochemistry of adherens junction proteins of a native cornea (Figure 3A,D,G,J,M) may be ... Adherens junction complexes are also essential in establishing distinct basolateral and apical domains [2]. The polarized ... Epithelial cells are attached to each other by E-cadherin, an adherens junction protein. Other classical cadherins such as N-, ...
more infohttp://www.molvis.org/molvis/v20/386/
Alpha-catenin-dependent recruitment of the centrosomal protein CAP350 to adherens junctions allows epithelial cells to acquire...  Alpha-catenin-dependent recruitment of the centrosomal protein CAP350 to adherens junctions allows epithelial cells to acquire...
Our results indicate that CAP350 may act as an adaptor between adherens junctions and microtubules, thus regulating epithelial ... Alpha-catenin-dependent recruitment of the centrosomal protein CAP350 to adherens junctions allows epithelial cells to acquire ... Here, we report that the centrosomal microtubule (MT)-binding protein CAP350 localises at adherens junctions in epithelial ... mediated cell-cell adhesion or α-catenin depletion prevented CAP350 localisation at cell-cell junctions. Knocking down junction ...
more infohttps://www.sigmaaldrich.com/catalog/papers/25764135
  • Moreover, both transgenic mouse embryos overexpressing Vangl2 in neural stem cells and loop-tail Vangl2 loss-of-function embryos displayed impaired adherens junctions, a cytoskeletal unit essential for neural tube rigidity and neural tube closure. (biologists.org)
  • These factors include the components of adherens junctions (such as E-cadherin and the catenins), a heterotrimeric G protein, and the cytoskeletal regulators RhoGEF2, Abl, and Ena ( 5 , 19 , 28 , 37 , 58 ). (asm.org)
  • 11 12 VE-cadherin is a fully functional cadherin, because its expression in Chinese hamster ovary cells leads to association with catenins, adherens junctions formation, contact inhibition of cell growth, and restriction of monolayer permeability. (ahajournals.org)
  • E-cadherin en- gagement at adherens junction suppresses the nuclear location and activity of YAP by regulating MST1 and 2 activity, or via alpha-catenin by sequestrating 14-3-3 protein complexes within the cytoplasm. (covalab.com)
  • Beneath this, anchoring the junction to the cell cytoplasm , are loosely structured mats of fibres, 7 nm in diameter, thought to be actin filaments. (encyclopedia.com)
  • In seeking to elucidate the pathogenesis of BHD, we discovered a physical interaction between folliculin (FLCN), the protein product of the BHD gene, and p0071, an armadillo repeat containing protein that localizes to the cytoplasm and to adherens junctions. (harvard.edu)
  • Non-muscle myosins are expressed in a wide variety of tissues, but NM-IIB is the only non-muscle myosin II isoform expressed in cardiac muscle, where it localizes to adherens junctions within intercalated discs. (wikipedia.org)
  • Although loss of Crb or overexpression of the FERM binding domain causes mislocalization of adherens junctions, they do not result in a significant loss of photoreceptor polarity. (nih.gov)
  • In this Cell Science at a Glance article, we present the example of the so-called cerebral cavernous malformation (CCM), where adherens junctions are dismantled in the vessels contributing to brain microcirculation. (biologists.org)
  • We generated null alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function. (rupress.org)