Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADHESIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed1982

Altered adhesiveness of tumor cell surface variants with reduced metastasizing capacity--reduced adhesiveness to vascular wall components in culture.

Heterotypic adhesiveness of surface variant clones of B-16 melanoma cells exhibiting different metastasizing capacity was studied with respect to components of the vascular wall in culture including endothelial (E) and smooth muscle (SM) cells from adult bovine aorta, and the extracellular matrices laid down by them. The ricin-resistant cells (ricinR) and the wheat-germ agglutinin-resistant (WGAR) cells, both of which showed reduced hematogenous metastases in vivo, showed reduced adhesiveness specifically to endothelial cells and extracellular matrices. This reduced heterotypic adhesiveness is in contrast to the homotypic adhesive properties in which respect the ricinR cells had similar values to the parental cells, while the WGAR cells had much higher values than the latter. There appeared to be a positive correlation between metastasizing capacity and specific adhesiveness to E cells and the extracellular matrix surfaces.

Blood Vessels↗
PubMed1989

Oligomers with pendant isocyanate groups as tissue adhesives: II. Adhesion to bone and other tissues.

The adhesive properties of a series of oligomers prepared from 2-isocyanatoethyl methacrylates (IEM) and/or m-isopropenyl-alpha,alpha-dimethylbenzyl isocyanate (TMI) and various acrylates or methacrylates were studied. The bond strength of bone, dentin, or soft tissue specimens joined with these oligomers respectively to bone, dental composite restorative, or denture base resin were determined by tensile adhesion or shear tests. These oligomers are more effective in forming stronger bonds to bone than are other tissue adhesives. Fracture occurs cohesively, usually within the bone. Thermocycling in water for 1 week between 5 degrees C and 55 degrees C did not decrease adhesion indicating that exposure to water or thermal shock produced no deterioration of the bond. Tensile adhesion of bovine or human dentin joined to composite restorative resin by means of the oligomers is similar to that of the best dental bonding agents such as Gluma (glutaraldehyde and 2-hydroxyethyl methacrylate) or ferric oxalate + N-phenylglycine + dimethylacryloxyethyl-pyromellitate. These oligomers also strongly bond soft tissues and calfskin and to acrylic resins and composites.

Biopolymers↗
PubMed1989

A micromechanical technique for monitoring cell-substrate adhesiveness: measurements of the strength of red blood cell adhesion to glass and polymer test surfaces.

We report a novel method for rapid comparison of the relative strength of adhesion of cells to different solid surfaces. A vertically oscillating micropipette is brought above an individual cell in such a manner that it makes contact with the cell at the lower limit of its travel. The pressure within the micropipette is gradually reduced until the cell attaches to the micropipette by suction and is lifted from the solid surface. The reduction in pressure required to detach a cell depends on the specific cell/substrate combination and serves as a relative measure of the strength of cell adhesion. A particular advantage of this approach over conventional methods is the ability to select particular cells from a population. As a test of the reproducibility of the method and its ability to distinguish the strength of adhesion of cells to different solid surfaces, we have used it to measure the adhesiveness of human red blood cells to hydrophilic glass, tissue culture grade polystyrene, polyethylene terephthalate, and polymethyl methacrylate. We find that results for the same surface are highly reproducible and that the method is capable of distinguishing small differences in the adhesiveness of red blood cells to the above surfaces.

Biocompatible Materials↗
PubMed1994

Role of cell surface O-linked oligosaccharides in adhesion of HL60 cells to fibronectin: regulation of integrin-dependent cell adhesion by O-linked oligosaccharide elongation.

The adhesion of the myelogenous leukemia cell line, HL60, to fibronectin and its fragments, heparin binding fragment (40 kDa) and cell attachment fragment (120 kDa), was enhanced by culturing with benzyl-alpha-GalNAc (BZ alpha GalNAc). Enhancement of cell adhesion to fibronectin was also observed on treatment of HL60 cells with 12-O-tetradecanoylphorbol 13-acetate (TPA). However, an additive effect of BZ alpha GalNAc and TPA treatments was not observed. The expression of VLA4 and VLA5 did not change during treatment with BZ alpha GalNAc or TPA. Cell adhesion to fibronectin before and after treatment with BZ alpha GalNAc or TPA was inhibited by anti-VLA4 and anti-VLA5 monoclonal antibodies. Staining of the cells with Helix pomatia lectin demonstrated that culturing of the cells with BZ alpha GalNAc blocked elongation of O-linked oligosaccharides on the cell surface and led to accumulation of GalNAc-O-Ser/Thr. Labeling of cell surface carbohydrates with [3H]-glucosamine followed by treatment with TPA revealed that O-glycosylated glycoproteins including CD43 were released from the cell surface during this treatment. These findings indicate that integrin-dependent cell adhesion, particularly VLA4- or VLA5-dependent cell adhesion, of HL60 cells is prevented with the extension of O-linked oligosaccharides and recovers with the disappearance of O-linked oligosaccharides from the cell surface.

Acetylgalactosamine↗
PubMed1993

T cell adhesion to endothelium: the FRC conduit system and other anatomic and molecular features which facilitate the adhesion cascade in lymph node.

Since T cell surveillance depends on movement from blood into tissue and back again, rapid, efficient and selective T cell adhesion to vascular endothelium is essential. This adhesion involves a multistep cascade clarified by a recent consensus model: (1) initial tethering by selectin-mediated interactions; (2) triggering of adhesive function of T cell integrins by ligands at or near the endothelial surface; and (3) strong adhesion mediated by T cell integrins. We recapitulate this model, particularly as it pertains to the lymph node, and explore additional molecular and anatomic elements which contribute to the effectiveness of the adhesion cascades at that site: (1) importance of cytokines/soluble mediators as triggering ligands; (2) role of glycocalyx and proteoglycans on high endothelial venule (HEV) endothelium in capturing and presenting triggering cytokines; (3) remarkable function of what we designate the 'fibroblastic reticular cell (FRC) conduit system' in rapidly transporting cytokines to the HEV; (4) importance of the unique anatomy of the flap-valve junctions between HEV endothelium in enabling intravasation of cytokines and transmigration of lymphocytes. Taken together, these molecular mechanisms and these three anatomic features of lymph node facilitate extremely efficient lymphocyte traffic to this site critical for T cell-mediated immune responses. Analogous mechanisms contribute to T cell interaction with endothelium at other sites.

Animals↗
PubMed2004

Phospholipids reduce the intraperitoneal adhesion of colonic tumor cells in rats and adhesion on extracellular matrix in vitro.

OBJECTIVE: To evaluate the influence of intraperitoneal treatment with phospholipids on the formation of peritoneal carcinosis after inoculation of colonic tumor cells in rats. The presence of tumor cells in the peritoneal cavity serves as a prognostic marker for postoperative survival after resection of gastrointestinal cancer. Intraperitoneal tumor cell attachment is a pivotal step in developing peritoneal carcinosis. Intraabdominal application of phospholipids resulted in a significant decrease of adhesion formation, especially at sites of peritoneal lesions. METHODS: 2x10(6) colonic tumor cells (DHD/K12/TRb) were injected intraperitonely in female BD-IX rats. A total of 90 rats were divided into three groups with treatments of phospholipids at 75 mg/kg or 150 mg/kg bodyweight or sodium chloride at 0.9% in the control group. The treatment groups were subdivided into animals with defined peritoneal lesions and animals without lesions. After 30 days, the extent of peritoneal carcinosis was determined by measuring the tumor volume, the area of tumor attachment and the Peritoneal Cancer Index. Over a 90-day observation period, the survival rate was analyzed. In vitro, we examined the reduction of tumor cell adhesion on extracellular matrix components after treatment with phospholipids. Microtiter plates were coated with laminin, fibronectin or collagen IV for adhesion experiments. RESULTS: In our study, we found a significant reduction of peritoneal dissemination with respect to all evaluation methods after treatment with phospholipids at 150 mg/kg in animals without peritoneal lesions. This could not be achieved using the lower concentration of phospholipids (75 mg/kg). In vitro, the maximum reductions of tumor cell adhesion by phospholipids compared with the control values for laminin and fibronectin were 46% and 37%, respectively, whereas for collagen IV the reduction was only 24% ( p<0.0001). CONCLUSIONS: A new method of prevention of intraperitoneal tumor cell adhesion, possibly leading to a reduced incidence of peritoneal carcinosis after surgery of gastrointestinal tumors, is introduced.

Adenocarcinoma↗
PubMed2005

Paclitaxel impairs endothelial cell adhesion but not cytokine-induced cellular adhesion molecule expression.

Local delivery of antiproliferative agents using drug-eluting stents has become a productive area of research for preventing in-stent restenosis. Recently, the microtubule stabilizing drug paclitaxel has been used to coat stents. While the actions of paclitaxel on smooth muscle are well documented, effects on endothelial cells (ECs) are largely unknown. Nevertheless, restoration of EC function is a critical step in repairing the vascular lesion. We assessed the effects of paclitaxel by examining three events that are critical in controlling the severity of vascular injury: (1) adhesion of ECs to matrix proteins, (2) EC migration, and (3) cytokine-stimulated cellular adhesion molecule (CAM) expression on the surface of ECs. Paclitaxel inhibited both EC adhesion and migration of ECs; however, it had no effect on tumor necrosis-stimulated CAM expression on ECs. The mechanisms of paclitaxel action on matrix adhesion and migration are not clear, but protein kinase C and myosin light chain kinase do not appear to play a role as they are unaffected by treatment of the cells with paclitaxel. On the other hand, the MAP kinase ERK1/2 is modestly inhibited by paclitaxel. While paclitaxel-coated endovascular stents may prevent smooth muscle proliferation, their attenuation of EC migration and adhesion to the lesion coupled with an inability to reduce cytokine-induced CAM expression on ECs may limit their effectiveness.

Antineoplastic Agents↗
PubMed1991

Inhibition of adhesion-promoting activity of a human salivary protein which promotes adhesion of Streptococcus mutans JBP to hydroxyapatite.

The adhesion-promoting proteins (APP) (molecular mass approx. 300 kDa), which promote adhesion of Streptococcus mutans JBP (serotype c) to hydroxyapatite, were isolated from human submandibular-sublingual (SMSL) saliva by gel filtration on a Trisacryl GP2000 M column. The effects of hexoses, pentoses, methyl-pentoses, hexosamines, N-acetylhexosamines, a basic amino acid, polyamines and ammonium chloride on the bacterial adhesion-promoting activity of the APP were examined. Galactosamine, mannosamine, L-lysine, spermine, putrescine, and ammonium chloride inhibited the adhesion-promoting activities of the APP. The other sugars, including the N-acetylhexosamines, were without effect. Thus, compounds containing a primary amino-group appear to have a specific inhibitory effect on adhesion of S. mutans JBP to APP adsorbed onto hydroxyapatite, an activity which is lost if the amino-group is acetylated.

Bacterial Adhesion↗
PubMed2004

Reduction in adhesiveness to extracellular matrix components, modulation of adhesion molecules and in vivo migration of murine macrophages infected with Toxoplasma gondii.

Toxoplasma gondii is an obligate intracellular parasite, able to disseminate into deep tissues and cross biological barriers, reaching immunoprivileged sites such as the brain and retina. In order to investigate whether the parasite uses leukocyte trafficking to disseminate throughout the host, the adhesive potential to extracellular matrix components, the expression of adhesion molecules and the in vivo migration of murine macrophages infected with RH strain of T. gondii were investigated. Cellular adhesion to fibronectin, laminin and collagen IV decreased after 24 h of T. gondii infection. However, the decrease in adhesion of infected macrophages observed at early infection was reversed after 48 h. Moreover, decreased adhesion was dependent on active penetration, since heat-killed parasites were unable to reproduce it. Expression of integrins alphaL, alpha4 and alpha5 chains was downmodulated early postinfection, but a progressive regain of expression was observed after 12 h of infection. Expression of beta2, alphav and alpha4 integrins by peritoneal macrophages at late infection was also gradually reestablished. The assessment of in vivo migration of infected macrophages labeled with the fluorescent dye 5-chloromethylfluorescein diacetate showed a 48-h delay in migration to cervical lymph nodes when compared to LPS pre-stimulated macrophages. Furthermore, cells that migrate to distal lymph nodes were loaded with live parasites. Taken together, these results provide insights about T. gondii escape from the host immune response, placing the macrophage as a "Trojan horse", contributing to parasite dissemination and access to immunoprivileged sites.

Animals↗
PubMed2004

Integrin alpha4beta1 involvement in stromal cell-derived factor-1alpha-promoted myeloma cell transendothelial migration and adhesion: role of cAMP and the actin cytoskeleton in adhesion.

The chemokine stromal cell-derived factor-1alpha (SDF-1alpha) is expressed by bone marrow (BM) stromal cells and plays key roles in cell homing to and retention into the bone marrow. In multiple myeloma, blood-borne malignant plasma cells home to the BM and accumulate in contact with stromal cells, implicating myeloma cell migration across endothelium. Myeloma cells express the SDF-1alpha receptor CXCR4, as well as the integrin alpha4beta1, which mediates their attachment to BM stroma. We show here that SDF-1alpha promotes transendothelial migration of purified BM myeloma cells and myeloma-derived NCI-H929 cells, involving a transient upregulation of alpha4beta1-dependent cell adhesion to the endothelium. Characterization of intracellular signaling pathways involved in the modulation by SDF-1alpha of alpha4beta1-mediated myeloma cell adhesion revealed that intracellular cAMP amounts associated with the activation of protein kinase A play key roles in this modulation. Furthermore, a functional link between cAMP actions on the dynamics of actin cytoskeleton, RhoA activation, and alpha4beta1-dependent cell adhesion in response to SDF-1alpha has been found. The regulation of alpha4beta1-mediated myeloma cell adhesion by SDF-1alpha could play key roles during myeloma cell homing into and trafficking inside the BM, and characterization of the molecular events involved in SDF-1alpha-activated modulation of this adhesion will contribute to a better understanding of mechanisms participating in cell migration.

Actin Cytoskeleton↗
PubMed1998

Gonadotropin-releasing hormone agonist (GnRH-a) therapy alters activity of plasminogen activators, matrix metalloproteinases, and their inhibitors in rat models for adhesion formation and endometriosis: potential GnRH-a-regulated mechanisms reducing adhesion formation.

OBJECTIVE: To evaluate the effects of a gonadotropin-releasing hormone agonist (GnRH-a) on plasminogen activator (PA), matrix metalloproteinase (MMP), plasminogen activator inhibitor (PAI) and matrix metalloproteinase inhibitor (MMPI) activities in peritoneal fluid relative to GnRH-a-induced reduction of adhesion formation. DESIGN: Continuation of prospective randomized study using surgical models for adhesion formation. SETTING: Department of Obstetrics and Gynecology research laboratory at the University of Missouri School of Medicine. PATIENT(S): Forty reproductively cycling female Sprague-Dawley rats. INTERVENTION(S): Female rats were injected with depot GnRH-a or diluent and randomly assigned to adhesion and endometriosis surgeries. Peritoneal fluid was collected prior to (time 1) and 7 weeks from (time 2) initial surgery. MAIN OUTCOME MEASURE(S): Peritoneal fluid was analyzed for PA, PAI, MMP, and MMPI activities. RESULT(S): At time 1, MMP and MMPI activities were similar in all rats; however, PA and PAI activities were less in rats pretreated with GnRH-a than with diluent. Between time 1 and time 2, GnRH-a-treated rats showed an increase in PAI and MMPI activities without significant changes in PA or MMP activities, whereas rats receiving diluent showed a significant increase in PAI and MMP activities but no significant changes in PA or MMPI activities. At time 2, rats receiving GnRH-a had less PA and MMP activities than those receiving diluent. Adhesion scores showed a positive correlation with MMP activity. CONCLUSION(S): In the absence of GnRH-a therapy, surgical tissue manipulation increased peritoneal fluid MMP and PAI activity. Gonadotropin-releasing hormone agonist therapy decreased PA and MMP activities and also increased PAI and MMPI activities. This GnRH-a-induced shift to a less invasive phenotype may alter fibrinolysis and extracellular matrix remodeling and thereby play a role in the mechanism of GnRH-a-induced reduction in adhesion formation.

Animals↗
PubMed2004

Molecular characterization of postoperative adhesions: the adhesion phenotype.

Postoperative adhesion development remains a very frequent occurrence, which is often unrecognized by surgeons because of limited ability to conduct early second-look laparoscopies. The consequences include infertility, pelvic pain, bowel obstruction, and difficult reoperative procedures. To date, approaches to limit adhesions primarily have involved barriers to separate tissue during reepithelization. Future progress in regulating adhesion development and tissue fibrosis likely will require an improved understanding of the molecular processes involved in normal peritoneal repair and its aberrations leading to adhesion development. We hypothesize that tissue hypoxia (in part resulting from tissue incision, fulguration, suture ligation, etc.) is the major inciting event, which leads to a coordinated series of molecular events that promote an inflammatory response leading to enhanced tissue fibrosis. These events are reduced plasminogen activator activity, extracellular matrix deposition, increased cytokine production, increased angiogenesis, and reduced apoptosis (programmed cell death). Improved understanding of these events and their regulation will provide the opportunity to regulate better postoperative adhesion development and tissue fibrosis, thereby reducing the morbidity and mortality they cause.

Extracellular Matrix↗
PubMed1988

ICAM, an adhesion ligand of LFA-1, is homologous to the neural cell adhesion molecule NCAM.

Antigen-specific cell contacts in the immune system are strengthened by antigen-nonspecific interactions, mediated in part by lymphocyte-function associated (LFA) antigens. The LFA-1 antigen is widely expressed on cells of haematopoietic origin and is a major receptor of T cells, B cells and granulocytes. LFA-1 mediates the leukocyte adhesion reactions underlying cytolytic conjugate formation, helper T-cell interactions, and antibody-dependent killing by natural killer cells and granulocytes. Recently, ICAM-1 (intercellular adhesion molecule-1) has been defined as a ligand for LFA-1. Monoclonal antibodies to ICAM-1 block T lymphocyte adhesion to fibroblasts and endothelial cells and disrupt the interaction between cytotoxic T cells and target cells. In addition, purified ICAM-1 reconstituted into artificial membranes binds LFA-1+ cells. ICAM-1 is found on leukocytes, fibroblasts, epithelial cells and endothelial cells and its expression is regulated by inflammatory cytokines. LFA-1 has been placed in the integrin family of cell surface receptors by virtue of the high sequence similarity between the LFA-1 and integrin beta chains. The adhesion ligands of the integrin family are glycoproteins bearing the Arg-Gly-Asp (RGD) sequence motif, for example, fibronectin, fibrinogen, vitronectin and von Willebrand factor. Here we show that a complementary DNA clone ICAM-1 contains no RGD motifs, but instead is homologous to the neural cell adhesion molecule NCAM.

Amino Acid Sequence↗
PubMed2001

In vitro bond strengths of resin modified glass ionomer cements and composite resin self-cure adhesives: introduction of an adhesive system with increased bond strength and inhibition of decalcification.

This study evaluated the shear bond strength and adhesive remnant index of 5 self-cure adhesives to comparatively evaluate a new adhesive system. Extracted human incisors were randomly divided into 7 test groups of 20 each. Incisor mesh-backed brackets were bonded to the tooth specimens in each group with their respective adhesive according to the manufacturer's instructions. The specimens were thermocycled for 2 weeks at temperatures from 5 degrees to 55 degrees C to simulate oral conditions and debonded using an Instron machine. Acceptable bond strength parameters were present with the Contacto No-Mix (composite resin containing glass ionomer 8.75 MPa) and Fuji Ortho SC with acid conditioning (6.98 MPa). Contacto No-Mix had a higher bond strength (11.2 MPa) when microetching and Megabond were employed than when these adjuncts were not employed. When FUJI Ortho SC specimens were conditioned with polyacrylic acid, they showed a higher bond strength (6.98 MPa) than when bonded to unetched teeth (5.41 MPa). In test 3, EXPT-fluoride adhesive (AF) demonstrated a higher bond strength (13.44 MPa) than both resin composite Contacto No-Mix (8.8 MPa, GAC 7.4 MPa) and FUJI Ortho SC (5.41 MPa). Expt AF (Test 3) and Concise had equal bond strengths, however, the former can potentially release fluoride from the glass ionomer. Although the Ex

Adhesiveness↗
PubMed1997

Up-regulation of the endothelial cell adhesion molecule intercellular adhesion molecule-1 (ICAM-1) by autoantibodies in autoimmune vasculitis.

Autoimmune vasculitis is characterized by the presence of autoantibodies, particularly anti-neutrophil cytoplasmic antibodies (ANCA) and anti-nuclear antibodies (ANA), in patient sera. These autoantibodies have an incompletely understood role in development of vascular injury. The expression or up-regulation of cell adhesion molecules is an early phase in the development of an inflammatory vascular lesion. Autoantibody-positive sera from patients with vasculitis were assessed for their ability to modulate adhesion molecule expression by human umbilical vein endothelial cells (HUVEC). Autoantibody-positive serum samples from 11 out of 21 patients with primary vasculitis produced substantial up-regulation of ICAM-1 on HUVEC. Autoantibody-negative samples did not produce adhesion molecule up-regulation. Up-regulation of adhesion molecules on HUVEC was observed with samples positive for ANA, a phenomenon not previously reported. Preincubation of the sera with purified antigens recognized by ANCA failed to block this activation. In addition, MoAbs to ANCA antigens were ineffective at inducing ICAM-1 up-regulation, suggesting that activation is independent of the molecular specificity of the antibody. This capacity of ANCA- and ANA-positive sera to up-regulate adhesion molecules on endothelial cells may be a factor in the vessel wall inflammation seen in ANCA-associated vasculitis.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1998

Inhibitory effect of bupleuri radix saponins on adhesion of some solid tumor cells and relation to hemolytic action: screening of 232 herbal drugs for anti-cell adhesion.

Anti-cell adhesive activity and hemolytic action of herbal drugs were investigated. Among 232 herbal drugs tested, six showed a remarkable anti-cell adhesive activity, and the extract from the roots of Bupleurum falcatum (Umbelliferae), the semen of Psorala corylifolia (Leguminosae), and the semen of Areca catechu (Palmae) showed an anti-cell adhesive action at non-cytotoxic concentrations. Saikosaponins-a, d and e, isolated from the roots of Bupleurum falcatum, exhibited a potent anti-cell adhesive activity and a strong hemolytic action. In a structure-activity relationship for both activities, it seems that a sugar moiety and an ether linkage between C-13 and C-28 are required for good bioactivities. In addition, saikosaponin d with a beta-hydroxy group at C-16 was more potent than saikosaponin a possessing an alpha-hydroxy group. Taken together, it is suggested that the mechanism for anti-cell adhesive activity of saikosaponin may resemble that for their hemolytic action.

Antineoplastic Agents, Phytogenic↗
PubMed2001

Suppression of chemically induced apoptosis but not necrosis of renal proximal tubular epithelial (LLC-PK1) cells by focal adhesion kinase (FAK). Role of FAK in maintaining focal adhesion organization after acute renal cell injury.

Decreased phosphorylation of focal adhesion kinase (FAK) is associated with loss of focal adhesions and actin stress fibers and precedes the onset of apoptosis in renal epithelial cells caused by nephrotoxicants (Van de Water, B., Nagelkerke, J. F., and Stevens, J. L. (1999) J. Biol. Chem. 274, 13328-13337). The role of FAK in the control of apoptosis caused by nephrotoxicants was further investigated in LLC-PK1 cells that were stably transfected with either green fluorescent protein (GFP)-FAK or dominant negative acting deletion mutants of FAK, GFP-FAT, and GFP-FRNK. GFP-FAT and GFP-FRNK delayed the formation of focal adhesions and prevented the localization of endogenous (phosphorylated) FAK at these sites. GFP-FAT and GFP-FRNK overexpression potentiated the onset of apoptosis caused by the nephrotoxicant dichlorovinyl-cysteine. This was associated with an increased activation of caspase-3. GFP-FAT also potentiated apoptosis caused by doxorubicin but not cisplatin. The potentiation of apoptosis by GFP-FAT was related to an almost complete dephosphorylation of FAK; this did not occur in cells overexpressing only GFP. This dephosphorylation was associated with a pronounced loss of focal adhesion organization in GFP-FAT cells, in association with loss of tyrosine phosphorylation of paxillin. In conclusion, the data indicate an important role of cell-matrix signaling in the control of chemically induced apoptosis; loss of FAK activity caused by toxic chemicals results in perturbations of focal adhesion organization with a subsequent inactivation of associated (signaling) molecules and loss of survival signaling.

Animals↗
PubMed2006

Regulation of cell adhesion by protein-tyrosine phosphatases: II. Cell-cell adhesion.

Cell-cell adhesion is critical to the development and maintenance of multicellular organisms. The stability of many adhesions is regulated by protein tyrosine phosphorylation of cell adhesion molecules and their associated components, with high levels of phosphorylation promoting disassembly. The level of tyrosine phosphorylation reflects the balance between protein-tyrosine kinase and protein-tyrosine phosphatase activity. Many protein-tyrosine phosphatases associate with the cadherin-catenin complex, directly regulating the phosphorylation of these proteins, thereby affecting their interactions and the integrity of cell-cell junctions. Tyrosine phosphatases can also affect cell-cell adhesions indirectly by regulating the signaling pathways that control the activities of Rho family G proteins. In addition, receptor-type tyrosine phosphatases can mediate outside-in signaling through both ligand binding and dimerization of their extracellular domains. This review will discuss the role of protein-tyrosine phosphatases in cell-cell interactions, with an emphasis on cadherin-mediated adhesions.

Animals↗