Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.7.10.2 (focal adhesion kinase)
44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from 34 patients with lepromatous leprosy were screened for the presence of autoantibodies by indirect immunofluorescence using two epithelial cell lines, PTK2 and HEp2, as substrates. Indirect immunofluorescence staining of both substrates with the serum of a patient with lepromatous leprosy revealed a cytoplasmic intermediate filament staining pattern. After exposure of PTK2 cells to colchicine, the filaments collapsed into thick perinuclear coils, confirming the presence of intermediate filament reactivity. Immunofluorescence of rat fibroblasts with the same serum also revealed an intermediate filamentous staining pattern. Human keratinocytes exposed to the patient's serum revealed a diffuse cytoplasmic staining pattern. Our study suggests the presence of autoantibodies to cytoskeletal intermediate filaments or to molecules associated with vimentin and possibly keratin subunit proteins in the serum of a patient with lepromatous leprosy.
...
PMID:A patient with lepromatous leprosy and anticytoskeletal antibodies. 245 40

Two distinct mechanisms by which bladder carcinoma cells of the NBT-II cell line dissociate and migrate away from an in vitro reconstituted epithelial sheet were examined as regards intercellular adhesion and cell locomotion. Scattering of NBT-II bladder carcinoma cell line was promoted by 2 distinct culture protocols: (i) deposition of some components of the extracellular matrix onto the culture substratum (glass or plastic) induced cell dispersion of the epithelial sheet of carcinoma cells, and (ii) addition of Ultroser G, a serum substitute, to the culture medium induced scattering and acquisition of motility of NBT-II cells. Under both culture conditions, NBT-II cells dissociated, lost their epithelial morphology, acquired fibroblastic shape and migrated actively. We show that, among different extracellular matrix proteins, only collagens were able to promote the transition towards fibroblastic phenotype (referred as epithelium-to-mesenchyme transition or EMT). Furthermore, the native 3-dimensional helical structure of collagens was required for their function. During induction of EMT of NBT-II cells with Ultroser G, the junctions between epithelial cells were split, polarized epithelial cell organization was lost, and the resulting individual cells became motile and assumed a spindle-like fibroblastoid appearance. Using immunofluorescence microscopy techniques, we demonstrate that this change is accompanied by redistribution of desmosomal plaque proteins (desmoplakins, desmoglein, plakoglobin) and by reorganization of the cytokeratin and the actin-fodrin filament systems. Intermediate-sized filaments of the vimentin type were formed de novo in the fibroblastoid cell form. The observed transition towards fibroblastic phenotype (epithelium-to-mesenchyme transition or EMT) was fully reversed by removing the inducing factors from the culture medium, as shown by the disappearance of vimentin filaments and the reappearance of desmosomes in the newly formed epithelial cells.
...
PMID:Reversible transition towards a fibroblastic phenotype in a rat carcinoma cell line. 250 87

Serum from a patient with the CREST Syndrome and systemic lupus erythematosus contained an IgM antibody that reacted at dilutions up to 1:800 with a fibrous cytoplasmic network in several epithelioid and fibroblastic cell lines. The antibody was shown by immunofluorescence microscopy to label a specific subset of cytoskeletal polymers, the intermediate filaments. The reactive antigen from this biochemically heterogeneous group of filaments was established as the 58,000-mol wt protein, vimentin: (a) the patient's serum reacts with a range of cell lines that contain intermediate filaments composed of vimentin, but not with cells whose intermediate filaments are composed of different protein subunits; (b) in PTK2 epithelioid cells the serum reacts with the class of filaments that coils around the nucleus after colchicine treatment (vimentin) and not with the filaments that remain dispersed after colchicine (prekeratin); and (c) the component of reactive cells that combines with the serum is shown by immunoelectrophoresis to be a 58,000-mol wt protein antigen. A similar antibody that binds intermediate filaments of PTK2 cells was encountered at lower titer in some sera from other patients with connective tissue diseases and in control sera. Previous routine antinuclear antibody assays using mouse liver or commercially prepared HEp-2 cells have failed to reveal anticytoskeletal antibodies in patient sera, perhaps due to inadequate presentation or preservation of cytoplasmic antigens.
...
PMID:Immunoglobulin M autoantibody to vimentin intermediate filaments. 703 55

The expression patterns of low and high molecular weight cytokeratins (LCK and HCK) vimentin and desmin were investigated by immunocytochemistry in the rete testis and epididymis in the dog. The epithelium of the rete testis displayed coexpression of LCK, vimentin and desmin. The epithelium of the efferent ductules was composed of ciliated and nonciliated cells; the ciliated cells expressed LCK strongly. The epithelium of the epididymal duct was composed of principal, apical and basal cells. Principal cells in the duct of the head of the epididymis displayed LCK and vimentin, with a predominance of LCK in the apical cytoplasmic regions and vimentin in the basal portions of the cells. Expression of vimentin in the principal cells decreased towards the body of the epididymis and disappeared in the tail region, where LCK remained unchanged. Apical cells of the epididymal duct expressed LCK. Basal cells in the duct of the head and body of the epididymis showed LCK and those of the duct of the body of the epididymis also HCK expression.
...
PMID:Coexpression of different cytokeratins, vimentin and desmin in the rete testis and epididymis in the dog. 751 42

During the past two decades we have witnessed the identification of an expanding list of immunohistochemical and molecular markers linked to histopathologically defined subtypes of tumors. These markers offer new insights and approaches to the classification of tumors with important prognostic and/or therapeutic implications. We review the potentially diagnostic immunohistochemical and molecular markers of soft tissue tumors (STTs). The immunohistochemical markers reviewed include vimentin, cytokeratin, desmin, HHF35, S100, myoD1, alpha1-antitrypsin, vascular markers (factor VIII, CD31, CD34), MIC2, and others. The potentially diagnostic chromosomal translocations and associated genes identified in STT include Ewing's/PNET t(11;22)(q24;q12)(FLI1;EWS), t(21;22)(q22;q12)(ERG; EWS); t(7;22)(p22;q12)(ETV1;EWS); desmoplastic small round cell tumor t(11;22)(p13;q12)(WT1;EWS); extraskeletal myxoid chondrosarcoma t(9;22)(q22;q12) (TEC(CHN);EWS); malignant ectomesenchymoma t(11;22)(q24;q12)(FLI1;EWS); alveolar rhabdomyosarcoma t(2;13)(q35;q14)(PAX-3;FKHR); t(1;13) (p36;q14)(PAX-7;FKHR); myxoid and round cell liposarcoma t(12;16)(q13;p11)(CHOP;TLS(FUS)); synovial sarcoma t(X;18)(p11;q11)(SSX1&2;SYT), and others. The nature, utility, and limitations of these markers in diagnostic settings are explored.
...
PMID:Immunohistochemical and molecular genetic approaches to soft tissue tumor diagnosis: a primer. 934 17

Cultured fibroblasts from the cutaneous tissue of 16 schizophrenic patients were compared with 16 control cultured fibroblasts from the healthy subjects. The fibroblasts from the schizophrenic patients showed a decreased adhesion efficiency within 30 min after plating compared to that of the control subjects. However, after 90 min, there was no significant difference between the groups, where more than 90% of the cells from both groups had adhesed to the plate. By immunohistochemistry and western blotting using the antibodies against integrin (VLA5), talin, vinculin, fodrin, vimentin, ankyrin, plectin, fibronectin, and focal adhesion kinase (FAK), there was no significant difference in localization and amount between the groups. The amount of fibronectin released into the medium in which the fibroblast had already kept confluency showed no significant difference between the groups. However, the fibronectin content in cell lysate within 48 h after plating was significantly lower in the schizophrenic group.
...
PMID:Altered adhesion efficiency and fibronectin content in fibroblasts from schizophrenic patients. 968 89

Dendritic cells are professional antigen presenting cells that capture antigens and migrate to lymphoid tissues to elicit specific T cell responses. Here we used an in vitro differentiation system for generating highly motile dendritic cells from chicken bone marrow progenitors by employing the conditional v-Rel estrogen receptor (ER) fusion protein v-RelER. Molecular mechanisms of dendritic cell motility were investigated. Differentiation of v-relER progenitors into dendritic cells is associated with a reduction in cell-cell and cell-extracellular matrix interactions as cells acquire motility. We demonstrate that v-relER progenitors and dendritic cells express several adhesion receptors and components of adhesion complexes. Differentiation of v-relER cells was accompanied by downregulation of focal adhesion kinase (FAK), a key molecule of adhesion complexes, but ectopic FAK expression did not affect cell adhesion and motility. Interestingly, v-relER dendritic cells exhibit a polarised expression pattern of actin and vimentin, with actin being highly concentrated at the leading edge of the cells where lamellipodia are formed. FAK, paxillin and tyrosine phosphorylated proteins are found at both poles of the cell and colocalise with actin at the leading edge, while surface beta1 integrin is confined to the uropod at the rear. CD34(+ )stem cell-derived human dendritic cells also exhibited an elongated bipolar morphology, mode of migration and a polarised pattern of actin-vimentin expression similar to v-relER dendritic cells.
...
PMID:Polarised expression pattern of focal contact proteins in highly motile antigen presenting dendritic cells. 1031 61

The trabecular meshwork (TM) is a specialized eye tissue that regulates the aqueous humor outflow and controls intraocular pressure. Cells in this tissue are essential for maintenance of the outflow system. Disturbance of the TM cell status by insults such as oxidative stress may lead to elevation of the intraocular pressure and development of glaucoma. In the present study, we investigated the effect of oxidative stress on the adhesion of human TM cells to extracellular matrix (ECM) proteins. Treatment with 1 mM of H2O2 for 10 or 30 min did not affect cell viability, whereas the adhesion of TM cells to fibronectin, laminin, and collagen types I and IV was significantly reduced. Phalloidin and immunostaining also revealed reorganization of actin and vimentin structures. The level of integrins alpha5beta1, alphavbeta3, and beta1 was not altered, although the distribution of paxillin and focal adhesion kinase in focal contacts was reduced. Concomitantly, the level of transcription factor NF-kappaB was enhanced by the H2O2 treatment. Nuclear extracts of the treated cells also contained a heightened NF-kappaB binding activity. These changes persisted for up to 6 h after the H2O2 treatment but were partially recovered by 24 h. We concluded that under sublethal oxidative stress conditions, the TM cell adhesion to the ECM was impaired. The short-term loss of cell-matrix adhesiveness may be related to the rearrangement of cytoskeletal structures. Extensive and repeated oxidative stress in vivo may result in reduced TM cell adhesion, leading to cell loss, compromised TM integrity, and pathologic consequences.
...
PMID:Oxidative stress affects cytoskeletal structure and cell-matrix interactions in cells from an ocular tissue: the trabecular meshwork. 1039 88

In normal development, embryonic astrocytes progress through their cell lineage by acquiring differentiation, by apoptosis, and by proliferation. In this study, we show that embryonic astrocytes may maintain and make gains in differentiation as they simultaneously progress through one cell cycle when induced by prolactin (PRL). Prolactin induced the majority of astrocytes to incorporate bromodeoxyuridine (BrdU) with a four-fold increase over controls after 18 h of exposure. Investigating possible mitogenic signaling pathways we show for the first time that prolactin is coupled to a sustained phospholipase D (PLD) activation, with an efficacy similar to the phorbol ester and astrocytic mitogen 12-tetradecanoylphorbol-13-acetate (TPA). Both cyclosporine and suramin abolished this activation. Staurosporine and calphostin C also inhibited the PRL effect by 50%, consistent with involvement of protein kinase C-(PKC)-alpha, the major PKC isoform in astrocytes. Genistein and PP1 blocked the activation indicating additional regulation by cytosolic tyrosine kinases. This profile of PLD activation was suggestive of a PLD I isoform and a mitogenic response. Upon completion of the cell cycle, analysis of glia fibrillary acidic protein (GFAP) and vimentin abundance, and glutamine synthetase (GS) activity showed that astrocytes had gained in expression of differentiation markers. Moreover, the intensity of GFAP immunofluorescence was greater per cell, as was the length of the cell processes. In exploring the signaling for prolactin-induced differentiation we found that prolactin activated the tyrosine kinase Janus kinase (JAK) 2 and significantly stimulated tyrosine, phosphorylation of the prolactin receptor. Stat 1 and 3 were also activated presumably downstream to JAK2 activation. A rapid translocation of the cytosolic Stats over the nucleus was seen in nearly every astrocyte corresponding well with the gains in GFAP per cell. The Stats translocation did not depend on MEK-ERK inhibition by PD98059, inhibition of p38 by 1 microm SB203580, or Src kinase family inhibition by PP1. Our results demonstrate the ability of PRL to concurrently induce activation of PLD, a mitogenic signaling pathway in astrocytes, and prolonged stimulation of Stat1, compatible with the increased GFAP upregulation and cell differentiation. Considered together this data may provide an explanation on the fast gain in both numbers and differentiation in the astrocytic population during development (HD 09402, CRF).
...
PMID:Prolactin concurrently activates src-PLD and JAK/Stat signaling pathways to induce proliferation while promoting differentiation in embryonic astrocytes. 1097 48

We have derived a cell line, RE1, from a pre-implantation rat blastocyst, resembling morphologically the L2 cell line from a parietal yolk sac carcinoma of the rat, as well as parietal endoderm cell lines of the mouse. The sub-cellular organization and epithelial characteristics of RE1 cells are described. The cells express cytokeratins of simple epithelia, and vimentin; and demonstrate synthesis of proteins of the extracellular matrix, such as laminin and collagen IV. Extensive Reichert's-like basement membrane is formed by RE1 cells when grown in suspension as aggregates. Cells have a microvillous surface morphology and abundant, rough endoplasmic reticulum which is swollen with apparent secretory material. These morphological and cytochemical features are characteristic of parietal endoderm cells in vivo, and the RE1 cell line is deduced to be rat parietal endoderm. In addition, RE1 cells were examined for expression of stage-specific embryonic antigens: cells reacted with antibody against SSEA-1/TEC-1 and EMA-1, constituting the first observation of parietal endoderm cells expressing the respective epitopes. RE1-cell monolayers did not generate transepithelial resistances or potential differences in vitro, consistent with their formation of leaky epithelia. Our observations on RE1-cell morphology and ultrastructure are consistent with the occurrence of epithelial-mesenchyme transitions in culture.
...
PMID:Parietal endoderm cell line from a rat blastocyst. 1116 60


1 2 3 4 5 6 7 8 9 10 Next >>

---