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  • Life and Medical Sciences  (316)
  • General Chemistry  (128)
  • 1990-1994  (442)
  • 1905-1909  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Aluminum-Induced DNA synthesis in osteobalsts: Mediation by a G-protein coupled cation sensing mechanism (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 106-117 
    Details
    ISSN: 0730-2312
    Keywords: cation-sensing receptor ; BoPCaR ; diacyglycerol ; gadolinium ; fluoroaluminate ; de nove bone formation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Alumminium (Al3+) stimulates de novo bono formation in dogs and is a potent stimulate for DNA synthesis in non-transformed osteoblast in vitro. The recent identification of a G-protein couplked cation-sensing recepector(BoPCaR), which is activated by polycalant agonists [e.g., gadolinium (Gd3+) 〉 neomycin 〉 calcium(CA3+)], suggests that a similer physiologically inportant cation sensing receptor may be presant in obsoblasts and pharmacologically activated by Al3+. To evalute that possibility, we assessed whether known as BoPCaR agonists on DNA synthesis in a dose-dependent fashion, achiving 50% effective extracelluler concennetration (EC50) of 10 μM, 30 μM, 60 μM, and 2.5 mM, respectively. Al3+ displayed non-additive effect on DNA sunthesis with the BoPCAaR agonists as well as an unrelated G-porotien coupled receptor agonists, PGF2α, suggesting shared mechenisms of action. In contrast, the recepator tyrosine kinse agonist, IGF-1(10 ηg/ml), displayed additive proliferative effects when comboined with AlCl3, inducating distinct signalling pathways. AlCl3 (25 μM) induced DAG levels 2-fold and the phosphorylation of the myristoylated alanine-rich C kinase (MARKS) substrates 4-fold, but did not increase intracelluler calcium concenitrations. Doen-regardation of PKC by pre-treatment with phorbol 12-myristate 13-acetate as well as PKC inhebitation by H-7 and staurosporine blocked Al3+ -inducing DNA synthesis. Finally, Al3+, Gd3+, nemomycin, and Ca2+ activated G-proteins inn osteoblast membrans as evidenced by increased colvant binding pf [32P]-GTP-azidoanilide to putaitve Gα subunits. Our findings suggests that Al3+ stimulates DNA synthesis in ostoblasts through a cation sansing mechnism coupled to G-protein activation and signalling cascades involvings DAG and PCK- dependent pathways.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560115
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  • 2
    Electronic Resource
    Electronic Resource
    Myosin IB null mutants of Dictyostelium exhibit abnormalities in motility (1991)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 20 (1991), S. 301-315 
    Details
    ISSN: 0886-1544
    Keywords: DMIB- cells ; F-actin ; cAMP ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Cellular and intracellular motility are compared between normal Dictyostelium amoebae and amoebae lacking myosin IB (DMIB-). DMIB- cells generate elongated cell shapes, form particulate-free pseudopodia filled with F-actin, and exhibit an anterior bias in pseudopod extension in a fashion similar to normal amoebae. DMIB- cells also exhibit a normal response to the addition of the chemoattractant cAMP, including a depression in cellular and intracellular particle velocity, depolymerization of F-actin in pseudopodia, and a concomitant increase in cortical F-actin. DMIB- cells do, however, form lateral pseudopodia roughly three times as frequently as normal cells, turn more often, and exhibit depressed average instantaneous cell velocity. DMIB- cells also exhibit a decrease in the average instantaneous velocity of intracellular particle movement and an increase in the degree of randomness in particle direction. These findings indicate that if there is functional substitution for myosin IB by other myosin I isoforms, it is at best only partial, with myosin IB being necessary for maintenance of the normal rate and persistence of cellular translocation, suppression of lateral pseudopod formation and subsequent turning, rapid intracellular particle motility, and the normal anterograde bias of intracellular particle movement. Furthermore, it is likely that the behavioral abnormalities observed here for DMIB- cells underlie the delay in the onset of chemotactic aggregation, the increase in the time required to complete streaming, and the abnormalities in morphogenesis exhibited by DMIB- cells.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970200406
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  • 3
    Electronic Resource
    Electronic Resource
    Actin dynamics during the cell cycle in Chlamydomonas reinhardtii (1992)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 22 (1992), S. 117-126 
    Details
    ISSN: 0886-1544
    Keywords: algae ; cell division ; cytokinesis ; mitosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We have used two monoclonal antibodies to demonstrate the presence and localization of actin in interphase and mitotic vegetative cells of the green alga Chlamydomonas reinhardtii. Commercially available monoclonal antibodies raised against smooth muscle actin (Lessard: Cell Motil. Cytoskeleton 10:349-362, 1988; Lin: Proc. Natl. Acad. Sci. USA 78:2335-2339, 1981) identify Chlamydomonasactin as a ∼43,000-Mr protein by Western immunoblot procedures. In an earlier study, Detmers and coworkers (Cell Motil. 5:415-430, 1985) first identified Chlamydomonas actin using NBD-phallacidin and an antibody raised against Dictyostelium actin; they demonstrated that F-actin is localized in the fertilization tubule of mating gametes. Here, we show by immunofluorescence that vegetative Chlamydomonas cells have an array of actin that surrounds the nucleus in interphase cells and undergoes dramatic reorganization during mitosis and cytokinesis. This includes the following: reorganization of actin to the ante- rior of the cell during preprophase; the formation of a cruciate actin band in prophase; reorganization to a single anterior actin band in metaphase; rearrange- ment forming a focus of actin anterior to the metaphase plate; reextension of the actin band in anaphase; presence of actin in the forming cleavage furrow during telophase and cytokinesis; and finally reestablishment of the interphase actin array. The studies presented here do not allow us to discriminate between G and F-actin. None the less, our observations, demonstrating dynamic reorganization of actin during the cell cycle, suggest a role for actin that may include the movement of basal bodies toward the spindle poles in mitosis and the formation of the cleavage furrow during cytokinesis. © 1992 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970220205
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  • 4
    Electronic Resource
    Electronic Resource
    The esem used to image crystalline structures of polymers and to image ink on paper (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Microscopy Research and Technique 25 (1993), S. 384-392 
    Details
    ISSN: 1059-910X
    Keywords: Spherulite ; Polymer etching ; Deinking ; Paper recycling ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Natural Sciences in General
    Notes: This article describes two cases in which the advantages of the ESEM have been exploited in unanticipated ways. First, we have found that etching occurs as the electron beam scans the surface of uncoated polymers in the ESEM. The surface topography caused by this etching, as seen in ESEM images, reflects the morphology of crystalline structures in the polymers. This technique has been valuable in the study of such textures in polymers. The second application is related to our use of the ESEM in support of research on the deinking of paper. In this effort we have learned that an unconventional contrast mechanism can be used during ESEM imaging to distinguish between inked and non-inked areas of newsprint. Under usual operating conditions, ESEM imaging does not distinguish between inked and non-inked areas. However, at relatively low sample chamber pressures the non-inked areas appear brighter than inked areas in ESEM images. © 1993 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jemt.1070250506
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  • 5
    Electronic Resource
    Electronic Resource
    Preservation and visualization of the sea urchin embryo blastocoelic extracellular matrix (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Microscopy Research and Technique 22 (1992), S. 11-22 
    Details
    ISSN: 1059-910X
    Keywords: Rapid freezing ; Freeze-substitution fixation ; Confocal microscopy ; Blastocoel ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Natural Sciences in General
    Notes: Several methods were utilized to visualize the structure and orientation of the blastocoelic extracellular matrix (ECM) in Strongylocentrotus purpuratus embryos at the mesenchyme blastula stage. Rapid freezing in liquid propane cooled to LN2 temperatures followed by freeze substitution was used to preserve the ECM without shrinkage due to dehydration. Scanning, transmission, and light microscopy were employed to elucidate the ECMs' structure. The blastocoelic ECM consisted of parallel fibrillar sheets that were interconnected by finer filaments and oriented along the animal-vegetal axis. The ECM completely filled the blastocoelic cavity as viewed by scanning electron microscopy. The basal lamina could be distinguished from the blastocoelic ECM as a thin coat on the plasma membrane of epithelial cells; the ECM was in contact with this coat. In contrast, the blastocoelic ECM attached directly to the plasma membrane of primary mesenchyme cells (PMC) which did not possess a basal lamina. The blastocoelic ECM was isolated as an intact “bag” and probed in a hydrated state with Con A and alcian blue. Confocal microscopy confirmed that the entire blastocoel was filled with a fibrillar ECM. These approaches offer advantages for future studies of the ECMs of sea urchin embryos and their roles in gastrulation. © 1992 Wiley-Liss, Inc.
    Additional Material: 14 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jemt.1070220104
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  • 6
    Electronic Resource
    Electronic Resource
    Guanine nucleotide binding regulatory proteins in liver from obese humans with and without type II diabetes: Evidence for altered “cross-talk” between the insulin receptor and Gi-proteins (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 54 (1994), S. 309-319 
    Details
    ISSN: 0730-2312
    Keywords: diabetes ; G proteins ; insulin ; obesity ; insulin receptors ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A novel pathway for physiological “cross-talk” between the insulin receptor and the regulatory Gi-protein has been demonstrated. We tested the hypothesis that a coupling defect between Gi and the insulin receptor is present in the liver of obese patients with and without type li diabetes. Insulin 1 × 10-9 M (∼ ED50) and 1 × 10-7 M (Max) inhibited pertussis toxin-catalyzed ADP ribosylation of Gi in human liver plasma membranes from lean and obese nondiabetic patients. However, 1 × 10-7 M insulin was without effect in membranes from patients with type II diabetes. This coupling defect was not intrinsic to Gi, since Mg2+ and GTPγS inhibited pertussis toxin-catalyzed ADP ribosylation in both diabetic and nondiabetic patients. Binding of insulin of the α-subunit and activation of the tyrosine kinase intrinsic to the β-subunit of the insulin receptor are not responsible for the coupling defect. 125I insulin binding is the same in obese patients with or without diabetes. Tyrosine kinase of the insulin receptor is decreased in diabetes. However, a monoclonal antibody to the insulin receptor (MA-20) at equimolar concentrations with insulin equally inhibits pertussis toxin-catalyzed ADP ribosylation of Gi without activating tyrosine kinase or insulin receptor autophosphorylation. Immunodetection of G-proteins suggested that Gi3α was normal in diabetes and Gi1-2α was decreased by 40% in the diabetic group as compared to the obese nondiabetic group but was normal when compared to the lean non diabetic group. We conclude that the novel pathway of insulin signaling involving the regulatory Gi proteins via biochemical mechanisms not directly involving the tyrosine kinase of the insulin receptor is altered in obese type II diabetes and offers a new target for the search of the mechanism(s) of insulin resistance.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240540307
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  • 7
    Electronic Resource
    Electronic Resource
    Regulation of TGF-α expression in human keratinocytes: PKC-dependent and -independent pathways (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 151 (1992), S. 326-336 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Transforming growth factor-α (TGF-α) is an autocrine growth factor for epidermal keratinocytes that can induce its own expression (autoinduction). Because the regulation of this process may be important for the control of epidermal growth, we examined the roles of EGF receptor tyrosine kinase and protein kinase C (PKC) in TGF-α autoinduction in cultured human keratinocytes. Antiphosphotyrosine immunoblot analysis demonstrated that EGF and TGF-α rapidly and markedly stimulated tyrosine phosphorylation of a 170 kDa protein in growth factor-deprived keratinocytes. This protein was identified as the EGF receptor by immuno-precipitation using anti-EGF receptor mAbs. Tyrosine phosphorylation and TGF-α mRNA accumulation in response to EGF and TGF-α were both inhibited by a monoclonal antibody against the EGF receptor and by the EGF receptor tyrosine kinase inhibitor RG50864, demonstrating the involvement of the tyrosine kinase activity of the receptor in TGF-α autoinduction. The monoclonal antibody inhibited keratinocyte growth and TGF-α autoinduction with similar potency (IC50 ∼ 0.1 μg/ml). TGF-α and the PKC activator tetradecanoyl phorbol 12-myristyl, 13-acetate (TPA) had similar effects on TGF-α steady-state mRNA levels, suggesting that PKC activation might be a downstream mediator of TGF-α autoinduction. However, down-regulation of more than 90% of keratinocyte PKC activity by bryostatin pretreatment abrogated the induction of TGF-α mRNA in response to TPA without affecting the autoinductive response or EGF-stimulated tyrosine phosphorylation. These results indicate that EGF receptor and PKC stimulate TGF-α gene expression by different pathways, and suggest that PKC is not required for TGF-α autoinduction in this system. Moreover, the fact that EGF-stimulated tyrosine phosphorylation and TGF-α autoinduction were not potentiated after PKC down-regulation suggests that PKC does not exert a tonic inhibitory influence on EGF receptor tyrosine kinase activity in normal human keratinocytes. © 1992 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041510214
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  • 8
    Electronic Resource
    Electronic Resource
    Transforming growth factor beta inhibits plasminogen activator (PA) activity and stimulates production of urokinase-type PA, PA inhibitor-1 mRNA, and protein in rat osteoblast-like cells (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 149 (1991), S. 34-43 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Transforming growth factor(β)(TGFβ) treatment of rat osteoblast-rich calvarial cells or of the clonal osteogenic sarcoma cells, UMR 106-01, resulted in dosedependent inhibition of plasminogen activator (PA) activity, and increased production of 3.2 kb mRNA and protein for PA inhibitor-1 (PAI-1). Although tissue-type PA(tPA) protein was not measured, TGF(β)did not influence production of mRNA for tPA. Production of 2.3 kb mRNA for urokinase-type PA (uPA) was also increased by TGF(β)in a dose-dependent manner. The effects of TGFβ on synthesis of mRNA for PAI-1 and uPA were maintained when protein synthesis was inhibited, and were abolished by inhibition of RNA synthesis. Although uPA had not been detected previously as a product of rat osteoblasts, treatment of lysates of osteoblast-like cells with plasmin yielded a band of PA activity on reverse fibrin autography, corresponding to a low Mr form of uPA. Untreated conditioned media from normal osteoblasts or UMR 106-01 cells contained no significant TGFβ activity, but activity could be detected in acidified medium. Treatment of conditioned media with plasmin resulted in activation of approximately 50% of the TGFβ detectable in acidified media. The results identify several effects of TGFβ on the PA-PA inhibitor system in osteoblasts. Net regulation of tPA activity through the stimulatory actions of several calciotropic hormones and the promotion of PAI-1 formation by TGFβ could determine the amount of osteoblast-derived TGFβ activated locally in bone. Stimulation of osteoblast production of mRNA for uPA could reflect effects on the synthesis of sc-uPA, a precursor for the active form of the enzyme.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041490106
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  • 9
    Electronic Resource
    Electronic Resource
    Plasminogen-dependent activation of latent transforming growth factor beta (TGFβ) by growing cultures of osteoblast-like cells (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 157 (1993), S. 528-534 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Osteoblasts secrete transforming growth factor beta (TGFβ) as a biologically inert, latent complex that must be dissociated before the growth factor can exert its effects. We have examined the production and proteolytic activation of latent TGFβ (LTGFβ) by clonal UMR 106-01 rat osteosarcoma cells and neonatal mouse calvarial (MC) osteoblast-like cells in vitro. Synthetic bPTH-(1-34) increased the activity of tissue-type (tPA) and urokinase-type (uPA) plasminogen activators (PA) in cell lysates (CL) of UMR 106-01 cells. The concentration of active TGFβ in serum-free CM from cultures treated with bPTH-(1-34) and plasminogen was significantly greater than in CM from untreated controls and cultures treated with either bPTH-(1-34) or plasminogen alone. This effect occurred at concentrations of PTH-(1-34) that increased PA activity and was prevented by aprotinin, an inhibitor of plasmin activity. Treatment with bPTH-(1-34) had no effect on the concentration of TGFβ in acid-activated samples of CM. Functional consequences of proteolytically activated TGFβ was examined in primary cultures of neonatal MC osteoblast-like cells. Human platelet TGFβ1 caused a dose-dependent increase in the migration of these cells in an in vitro wound healing assay. Cell migration was also stimulated in cultures treated with bPTH-(1-34) and plasminogen together. This effect was blocked by an anti-TGFβ1 antibody. The results of these studies demonstrate that (1) LTGFβ secreted by osteoblasts in vitro is activated under conditions where the plasmin activity in the cultures is increased, and (2) the TGFβ generated by plasmin-mediated proteolysis is biologically active. We suggest that the local concentration of TGFβ in bone may be controlled by the osteoblast-associated plasminogen activator/plasmin system. Furthermore, since several calciotropic factors influence osteoblast PA activity, this system may have an important role in mediating their anabolic and/or catabolic effects. © 1993 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041570312
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  • 10
    Electronic Resource
    Electronic Resource
    Plasminogen activator regulation in osteoblasts: Parathyroid hormone inhibition of type-1 plasminogen activator inhibitor and its mRNA (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 152 (1992), S. 346-355 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In order to determine the mechanism by which parathyroid hormone (PTH) stimulates plasminogen activator (PA) activity in rat osteoblasts, we investigated the effect of human PTH(1-34) [hPTH(1-34)] on the synthesis of mRNAs for tissue-type PA (tPA), urokinase-type PA (uPA), and PA inhibitor-1 (PAI-1), and on release of PA activity and PAI-1 protein in both normal rat calvarial osteoblasts and UMR 106-01 osteogenic sarcoma cells. hPTH(1-34) (0.25-25 nM) decreased PAI-1 mRNA and protein, and increased PA activity in both cell types in a dose-dependent manner with ED50 of about 1 nM for both responses. Forskolin and isobutylmethylxanthine also stimulated PA activity and decreased PAI-1 protein and mRNA in both cell types. hPTH(1-34) did not show any consistent effect on tPA and uPA mRNA in calvarial osteoblasts, but a modest (two-fold) increase of both mRNAs was observed in UMR 106-01 cells treated with 25 nM hPTH(1-34). However, when protein synthesis was inhibited with 100 μM cycloheximide, the increase of tPA and uPA mRNA by hPTH(1-34) was enhanced in UMR 106-01 cells and became evident in calvarial osteoblasts. Fibrin autography also revealed that hPTH(1-34) increases tPA and uPA activity, especially after cycloheximide treatment in UMR 106-01 cells. These results strongly suggest that PTH increases PA activity predominantly by decreasing PAI-1 protein production through a cyclic adenosine monophosphate (cAMP)-dependent mechanism in rat osteoblasts. The reduction of PAI-1 protein by PTH results in enhanced action of both tPA and uPA, and would contribute to the specific roles of these PAs in bone. © 1992 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041520216
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