SEARCH · Search PubMed

Results for “Intercellular Junctions”

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.

SourceResearch connectionFrom yearThrough year

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

At least 955 records · Page 53Linked to original sources

PubMed1986

Extracellular matrix regulation of cell-cell communication and tissue-specific gene expression in primary liver cultures.

Epithelial-mesenchymal interactions are effected, in part, by extracellular matrix components. We have spent many years analyzing the influence of extracellular matrix, both as extracts of matrix and as purified matrix components, on the growth and differentiation of normal and neoplastic liver cells. Currently we are focused on analyzing the influence of the extracellular matrix components, glycosaminoglycans and proteoglycans. We have found that these factors induce dramatic morphological changes, are potent inducers of gap junction synthesis and can regulate tissue-specific gene expression. With respect to gap junctions: intercellular communication via gap junctions, as measured by dye and electrical coupling, disappears within 12 hrs in primary rat hepatocytes cultured in serum supplemented media or within 24 hrs in cells in a serum free, hormonally defined medium designed for hepatocytes. Glucagon and linoleic acid/BSA were the primary factors in the HDM responsible for the extended life span of the electrical coupling. Addition of proteoglycans or glycosaminoglycans to hormonally defined medium after 24 hrs resulted in reexpression of electrical and dye coupling when assayed at 96 hrs of culture. The incidence of coupling was less than 5% in hormonally defined medium alone. Coupling incidence increased to 10-30% with the addition of 10 micrograms/ml of glycosaminoglycans (i.e., hyaluronic acid, dermatan sulfate, chondroitin 4- or 6-sulfate, and iota- or kappa-carrageenan) to hormonally defined medium. By contrast, the same concentrations of chondroitin sulfate proteoglycan, dermatan sulfate proteoglycan, or lambda-carrageenan resulted in dye coupling in more than 70% of the cells, with numerous cells showing dye spread from a single injected cell (in the case of the proteoglycans). The greatest effect of those tested was elicited by the dermatan sulfate proteoglycans, which induced cell-cell communication in 90-100% of the cells. Heparins gave intermediate responses (30-50%). Western blots demonstrated that the amounts of the main intrinsic gap junction polypeptide (27 KDa) extractable from cells correlated with the degree of electrical and dye coupling. Thus, proteoglycans and glycosaminoglycans appear to elicit the formation and function of gap junctions and may thus play a role in the regulation of intercellular communication under normal and pathological conditions. With respect to gene expression: normal rat hepatocytes maintained in culture on tissue culture plastic and in serum supplemented medium lose their tissue-specific functions within hours to a few days due to loss of synthesis and to rapid degradation of tissue-specific mRNAs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1998

Enhanced in vivo airway gene transfer via transient modification of host barrier properties with a surface-active agent.

Effective adenoviral gene therapy requires efficient viral vector entry into epithelial cells. Injured airway epithelia display enhanced gene transfer, reflecting in part increased vector access to protected cell populations and/or protected basolateral membranes. We tested whether adenoviral gene transfer is enhanced by modification of the epithelial barrier in mouse nasal airways with a nonionic detergent (polidocanol, PDOC). In C57BL/6 mice, 1.6 x 10(9) PFU of Ad5CMV LacZ (AdLacZ) instilled into the right nostril produced negligible gene transfer to the nasal epithelium 2 days after dosing, but significant, dose-dependent increases in gene transfer were achieved by pretreatment with PDOC. Permeation of the electron-dense tracer lanthanum into the intercellular junctions of PDOC (0.1%)-treated murine nasal epithelium, but not into intercellular junctions of vehicle controls, is consistent with PDOC-mediated increases in tight junctional permeability. In CF(-/-) mice, significant gene expression was not detectable after exposure to Ad5CBCFTR alone (1.4 x 10(9) PFU in 20 microl; AdCFTR), but PDOC pretreatment prior to AdCFTR instillation produced functional expression of CFTR (measured as deltaPD) 5 days after instillation. Because the development and testing of lung gene therapy will principally occur in children and adults with airway disease, AdLacZ gene transfer with and without PDOC pretreatment was examined in infected nasal airways. Gene expression was significantly reduced in infected as compared with uninfected airways. We conclude that the use of adjuvant surface-active and/or membrane-perturbing agents, synthetic or naturally derived, may provide a novel approach to enhancing the efficiency of adenoviral gene transfer.

Adenoviridae↗

PubMed1982

Ultrastructure of odontoblasts in kitten tooth germs as revealed by freeze-fracture.

Fifteen kittens were perfused with 2.5 per cent glutaraldehyde or modified Karnovsky fixative. Distribution and structural features of the three kinds of intercellular junctions; gap junctions, macular tight junctions and desmosome-like junctions were clarified by correlated observations using thin sections and freeze-fracture replicas. Distal junctional complexes of the odontoblasts were composed of both gap and macular tight junctions and sealed extracellular spaces incompletely, because of the poor sealing capacities of macular tight junctions. Therefore, there was no predentine-pulp barrier in the odontoblast layer. Except for the junctional complex, no tight junction was observed in the odontoblasts. Gap junctions and desmosome-like junctions were found between adjacent odontoblasts and between odontoblasts and neighbouring pulp cells. Gap junctions were similar to those of many other tissues but the desmosome-like junctions were different from mature desmosomes in the epithelial cells and showed immature features. Each intercellular junction of odontoblasts is considered to form a site of intercellular communication and cell-to-cell attachment.

Animals↗

PubMed1990

Modulation of intercellular communication during radiation and chemical carcinogenesis.

Carcinogenesis is a multistep process, involving the irreversible conversion of a stem cell to a terminal-differentiation-resistant cell ("initiation"), followed by the clonal expansion of this cell ("promotion") and by the acquisition of other genetic alterations leading to malignancy ("progression"). The initiation and progression steps seem to be facilitated by mutagenesis. Promotion has been associated with agents and conditions that cause mitogenesis. Gap junctional intercellular communication, a fundamental biological process regulating cell growth and differentiation, has been postulated to play a major role in carcinogenesis. The hypothesis is supported by the fact that many cancer cells have some dysfunction in gap junctional intercellular communication, many tumor-promoting chemicals and several oncogenes (i.e., ras, src, mos, neu, but not myc) reduce gap junctional intercellular communication, and several growth factors (i.e., EGF, TGF-beta, bovine pituitary extract) inhibit gap junction function. This integrative concept postulates that chemical promoters, oncogenes coding for growth factors, receptors, or transmembrane signaling elements, and growth factors can isolate an initiated cell from the suppressing influence of surrounding normal cells by down-regulating the transfer of ions and small molecules through gap junctions.

Animals↗

PubMed1988

Junctional specializations in the seminiferous epithelium of an insect (Triatoma infestans): a freeze fracture and lanthanum tracer study.

Intercellular junctions in the seminiferous epithelium of the testis of Triatoma infestans were examined by conventional electron microscopy, tannic acid fixation, electron-opaque tracers, and freeze-fracture techniques. Distinctive aspects of the intercellular junctions are described in different regions of the testis follicles. In the basal region, close to the basal lamina, smooth septate junctions intermingled with gap junctions were observed between sustentacular cells. In the parabasal regions of the seminiferous epithelium, plated septate junctions, 'molluscous and arthropod' type (according to the classification of Green, 1981), were observed. Over the above junctions, in the central regions, also located between sustentacular cell membranes, parallel rows of intramembrane particles form successive belts of widely spaced septate junctions in an atypical configuration. Invertebrate gap junctions were also observed between adjacent spermatocyte membranes.

Animals↗

PubMed1998

Targeting of the myosin-I myr 3 to intercellular adherens type junctions induced by dominant active Cdc42 in HeLa cells.

Myr 3, a member of the myosin-I family from rat, is shown in this study to be localized at adherens-type intercellular junctions in epithelial and nonepithelial tissues. Formation of intercellular junctions and the accompanying recruitment of myr 3 to these junctions involves signaling by the Rho subfamily of small GTP-binding proteins. This conclusion is based on studies with HtTA-1 HeLa cells that were induced by overexpression of constitutively active Cdc42Hs to form typical adherens-type intercellular junctions enriched in cadherins (N-cadherin), beta-catenin, filamentous actin and myr 3. Recruitement of myr 3 to Cdc42-induced adherens junctions in HeLa cells was dependent on a short region of the tail domain and a functional myosin motor domain, but was independent of its myosin-I tail homology and SH3 regions. Overexpression of constitutively active Rac1 induced a distinct type of adherens junction in HeLa cells that was characterized by elaborate intercellular interdigitations enriched in N-cadherin, beta-catenin and F-actin. Myr 3 was often present, but not specifically enriched in the intercellular junctions induced by constitutively active Rac1.

Amino Acid Sequence↗

PubMedDate not supplied

Inhibition of gap junctional-mediated intercellular communication in vitro by aldrin, dieldrin, and toxaphene: a possible cellular mechanism for their tumor-promoting and neurotoxic effects.

Several mechanisms have been postulated to be responsible for the pleiotropic effects of toxic chemicals. Although the cytotoxicity and mutagenicity of chemicals are well studied and relatively easily detected, the noncytotoxic and nonmutagenic (i.e., epigenetic) mechanisms of chemical toxicity are less well understood. An in vitro assay, using cocultures of Chinese hamster cells to measure metabolic cooperation between V79 6-thioguanine-sensitive (6TGs) and resistant (6TGr) cells, has been developed to detect noncytotoxic and nonmutagenic chemicals that inhibit, quantitatively, gap junctional communication. The insecticides aldrin, dieldrin, and toxaphene, known to have pleiotropic toxic effects in animals, were shown to inhibit gap junctional communication. Interpretation of results suggests that chemical inhibition of gap junctional communication could be a possible mechanism to explain their tumor-promoting and neurotoxic effects.

Aldrin↗

PubMed1991

Three-dimensional structure of an invertebrate intercellular communicating junction.

Gap junctions containing extensive, highly ordered crystalline arrays of hexagonally packed connexons have been isolated from the hepatopancreas of the arthropod, Homarus americanus (American lobster). The structure of such junctions has been studied to a resolution of approximately 25 A in three dimensions by electron microscopy of negatively stained specimens. The structure, which has the crystallographic symmetry of the two-sided plane group p6, reveals the connexon as an annular oligomer which projects approximately 30-45 A from the cytoplasmic surface. The stain-filled channel structure appears to be approximately 40-45 A wide in the extracellular region. Projection images of glucose-embedded specimens extend to a resolution of 10 A, and show a strong contrast from the connexon subunits. Overall the structure is quite similar to that of rat liver junctions, except that less stain is seen in the aqueous region of the gap and more surrounding the protrusions of the protein into the cytoplasm.

Animals↗

PubMed1980

On the developing rat placenta. I. Differentiation and junctional alterations of labyrinthine layers II and III.

The differentiation of chorionic layers II and III and alterations of intercellular junctions within the developing placental labyrinth were investigated in rats. Between the 14th and 16th day of gestation, the trabecular structures of the labyrinth alter and increasing numbers of primary, secondary, and tertiary lamellae develop. Trophoblastic layer I remains multicellular. Layer III rearranges and cytoplasmic fusions result in a continuous cytoplasmic barrier intervening between the already syncytial trophoblastic layer II and fetal capillaries. Simultaneously, most of the "undifferentiated" cells within the labyrinth disappear. Thin sectioning anf freeze-fracturing reveal multiple images of intercellular junctions, particularly gap and tight junctions in the cellular and syncytial parts of layers II and III. Continuous and regularly arranged tight junctions occur as well as fragmented structures which are spaced irregularly. Gap junctions are occasionally found between the juxtasinusoidal regions of layers II and III on the 14th day. More often they occur within restricted areas near the center of the trabeculae, integrated within extensive tight junctional strands. Gap junctions increase in later stages of pregnancy and eventually become distributed between the interfaces of layers II and III in the primary lamellae.

Animals↗

PubMed2002

Connexins and cancer.

The hypothesis, that gap junctional intercellular communication plays a key role in carcinogenesis and more generally in growth control was formulated nearly 40 years ago. From this time, data accumulated, showing that this type of communication is frequently decreased or absent in cells treated with tumor promoting agents, among transformed cells or between transformed/tumor cells and normal cells. This observation has been made on various cell types and whatever their tissue and species origins, by using in vitro and in vivo models. It led to the general assumption that the inhibition of gap junctional intercellular communication may play a role in carcinogenesis at two levels: (1) during tumor promotion by favoring the clonal expansion of initiated cells and (2) after the phenotypic transformation of cells by preventing the diffusion of putative "normalizing" factors between tumor cells and surrounding normal cells. During the past decade, the discovery that gap junction proteins, the connexins (Cx), may act as tumour suppressors, by reverting the phenotype of transformed cells confirmed the idea that their lack of function would be actively involved in carcinogenesis. However, we still do not know precisely what are the molecular processes that gap junctional intercellular communication may regulate and still do have very few data concerning the gap junction situation in human cancers. All these aspects are presented from an historical point of view and discussed below.

Animals↗

PubMed1994

Pathological changes induced by BaH1, a hemorrhagic proteinase isolated from Bothrops asper (Terciopelo) snake venom, on mouse capillary blood vessels.

The pathological changes induced in capillaries by BaH1, a hemorrhagic metalloproteinase isolated from the venom of Bothrops asper, were studied after i.m. injection in mouse gastrocnemius. Hemorrhage was observed macroscopically, and corroborated histologically, within the first 5 min. At the ultrastructural level, the earliest changes in endothelial cells, observed 1 min after toxin administration, consisted of a decrease in the number of pinocytotic vesicles, the presence of blebs and cytoplasmic projections pinching off to the vascular lumen and the detachment of endothelial cells from the surrounding basal lamina. These processes occurred concomitantly with a thinning of endothelial cells. In capillaries undergoing more advanced degenerative stages, there were gaps or breaks in endothelial cells through which erythrocytes were escaping to the extravascular space. In these cells, the basal lamina was usually absent. Throughout this process, intercellular junctions remained apparently intact and no evidence was found of extravasation through widened intercellular junctions. In addition to this morphological pattern of degeneration, some capillaries presented swollen endothelial cells with dilated endoplasmic reticulum and lacking pinocytotic vesicles. Many capillaries contained platelet plugs and fibrin. Thus, hemorrhage induced by BaH1 occurs per rhexis, as has been also described for other venoms and hemorrhagic toxins.

Animals↗

PubMed1986

Changes in membrane-microfilament interaction in intercellular adherens junctions upon removal of extracellular Ca2+ ions.

EGTA-induced depletion of Ca2+ ions from the culture medium of Madin-Darby bovine kidney epithelial cells results in rapid splitting of adherens-type junctions and the detachment of the vinculin- and actin-containing filament bundle from the cytoplasmic faces of the plasma membrane of the zonula adhaerens. This process was monitored by phase-contrast microscopy, combined with electron microscopy and immunofluorescent localization of the two proteins. It is shown that shortly after extracellular free Ca2+ concentration is lowered to the micromolar range, the actin-containing, junction-associated belt of microfilaments, together with the vinculin-rich junctional plaque material, is irreversibly detached as one structural unit from the plasma membrane, contracts, and is displaced towards the perinuclear cytoplasm where it gradually disintegrates. Other actin- and vinculin-containing structures present in the same cells, notably the focal contacts at the substratum, are not similarly affected by the Ca2+ depletion and retain both the adhesion to the external surface and the association with the plaque and microfilament components. Electron microscopic examination has shown that the membrane domain of the zonulae adhaerentes, unlike that of desmosomes, is not endocytosed after Ca2+ removal and that the displaced actin- and vinculin-containing plaque and filament belt are not associated with a particular membrane. It is further shown that upon restoration of normal Ca2+ levels in the culture medium, new intercellular contacts are established gradually by accretion of both vinculin and actin into new belt-like plaque- and microfilament-containing structures.

Actin Cytoskeleton↗

PubMed2005

Surface-modified PLGA nanosphere with chitosan improved pulmonary delivery of calcitonin by mucoadhesion and opening of the intercellular tight junctions.

Surface-modified DL-lactide/glycolide copolymer (PLGA) nanospheres with chitosan (CS) were prepared by the emulsion solvent diffusion method for pulmonary delivery of peptide, i.e., elcatonin. The nanosphere suspension was successfully aerosolized with a nebulizer similar to the drug solution, whereas the microsphere suspensions could not be aerosolized. After pulmonary administration, CS-modified PLGA nanospheres were more slowly eliminated from the lungs than unmodified PLGA nanospheres. CS-modified PLGA nanospheres loaded with elcatonin reduced blood calcium levels to 80% of the initial calcium concentration and prolonged the pharmacological action to 24 h, which was a significantly longer duration of action than that by CS-unmodified nanospheres. These results were attributed to the retention of nanospheres adhered to the bronchial mucus and lung tissue and sustained drug release at the adherence site. In addition, CS and CS on the surface of the nanospheres enhanced the absorption of drug. The rank order of the absorption of the model drugs with CS solution was carboxyfluorescein>FITC-dextran-4 (FD-4; Mw. 4000)>FD-21 (Mw. 21,000)>FD70 (Mw. 70,000), which corresponded to the molecular weights ([Mw.] given in parentheses). The absorption-enhancing effect may have been caused by opening the intercellular tight junctions.

Absorption↗

PubMed2001

Fenamates: a novel class of reversible gap junction blockers.

The effect of fenamates on gap junctional intercellular communication was investigated in monolayers of normal rat kidney (NRK) fibroblasts and of SKHep1 cells overexpressing the gap junction protein connexin43 (Cx43). Using two different methods to study gap junctional intercellular communication, single electrode voltage-clamp step response measurements and dye microinjection, we show that fenamates are reversible blockers of Cx43-mediated intercellular communication. After adding fenamates to a confluent monolayer of electrically coupled NRK fibroblasts, the voltage step-induced capacitive current transient changed from a transient characteristic for charging multiple coupled cell capacitances to one characteristic for a single cell in isolation. The capacitance of completely uncoupled cells was 19.7 +/- 1.0 pF (mean +/- S.E.M.; n = 11). Junctional conductance between the patched cell and the surrounding cells in the monolayer changed from >140.7 +/- 9.6 nS (mean +/- S.E.M.; n = 14) to <1.4 +/- 0.4 nS (mean +/- S.E.M.; n = 11) after uncoupling. Electrical coupling could be restored to >51.8 +/- 4.2 nS (mean +/- S.E.M.; n = 11) by washout of the fenamates. Voltage-clamp step response measurements showed that the potency of fenamates in inhibiting electrical coupling decreases in the order meclofenamic acid > niflumic acid > flufenamic acid. The half-maximal concentration determined by dye-coupling experiments was 25 and 40 microM for meclofenamic acid and flufenamic acid, respectively. Inhibition of gap junctional communication by fenamates did not involve changes in intracellular calcium or pH, and was unrelated to protein kinase C activity or an inhibition of cyclooxygenase activity. Voltage-clamp step response measurements in confluent monolayers of SKHep1 cells that had been stably transfected with Cx43 revealed that fenamates are potent blockers of Cx43-mediated intercellular communication. In conclusion, fenamates represent a novel class of reversible gap junction blockers that can be used to study the role of Cx43-mediated gap junctional intercellular communication in biological processes.

Cell Communication↗

PubMed1995

Melatonin enhances junctional transfer in normal C3H/10T1/2 cells.

Gap junctional intercellular communication is known to be involved in controlling cell proliferation and differentiation, and seems to play a crucial role in suppression of tumor promotion. The pineal gland and its hormone, melatonin, are believed to intervene in the control of neoplastic processes. Several possible mechanisms have been suggested to be potentially responsible for melatonin's oncostatic action; however, the actual mechanisms involved in melatonin's effects at the cellular level remain unidentified. In the present study low-density cultures of C3H/10T1/2 mouse embryo fibroblasts were incubated until relatively quiescent monolayers were established (17-18 days). Gap junctional intercellular communication in control samples and in cells treated with 10(-12) to 10(-8) M melatonin was determined by the scrape-loading assay using the fluorescent dye Lucifer yellow. The results showed that concentrations of melatonin considered physiological (10(-11) and 10(-10) M) induced a significant increase in the transfer of the dye to adjacent cells through gap junctions; both higher and lower concentrations were ineffective. These results suggest that melatonin could exert its putative oncostatic action, in part, by modulating the levels of gap junctional intercellular communication.

Animals↗

PubMed1996

Spatially dynamic intercellular adhesion junction is coupled to a microtubule-based motility system: evidence from an in vitro binding assay.

During spermatogenesis, spermatids change position in the seminiferous epithelium along an axis that is perpendicular to the seminiferous tubule wall. During this period, spermatids are attached to apical invaginations of Sertoli cells. In areas of this attachment, unique junction plaques occur in Sertoli cells. These plaques consist of regions of the plasma membrane involved with intercellular adhesion, a layer of actin filaments that are hexagonally packed, and an underlying cistern of endoplasmic reticulum (ER). It previously has been proposed that these junction plaques, and therefore the attached spermatids, are translocated, by motor proteins, along microtubule tracts in the Sertoli cell. If this is true, microtubules should bind to the junction plaque in a nucleotide dependent fashion. To verify this prediction, seminiferous epithelia of the rat were separated from tubule walls and then mechanically fragmented. These epithelial preparations were incubated, in both the presence and absence of 10 mM Mg(+)(+)ATP, with exogenous microtubules stabilized with taxol. Then unbound microtubules were separated from microtubules bound to larger epithelial components by centrifuging the samples through a step sucrose gradient. The fraction enriched for elongate spermatids was collected and processed for electron microscopy. The results indicate that the junction plaques remain attached to spermatids, the plaques are intact, and the cytoplasmic face of the ER binds microtubules in a nucleotide dependent fashion. The results are consistent with the presence of motor proteins on the ER component of the junction plaques and with the general hypothesis of microtubule-dependent spermatid translocation.

Adenosine Triphosphate↗

PubMed1998

Shear stress induces spatial reorganization of the endothelial cell cytoskeleton.

The morphology of endothelial cells in vivo depends on the local hemodynamic forces. Cells are polygonal and randomly oriented in areas of low shear stress, but they are elongated and aligned in the direction of fluid flow in regions of high shear stress. Endothelial cells in vitro also have a polygonal shape, but the application of shear stress orients and elongates the cells in the direction of fluid flow. The corresponding spatial reorganization of the cytoskeleton in response to the applied hemodynamic forces is unknown. In this study, we determined the spatial reorganization of the cytoskeleton throughout the volume of cultured bovine aortic endothelial cells after the cells had been exposed to a physiological level of shear stress for 0, 1.5, 3, 6, 12, or 24 h. The response of the monolayer to shear stress was not monotonic; it had three distinct phases. The first phase occurred within 3 h. The cells elongated and had more stress fibers, thicker intercellular junctions, and more apical microfilaments. After 6 h of exposure, the monolayer entered the second phase, where the cells exhibited characteristics of motility. The cells lost their dense peripheral bands and had more of their microtubule organizing centers and nuclei located in the upstream region of the cell. The third phase began after 12 h of exposure and was characterized by elongated cells oriented in the direction of fluid flow. The stress fibers in these cells were thicker and longer, and the heights of the intercellular junctions and microfilaments were increased. These results suggest that endothelial cells initially respond to shear stress by enhancing their attachments to the substrate and neighboring cells. The cells then demonstrate characteristics of motility as they realign. The cells eventually thicken their intercellular junctions and increase the amount of apical microfilaments. The time course of rearrangement can be described as a constrained motility that produces a new cytoskeletal organization that alters how the forces produced by fluid flow act on the cell and how the forces are transmitted to the cell interior and substrate.

Animals↗

PubMed1994

Augmentation of adherens junction formation in mesenchymal cells by co-expression of N-CAM or short-term stimulation of tyrosine-phosphorylation.

Adherens-type junctions (AJ) are specialized intercellular contacts, mediated by cadherins and characterized by the association with actin filaments through a vinculin- and catenin-rich submembrane plaque. We describe here two mechanisms which potentiate AJ formation in mesenchymal cells. These include the augmentation of AJ by the co-expression of another adhesion molecule, namely NCAM, and the stimulation of tyrosine phosphorylation. These effects were obtained in NIH-3T3 cells, which, under normal conditions, have poor cadherin- and vinculin-containing intercellular junctions. The transfection of these cells with cDNA encoding the 140kD NCAM resulted in the extensive formation of cadherin- and vinculin-rich AJ, demonstrating a cooperativity between the two junctional systems. AJ could also be induced in 3T3, and in CEF and COS cells, upon a brief exposure to H2O2/vanadate, which elevates cellular levels of phosphotyrosine due to inhibition of tyrosine-specific phosphatases. This induction was, however, transient since prolonged exposure to H2O2/vanadate resulted in an overall destruction of AJ and detachment of cells from each other and from the extracellular matrix. AJ formation appears, therefore, to be modulated by a variety of factors including the level of expression of its intrinsic components, the cooperative effect of other adhesion molecules, and by tyrosine-phosphorylation.

3T3 Cells↗