2 edition of Resistance to cytochalasins in mouse erythroleukaemic cells. found in the catalog.
Resistance to cytochalasins in mouse erythroleukaemic cells.
Rosemary Anne Neill
Written in English
Thesis (Ph. D.)--The Queen"s University of Belfast, 1984.
|The Physical Object|
Cytochalasins D (60 microM) and H (30 microM) were found to be most suited for fast and reversible inhibition of actin-based motility, while cytochalasins A and E arrested streaming at lower. Bioassay-guided fractionation of an EtOAc extract of the broth of the endophytic fungus Nemania sp. UM10M (Xylariaceae) isolated from a diseased Torreya taxifolia leaf afforded three known cytochalasins, 19,epoxycytochalasins C (1) and D (2), and deoxy,epoxy-cytochalasin C (3). All three compounds showed potent in vitro antiplasmodial activity and phytotoxicity with no Cited by: 4.
SPANDIDOS DA and Paul J: Transfer of human globin genes to erythroleukaemic mouse cells. EMBO Journal 1: , SPANDIDOS DA, Harrison PR and Paul J: Replication and amplification of recombinant plasmid molecules as extra chromosomal elements in transformed mammalian cells. Experimental Cell Research , Melanoma, one of the aggressive cancers, is known to be resistant to chemotherapy. Because of its aggressive nature, effectively inducing apoptosis is necessary to treat melanoma. Erythroid differentiation regulator 1 (Erdr1) is known to be a stress-related survival factor exhibiting anti-cancer effects in several cancers. However, little is known about the functions and underlying mechanisms Cited by: 6.
/cell, represents approximately 85% of the total sat- urable binding, displays a broad specificity interacting with cytochalasins C, D, and E, is not displaceable by D-glucose, is located mostly in a cytosol fraction, and exists in intimate relation to cytoskeletal actin. M site shows a Kd of 2 to 4 X M and Bt of 5 to 8 X /cell. Apoptotic resistance is the main obstacle for treating cancer patients with chemotherapeutic drugs. Multidrug resistance (MDR) is often characterized by the expression of P-glycoprotein (P-gp), a KD ATP-dependent drug efflux protein. Functional P-gp can confer resistance to activate caspase-8 and -3 dependent apoptosis induced by a range of different stimuli, including tumor necrosis and Cited by: 2.
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Resistance to cytochalasins in mouse erythroleukaemic cells Author: Neill, R. ISNI: Awarding Body: Queen's University Current Institution: Queen's University Belfast Date of Award: Availability of Full Text: Full text unavailable from EThOS.
It is proposed, therefore, that chloramphenicol resistance is a cytoplasmically inherited characteristic in this mouse cell line. Full text Get a printable copy (PDF file) of the complete article (K), or click on a page image below to browse page by by: Cytochalasins appear to preferentially damage malignant cells, as shown by their minimal effects on normal epithelial and immune cells.
Further, cytochalasins influence the end stages of mitosis, suggesting that such agents could be combined with microtubule-directed agents to elicit a profound synergistic effect on malignant by: cell resistance to cytotoxic T cells in mice Tangying Lu, 1 Rupal Ramakrishnan, Soner Altiok,2 Je-In Youn,1 Pingyan Cheng, 1 Esteban Celis, Vladimir Pisarev,3,4 Simon Sherman,3 Michael B.
Sporn,5 and Dmitry Gabrilovich1 1Department of Immunology and 2Department of Pathology, H. Lee Moffitt Cancer Center, Tampa, Florida, USA.
In Medical Cell Biology (Third Edition), Inhibitors of Actin-Based Function. Cytochalasins, a group of chemicals excreted by various molds, block cell cytochalasins bind to the plus end of microfilaments; block further polymerization; and inhibit cell motility, phagocytosis, microfilament-based trafficking of organelles and vesicles, and the production of lamellipodia and.
Cytochalasins are fungal toxins, well established inhibitors of actin polymerization and have been extensively used in studies of the cytoskeleton. 47 Different cytochalasins including cytochalasin D have been described to have antitumor capacities which probably can be explained by the rapid proliferation cycle of malignant cells, 49, 50 Author: Lisa Richter, Sonja Kropp, Peter Proksch, Stefanie Scheu.
Cytochalasins were discovered in during the screening of fungal culture filtrates for possible biological activity on cells (Carter, ), and are synthetized by a PKS-NRPS hybrid enzyme (Fig. ).They are able to bind to actin filaments and block polymerization of actin; consequently cytochalasins can change cellular morphology, inhibit cellular processes such as cell division, and.
First, the authors used cytochalasin D-resistant host cells (Cyt-1 cells; Ohmori and Toyama, ) to show that cytochalasin D inhibits invasion through an effect on the parasite, not the host cell. They then chemically mutagenized parasites, selected for cytochalasin D resistance, and isolated three clones that could invade host cells in the.
Drug resistance in cancer patients is complex. Reasons for clinical resistance include metabolic inactivation and excretion of antitumor agents by the liver, kidney, and other organs. In addition, it has been found that tumor cells can acquire resistance to anticancer drugs. It is generally accepted that drug resistance at the cellular level Cited by: Summary.
The hydraulic resistance was measured on internodal cells of Chara corallina and Nitellopsis obtusa using the method of transcellular osmosis described by Kamiya and Tazawa in The transcellular hydraulic resistances of N.
obtusa and C. corallina are and pm −1 s Pa, resepectively. These values correspond to osmotic permeability coefficients (P os) of and Cited by: Cancer cells are considered to express primary drug resistance, yet chemotherapeutics are the front line of cancer treatments and have achieved great successes.
In time, most neoplastic cells develop secondary resistance to chemotherapy, which remains the major obstacle to cancer : Zvi Malik, Abraham Nudelman, Benjamin Ehrenberg. Abstract. Chloramphenicol (CAP) resistance was the first cytoplasmic drug resistance marker to be described for mammalian cells.
CAP and a variety of structurally related analogs (Fig. 1) are potent inhibitors of both bacteria and mammalian by: Cytochalasins, a class of fungal metabolites, affect a wide variety of motile functions of eukaryotic cells 1–ly, several laboratories have shown that cytochalasins inhibit actin.
carcinoma sensitivity to cytochalasins B, C, D, dihydrocytochalasin B. Cell lines are arranged in order of increasing drug resistance from left to right. The IC. Volume Issue18 October In this article Peter J. Smith argues that a greater commitment (in deed as well as word) to community science by the Scientific Establishment might help.
Resistance to Friend virus in W/W v mice, Similar to fetal liver stromal cells, mouse spleen stromal cells are able to support the expansion of early erythroid progenitor cells, whereas bone marrow stromal cells cannot Rearrangements of the cellular p53 gene in erythroleukaemic cells transformed by Friend virus.
Nature Cited by: 8. In conclusion, collateral sensitivity to 5FU and the lipophilic AG and cross-resistance to other antifolates were observed in non-P-gp MDR SW/2R cells, as well as resistance to.
Lines of KB cells resistant to cytochalasin B have been isolated and characterized. The mutant Cyt 1 exhibits increased cross-resistance to cytochalasin E. Cyt 1 cells bind less cytochalasin B than parental KB cells. Two-dimensional gel analysis shows that Cyt 1 cells carry an alteration in β-actin.
This is further confirmed by one-dimensional peptide by: The Cytochalasins (Greek cytos, cell; chalasis, relaxation) are a group of related fungal metabolites.
They were discovered in during the screening of mold filtrates for possible biological activity on cells.1 These fungal toxins are related by chemical Size: KB. Abstract. The in vitro anticancer activity of eight natural cytochalasins and three hemisynthetic derivatives of cytochalasin B on six cancer cell lines was evaluated.
The IC 50 in vitro growth inhibitory concentrations, as determined by an MTT colorimetric assay, ranged between 3 and 90 µM and did not relate to the intrinsic sensitivity of the cancer cell lines to proapoptotic by:.
This conclusion was supported further by the observation that two MDR cell lines (FLC mouse erythroleukaemic and SKOV3 human ovarian carcinoma cells) showed sensitivity to EM. Fluorescent activated cell sorting analysis of the effects of EM on cell cycle traverse revealed that at EM concentrations up to 20 microM an increasing percentage of Cited by: Cytochalasin B, the name of which comes from the Greek cytos (cell) and chalasis (relaxation), is a cell-permeable was found that substoichimetric concentrations of cytochalasin B (CB) strongly inhibit network formation by actin filaments.
Due to this, it is often used in cytological al formula: C₂₉H₃₇NO₅.F2: Mechanisms of cytochalasins B and D. It is known that cytochalasins bind the growing barbed (+) end of microfilaments, thereby inhibitingpolymerization.
In addition, cytochalasin D stimulates ATP hydrolysis in formed G-actin dimers, preventing the formation of viable microfilaments.