ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Cell & Developmental Biology  (18)
  • Wiley-Blackwell  (18)
  • American Geophysical Union
  • PANGAEA
  • Springer
  • 1990-1994  (18)
  • 1993  (18)
Collection
Keywords
Publisher
  • Wiley-Blackwell  (18)
  • American Geophysical Union
  • PANGAEA
  • Springer
Years
  • 1990-1994  (18)
Year
  • 1
    Electronic Resource
    Electronic Resource
    PKC mediates 12(S)-HETE-induced cytoskeletal rearrangement in B16A melanoma cells (1993)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 26 (1993), S. 49-65 
    Details
    ISSN: 0886-1544
    Keywords: fatty acid ; MHC ; MLC ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The fatty acid 12(S)-HETE may be a new second messenger capable of activating PKC. In tumor cells 12(S)-HETE stimulates cytoskeleton-dependent cellular responses such as adhesion and spreading. Analysis of 12(S)-HETE effects on B16a melanoma cell cytoskeleton revealed reversible rearrangement of microtubules, microfilaments, the actin-binding proteins, vinculin, myosin heavy (MHC) and light chains (MLC), as well as bundling of vimentin intermediate filaments. The alterations in microfilaments and intermediate filaments occurred very rapidly, i.e., 5 min after exposure of tumor cells to 12(S)-HETE. The 12(S)-HETE-induced cytoskeletal alterations were accompanied by centrifugal organelle-translocation. Interestingly, MLC exhibited clear association with the cytoplasmic organelles. Biochemical analysis of the 12(S)-HETE effect indicated a PKC-mediated reversible hyperphosphorylation of MLC, vimentin, and a 130 kD cytoskeletal-associated protein. Optimal effects were obtained after 5 min treatment with 12(S)-HETE at 0.1 μM concentration. 12(S)-HETE pretreatment induced tumor cell spreading on a fibronectin matrix which required the intactness of all three major cytoskeletal components. The spreading process was dependent upon the activity of PKC. Our data suggest that 12(S)-HETE is a physiological stimulant of PKC. Further, it induces rearrangement of the cytoskeleton of tumor cells in interphase resulting in the stimulation of cytoskeleton-dependent cell activity such as spreading. © 1993 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970260106
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Computerized analysis of tumor cells flowing in a parallel plate chamber to determine their adhesion stabilization lag time (1993)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 26 (1993), S. 88-98 
    Details
    ISSN: 0886-1544
    Keywords: transglutaminase ; melanoma ; digital image analysis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The importance of cell adhesion in a variety of physiological phenomena requires development of an understanding of the factors and molecular mechanisms underlying these behaviors. Cell adhesion is a multistep process involving primary receptor-ligand interactions followed by secondary events that may lead to the formation of focal contacts. Due to the lack of well-defined assays to study adhesion stabilization, little is known about this process, except that it may involve signaling events, receptor recruitment, and, as we have demonstrated, covalent peptide cross-linking by cell membrane-associated transglutaminase [Menter et al.: Cell Biophys. 18:123-143, 1992]. To study the stabilization process we have developed a dynamic assay employing a parallel plate flow chamber coupled with video microscopy and digital image processing. Our studies utilize wheat germ agglutinin-selected human metastatic melanoma cell variants that exhibit differences in their experimental metastatic potential and expression of transglutaminase. Using this assay, quantifying cell-substrate stabilization was found to be quick, reliable, reproducible, and useful in evaluating agents that block this process. © 1993 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970260109
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Colchicine-induced stimulation of PMN motility related to cytoskeletal changes in actin, α-actinin, and myosin (1993)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 25 (1993), S. 10-18 
    Details
    ISSN: 0886-1544
    Keywords: microtubules ; blebs ; locomotion ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Colchicine-induced stimulation of polymorphonuclear leukocyte (PMN) locomotion is an interesting model because extension of blebs at the front occurs at a rate (about 2.4 μm/s) which is far above that reported for growth of actin filaments. The following cytoskeletal changes were observed in colchicine-treated PMNs: (1)a small increase in cytoskeleton-associated actin was noted, as well as a somewhate more pronounced increase in cytoskeleton-associated α-actinin, as compared with untreated or DMSO-treated controls. There was, however, no measurable increase in F-actin as determined by NBD-phallacidin blinding; (2)the values for the ratio (α-actinin/actin) are lower in PMNs treated with colchicine for 30 min, as compared with PMNs stimulated with fNLPNTL for 1 minute (non-polar ruffling cells) or 30 min (polarized locomoting cells); thus, this ratio may depend on the type of PMN motility; (3) in polarized PMNs F-actin was mainly located linearly all along the cell membrane; there was more intense staining at the front of the cells; (4) α-actining appeared to colocalize with F-actin at the leading front, but not with F-actin at the tail of polarized cells; (5) myosin was preferentially found at the rear part of polarized cells but not or only to a small extent at the front. Our data indicate a close functional correlation between microtubules and microfilaments. We speculate that F-actin in combination with α-actinin promotes expansion of pseudopods, whereas myosin combined with F-actin promotes contraction. In more general terms we suggest that different forms of PMN motility are generated by differential selective interaction of cytoskeletal compnents and variations in the composition of the cytoskeleton in different sites of the same cells. © 1993 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970250103
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Extracellular annexin II is associated with divalent cation-dependent tumor cell-endothelial cell adhesion of metastatic RAW117 large-cell lymphoma cells (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 265-276 
    Details
    ISSN: 0730-2312
    Keywords: calpactin ; lipocortin ; tumor metastasis ; liver endothelium ; tumor cell implantation ; cell surface ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Using fixed microvessel endothelial cell monolayers the molecules involved in the adhesion of liver-preferring murine RAW117 large cell lymphoma cells to murine liver-derived microvessel endothelial cells were identified by affinity isolation. Detergent lysates obtained from poorly (P) or highly (H10) liver-metastatic cells inhibited RAW117-H10 cell adhesion to hepatic sinusoidal endothelial (HSE) cell monolayers. Allowing detergent lysates of cell surface-labeled RAW117 cells to bind to fixed HSE cell monolayers and eluting the bound components indicated that several tumor cell surface molecules ( ∼ 70, ∼ 35, ∼ 32, ∼ 22, and ∼ 14 kDa) might be involved in RAW117 cell-HSE cell adhesion. The ∼ 35 kDa component was cation dependent in its binding to target HSE cells. Increasing detergent concentration had no effect on binding of the ∼ 35 kDa component to HSE cell monolayers, whereas treatment with 0.5 M NaCl resulted in its selective elution from HSE cells. Incubation of the HSE cell monolayers with detergent lysates from cell surface-labeled RAW117-H10 cells resulted in selective depletion of the ∼ 35 kDa component, suggesting that the binding is saturable. This divalent cation-dependent molecule is one of the major tumor cell surface components bound by several types of endothelial cells and murine hepatocytes, whereas there was poor binding of this component to unfixed or fixed human red blood cells. The purified, partially ( ∼ 40%) sequenced molecule had amino acid sequence identity with murine but not bovine annexin II, indicating that it was not bound from the bovine serum used to grow RAW117 cells. Using antibodies specific for annexin II flow cytometery indicated equivalent amounts of annexin II are expressed on RAW117 cell surfaces in the absence or presence of excess EDTA, whereas annexin I was only found in low amounts on the surfaces of RAW117 cells. Annexin II antibodies inhibited by ∼ 40-50% the adhesion of RAW117 tumor cells to live or fixed endothelial cells, and purified tumor cell surface fractions containing the ∼ 35 kDa component partially inhibited ( ∼ 35%) RAW117 cell-HSE cell adhesion. The data indicate that annexin II is expressed on the extracellular surface of RAW117 cells, and cell surface-annexin II mediates a portion of the Ca2+-dependent RAW117 cell adhesion to liver microvessel endothelial cells.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240530311
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Metabolic activation, DNA adducts, and H-ras mutations in human neoplastic and non-neoplastic laryngeal tissue (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 129-137 
    Details
    ISSN: 0730-2312
    Keywords: Cytochrome P-450 ; N-acetyltransferase ; 32P-postlabelling ; H-ras mutations ; larynx ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Metabolic activation, DNA adducts, and H-ras mutations were examined in human laryngeal tissue (n = 16) from both smoker and non/ex-smoker patients with laryngeal cancer. DNA adducts detected by 32P-postlabelling were evident only in smokers (n = 13); in fact, smoking cessation for as little as 10 months resulted in no DNA adducts detected (n = 3). Total DNA adduct levels in these samples were significantly correlated with levels of cytochromes P-4502C and 1A1 in laryngeal microsomes. Moreover, the P-4501A1 levels represent the highest yet found in human tissues. In contrast, laryngeal microsomes did not have detectable P-4501A2 activity, while laryngeal cytosols showed appreciable N-acetyltransferase activity for p-aminobenzoic acid (NAT1) but not sulfamethazine (NAT2).DNA was extracted from laryngeal specimens and amplified by PCR. Nylon filter dot or slot blots were hybridized with 32P-labelled probes for codons 12, 13, and 61 of the H-ras gene. Sixty percent of specimens demonstrated mutations in either codon 12, 13, or 61; a single common and specific mutation was a Gln → Glu transversion in codon 61. This mutation appeared in 5 laryngeal specimens, all from smokers.These results implicate cigarette smoke components, bioactivated by CYP1A1 and/or CYP2C, in DNA adduct formation. These results also demonstrate a probable smoking-related H-ras Gln → Glu transversion in codon 61.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531018
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    The chemoprevention of breast cancer by reducing sex steroid exposure: Perspectives from epidemiology (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 26-36 
    Details
    ISSN: 0730-2312
    Keywords: Breast cancer ; chemoprevention ; estrogen ; oral contraceptives ; progestogen ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Mitogenesis is a major driving force in neoplastic development. Blocking the effect of breast cell mitogens by reducing the actual exposure of the breast to these mitogens is an obvious strategy for breast cancer prevention. The ovarian hormones, estrogens and progesterone, are major effective (direct or indirect) breast cell mitogens. A woman's exposure to ovarian estrogens and progesterone is drastically reduced by the use of combination-type oral contraceptives (COCs), but the synthetic estrogen and progestogen in the COCs effectively replace ovarian estrogens and progesterone, so that breast cell exposure to these hormones is not decreased. Doses of estrogen and progestogen in modern COCs are close to the minimum attainable while still retaining both contraceptive efficacy and ovarian suppression (so that endogenous estrogen and progesterone do not add to the dose of estrogen and progestogen from the COC). Considerably lower effective breast cell exposure to estrogen and progestogen can, however, be achieved by using a gonadotropin-releasing hormone agonist (GnRHA) to suppress ovarian function and compensate for the resulting hypoestrogenemia with low-dose hormone replacement therapy. Compared to modern COCs, estrogen exposure can be reduced by approximately 60%, and progestogen dose by more than 80%. Such a contraceptive is predicted to reduce lifetime breast cancer risk by more than 50% if used for 10 years. The possibility that a practical contraceptive could achieve such a major benefit is shown by the dramatic decline in the incidence of both ovarian and endometrial cancer in young women in the U.S. over the last 3 decades - a direct result of COC use.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531105
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Chemoprevention of rat mammary carcinogenesis: Exceptional activity of dietary dehydroepiandrosterone (DHEA) (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 253-254 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A major determinant of progress in human breast cancer prevention is the identification of agents with significant anticarcinogenic activity and acceptable levels of toxicity in experimental animals. Over the past 20 years, more than 50 experimental regimens have been shown to have significant chemopreventive activity in the rat mammary gland. The most effective approaches to mammary cancer chemoprevention in rats involve surgical endocrine ablations such as bilateral ovariectomy. However, prophylactic surgical ablations are unlikely to be acceptable to the majority of the general public. All chemicals evaluated to date are less effective, and none has been shown to reduce mammary cancer incidence to zero. As a result, efforts continue to identify chemical agents whose protective activity is comparable to that of endocrine ablation. DHEA is an adrenal steroid with chemopreventive activity in several animal models for human cancer. In the present studies, the chemopreventive efficacy of DHEA was evaluated in rats exposed to the mammary gland carcinogen, N-methyl-N-nitrosourea (MNU). Groups of 20 female Sprague-Dawley rats were fed an AIN-76A diet supplemented with 0, 400, or 800 mg DHEA per kg diet; one week later, all rats received a single i.p. injection of 35 mg MNU per kg body weight. Animals were palpated weekly to monitor mammary tumor development, and all mammary tumors were histologically confirmed. When administered at 800 mg/kg diet, DHEA reduced mammary cancer incidence in controls from 95% to 15%; carcinoma multiplicity in rats receiving 800 mg DHEA per kg diet was reduced by more than 85% from control levels. In a separate study, the 400 mg/kg diet dose of DHEA reduced the incidence of mammary cancer to 5% from 80% found in controls fed the basal diet. Reductions in mammary cancer incidence and multiplicity associated with DHEA administration were accompanied by large increases in cancer latency. Evaluation of mammary gland wholemounts from animals fed DHEA demonstrated a massive induction of lobuloalveolar differentiation. These results indicate the dietary supplementation with non-toxic dose levels of DHEA has chemopreventive efficacy approaching that of endocrine ablation. This protection may be mediated by the induction of differentiation in the mammary gland, during which sensitive mammary parenchymal structures (terminal end buds) are stimulated to develop into structures (alveolar buds) less sensitive to carcinogenic insult.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531154
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Protein kinase C: Mediator or inhibitor of insulin action? (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 52 (1993), S. 8-13 
    Details
    ISSN: 0730-2312
    Keywords: signal transduction ; metabolism ; diabetes ; PKC ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The role of protein kinase C in insulin signal transduction i s controversial It has been postulated that protein kinase C i s activated by insulin and that the kinase i s directly involved in insulin-mediated metabolic processes. In opposition to this view i s the hypothesis that protein kinase C is not activated by insulin and, more importantly, may be responsible for attenuation of the insulin signal The evidence for and against protein kinase C as a mediator of the insulin signal will be put in perspective followed by discussion of the possible role of the kinase in the pathogenesis of insulin resistance in type II diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240520103
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    DNA repair and repair fidelity in metastatic variants of the B16 murine melanoma (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 51 (1993), S. 336-344 
    Details
    ISSN: 0730-2312
    Keywords: DNA repair ; repair fidelity ; genomic instability ; metastasis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We have examined the concept of genomic instability in relation to the metastatic progression of low (F1) and high metastasis (BL6, ML8) clones of the B16 mouse melanoma, by using a mutation assay, and DNA strand break repair and repair fidelity assays. The frequency of induced ouabain resistant colonies between the variant cell lines was consistent with the difference between their metastatic properties. Survival data for X-irradiation and bleomycin were similar among the 3 cell lines. When X-rays or bleomycin were used to induce strand breakage, no difference was detectable in either the rate or extent of DNA repair using the techniques of alkaline unwinding and alkaline elution for total strand breaks, and neutral elution for double strand breaks. DNA repair fidelity was measured using the PMH16 plasmid. A Kpn I restriction site was used to introduce a break within the gpt gene of the plasmid, prior to transfection. We found that ∼ 100% and ∼ 65% of the highly metastatic ML8 and BL6 clones, respectively, religated the gene with the required fidelity, compared with only ∼ 25% of the low metastasis F1 clones. In summary, the metastatic variants show similar sensitivities to X-irradiation and bleomycin, but a differential response to EMS. This difference is not reflected in any subsequent DNA strand break religation, but the variants do differ in their fidelity of repair. However, although the fidelity of DNA religation is related to metastatic potential, it is not consistent with the mutation frequency data. © 1993 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240510313
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Cytochemical characterization of the hemocytes of Leucophaea maderae (Dictyoptera: Blaberoidea) (1993)
    New York, NY : Wiley-Blackwell
    Journal of Morphology 218 (1993), S. 115-126 
    Details
    ISSN: 0362-2525
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A correlated morphological and cytochemical approach to the hemocytes in Leucophaea maderae characterizes the granule contents of blood cells with May Grunwald-Giemsa (MGG), periodic acid-Schiff (PAS), Alcian blue (AB), and Sudan black B stainings, and after fluorochroming with acridine orange (AO). The cell nucleus and nuclear DNA is demonstrated with the Feulgen reaction. The activities of α-naphtyl butyrate esterase (ANBE) and acid phosphatase (AcPase) have been investigated in hemocytes, by both light and electron microscopy. The study discloses five cells types: prohemocyts, plasmatocytes, granulocytes, spherulocytes, and cytocytes. Occasional Sudan black-positive cells could represent an adipohemocyte category. The different patterns of cytochemical staining suggest a variety of functional roles for hemocytes. The most selective reaction pattern in terms of cytological differentiation among hemocytes occurred with the ANBE reaction. Ultrastructural analysis of intercellular granule contents, and the demonstration of cells with intermediate features, suggests that the hemolymph of Leucophaea maderae contains a developmental series from prohemocyte to plasmatocyte to granulocyte and then to spherulocyte. © 1993 Wiley-Liss, Inc.
    Additional Material: 21 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jmor.1052180202
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...