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At least 19 recordsLinked to original sources
PubMed1983

Binding of 18F by cell membranes and cell walls of Streptococcus mutans.

The binding of 18F to isolated cell membranes and cell walls of Streptococcus mutans GS-5 or other bacteria was assayed. The attachment of 18F to these cell envelopes proceeded slowly and reached equilibrium within 60 min. 18F binding was stimulated by Ca2+ (1 mM). The binding of 18F to cellular components was dependent upon the pH, as well as the amount of 18F and dose of the binder employed. The binding of 18F by cell walls prepared from fluoride-sensitive and fluoride-resistant cells of S. salivarius and S. mutans did not differ significantly. The pretreatment of cell walls or cell membranes for 60 min at 30 degrees C with 1 mg of RNase, DNase, or trypsin per ml did not influence the binding of 18F by the walls and membranes of S. mutans GS-5. However, prior exposure of cell membranes to sodium dodecyl sulfate caused a significant reduction in the number of 18F atoms bound by the membranes. In saturated assay systems, cell membranes of S. mutans GS-5 bound 10(15) to 10(16) atoms of 18F per mg (dry weight), whereas cell walls from S. mutans GS-5, FA-1, and HS-6 or Actinomyces viscosus T14V and T14AV bound 10(12) to 10(13) atoms of 18F per mg (dry weight). 18F in this quantity (10(12) to 10(13) atoms) cannot be detected with the fluoride electrode. The data provide, for the first time, a demonstration of 18F binding by cell membranes and walls of oral flora.

Actinomyces↗
PubMed1984

Inhibition of normal lymphocyte responses by cell membranes.

Cell membranes bearing the appropriate antigen are known to stimulate a variety of cell-mediated immune responses. This report confirms that tumor cell membranes at doses of 2-5 micrograms protein/ml will stimulate in vitro generation of allogeneic cytotoxic T lymphocytes (CTL). However, higher doses (50-100 micrograms protein/ml) of the same membranes completely abrogate the generation of lytic activity. Responding lymphocytes are inhibited by membranes from either syngeneic or allogeneic cells. The inhibition appears to act at a proliferative or differentiation step in the generation of the CTL response, since membranes are known to have little direct effect on the lytic phase of CTL activity. Similar doses of membranes also inhibit LPS-induced B-cell proliferation. B-Cell proliferation is inhibited equally well by allogeneic and syngeneic membranes, and membranes from normal spleen cells are as inhibitory as tumor cell membranes. The inhibitory activity copurifies with the plasma membrane. The results raise important considerations regarding the use of subcellular forms of antigen in studies of lymphocyte recognition. In addition, these data suggest that cell-cell contacts might provide signals regulating the proliferation of lymphocytes.

Animals↗
PubMed1979

Lithium transport across red cell membrane: a cell membrane abnormality in manic-depressive illness.

In the families of manic-depressive patients, relatives with a history of affective disorders had a significantly higher ratio of mean red cell lithium to plasma lithium in vitro than relatives with no such history. A genetically controlled abnormality in lithium-sodium transport, the mechanism that determines the lithium ratio, may play a role in the etiology of some forms of affective disorders.

Biological Transport↗
PubMed1981

Evidence for a folic acid binding protein in human cell membrane.

Cell membranes were prepared by sucrose discontinuous gradient from human liver and human peripheral leukocytes and erythrocytes and from circulating leukocytes from patients with chronic granulocytic leukemia (CGL) and acute myeloblastic leukemia (AML). The membrane preparations from liver and from leukemic leukocytes were shown to bind tritiated folic acid. The membranes from normal leukocytes and erythrocytes did not show this binding capacity. The membrane preparation from liver and CGL leukocytes showed two peaks of binding eluting with proteins from Sephadex G-200. However, protein extracts of these membrane preparations showed only a single peak for labelled folic acid, eluting near but just after albumin. The binding capacity of the membranes for folic acid was partially inhibited by reduced folate analogues. It is concluded that the liver plasma cell membrane and the membranes of myeloblasts in AML and circulating leukocytes in CGL contain a binding protein for folic acid which may be concerned in the transport of folates into these cells.

Animals↗
PubMed1977

Separation of the Moloney leukemia virus-determined cell surface antigen (MCSA) from known virion proteins associated with the cell membrane.

Cell membranes of Moloney lymphoma cells (YAC, of strain A origin) were solubilized by NP40. The antigenicity of the solubilized protein fraction was assayed by inhibition of the corresponding cytotoxic reaction against YAC target cells. The Moloney leukemia virus (MLV)-determined cell surface antigen (MCSA) was detected with mouse antisera, produced by the repeated inoculation of heavily irradiated YAC cells into syngeneic mice. Virion proteins gp71, p30, p15, p12 and p10 were identified with goat or rabbit antisera against purified Rauscher and Friend leukemia virus proteins. MCSA was found to bind to Con-A--Sepharose and was eluted by mannoside together with H-2A AND GP71. In contrast, p30, p12, p10 and part of p15 and p15(E), were not retained on the column and could be separated from MCSA. Passage of the glycoprotein fraction through Sephadex G-200 led to the separation of MCSA activity from gp71 and H-2A. MCSA eluted between the immunoglobulin (IgG) and the bovine serum albumin (BSA) size markers. MCSA could be also separated from the known viral proteins and from H-2 by velocity centrifugation in sucrose gradients. It sedimented with approximately 6.6 S ahead of gp71 (4.4 S) and H-2 (3.2 S). It is suggested that MCSA may be a glycoprotein with an approximate molecular weight of 110,000 and distinct from the known viral proteins gp71, p30, p15(E), p12, p10 and from H-2.

Animals↗
PubMed1994

Direct correlation between cell membrane fluctuations, cell filterability and the metastatic potential of lymphoid cell lines.

Cell membrane fluctuations, which reflect local bending deformability of the cell surface, are composed of submicron aperiodic reversible displacements of the cell membrane in the frequency range of 0.5-20Hz. Measurements of time-dependent light scattering from small areas (0.25 micron 2) of the cell surface reveal a higher level of cell membrane fluctuations in high metastatic BW5147 T-lymphoma derived cell lines than in their corresponding non-metastatic cell lines. Filterability measurements, carried out by recording the passage time of equal volumes of cell suspensions and media through 8 microns and 10 microns pores of a polycarbonate filter, demonstrate a higher filterability (lower rigidity index) for the high metastatic cell lines than their matched non-metastatic ones. Hence, the present study demonstrates a positive correlation between the metastatic potential of BW5147 lymphoma derived cell lines, their relative level of cell membrane fluctuations and their in-vitro cell filterability.

Animals↗
PubMed1990

Intracellular regulation of ion channels in cell membranes.

Cells communicate with their environment through receptor proteins on the cell membrane. Some ion channels are receptors, whereas others are linked to receptors through guanine nucleotide-binding proteins (G proteins). Ion channels control intracellular concentrations of ions such as calcium, and these concentrations control cell functions such as secretion and cell division. This review summarizes the current state of knowledge about the control of ion channels.

Cell Communication↗
PubMed1997

On periodic curvature and standing wave motions in cell membranes.

Cell membranes can form cubic arrangements and there is evidence for the occurrence of periodic curvature in simple membranes. The periodicity of the bilayer implies a standing wave character of vibrational motions. It is proposed that the periodic curvature reflects a dominating mode of standing wave oscillations, with the different cubic bilayer structures representing alternative standing wave conformations of the bilayer. The wave motions in lamellar liquid-crystalline phases, as well as in vesicles and membranes, which lack lateral periodicity, are known to exhibit statistically distributed undulations. The standing wave character of conformational fluctuations of periodically curved membranes, on the other hand, results in an organisation in time and space. Calculated models of standing wave conformations of membranes are demonstrated, and functional aspects of such biomembranes are discussed.

Cell Membrane↗
PubMed1980

A rapid method for the detection of antibodies to cell surface antigens: a solid phase radioimmunoassay using cell membranes.

Cell membranes isolated from murine lymphocytes or ascites tumors bind tightly to the surface of flexible plastic microtiter plates in the absence of additional proteins. This allows the detection of membrane associated molecules by specific antibodies and thus forms the basis for a rapid and sensitive radioimmunoassay for antibodies to membrane-bound components. The assay compares favorably with a variety of methods currently used to detect antibodies to cell surface antigens. The assay detects a variety of well characterized murine cell surface antigens (H-2, I-A, T-200, Thy-1.2, Ig). The level of antibody binding to membranes on plates correlates well with antigen density on intact cells. A modification of the assay involving competition between cross-reacting antibodies allows detection and resolution of closely spaced antigenic determinants.

Animals↗
PubMed1976

Cell membrane and cell junctions in differentiation of preimplanted mouse embryos.

Cell membrane and cell junctions in differentiation of preimplanted mouse embryos, (membrana celular y uniones celulares en la diferenciación del embrión de ratón antes de la implantación). Arch. Biol. Med. Exper. 10: 130-134, 1976. The development of cell junctions that seal the peripheral blastomeres could be a decisive step in the differentiation of morulae into blastocysts. The appearance of these junctions is studied by electron microscopy of late morulae and initial blastocysts. Zonulae occludentes as well as impermeability to lanthanum emulsion precedes the appearance of the blastocel and hence might be considered as one of its necessary causes.

Animals↗
PubMed1990

The cell membrane and cell signals: new targets for novel anticancer drugs.

In the concluding Discussion session, emphasis focussed on the potential for interfering selectively with cell membranes and cell signalling in tumour as against normal tissues. There could be no doubt that tremendous advances are being made in our understanding of the molecular changes associated with malignancy and that the information available for the rational design of inhibitors of particular signalling pathways is increasingly sophisticated. There was a consensus that we need more information on the qualitative and quantitative differences in the structure and function of membranes and the signalling machinery in various normal tissues as compared to their cancerous counterparts. Ideally we will develop drug against, for example, specific forms of, let us say, protein kinase C or tyrosine kinase which are found to be predominantly active in neoplastic cells. This may well prove possible, at least in some instances, in which case a safe therapeutic margin will be assured. But differences may in other situations turn out to be in the level of expression rather than purely qualitative in nature, and the scale of the disparate expression may not always be great. Even in such situations, adequate therapeutic selectivity may still be achieved. This may derive from a "damping down" of signalling in the hyperactive tumour. Although there are legitimate concerns regarding the possible toxic effects of administering signal-wrecking molecules in man, we should not be pessimistic as there are clear precedents elsewhere in medicine for drugs acting on membrane signals proving to be safe and effective against expectation informed by hindsight. There may also be concerns about new forms of drug resistance. But this will be so for any new agent or novel target. And with mechanism of action clearly to the fore we should be able to predict resistance pathways in advance and devise appropriate circumvention strategies or targeted second line therapies. There was a palpable buzz at the meeting that this is a valid, different and above all rational approach. Not only that, but the new therapeutic molecules which we discover will themselves prove to be valuable tools with which to probe further into the mechanisms of malignancy and signal transduction. We had expected to see a bewildering amount of new information from the basic sciences of molecularbiology and cell physiology, and we got it. But it was also impressive to witness the number of new compounds coming through which look like real drugs or at least exciting lead compounds. The membrane-active ether lipids are in clinical trial. Bryostatin 1 will shortly join them.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1981

Increased cholesterol and decreased fluidity of red cell membranes (spur cell anemia) in progressive intrahepatic cholestasis.

Progressive hemolytic anemia occurred in a 4 1/2-year-old girl with familial intrahepatic cholestasis; a peripheral smear contained bizarre spiculated "spur" red cells. Analysis of this patient's fresh red cells revealed a 59% increase in cholesterol content with a normal phospholipid content and therefore an increase in the cholesterol/phospholipid molar ratio to 1.35 (normal = 0.92). A similar abnormality of lipid composition was present in serum lipoproteins. The lipid abnormality in red cell membrane was associated with a decrease in membrane fluidity, as assessed by the fluorescence polarization of the hydrophobic probe 1,6-diphenyl-1,3,5-hexatriene. Following incubation with patient's plasma, normal cells acquired a spur-shaped morphology with an associated decrease in osmotic fragility and a 25% increase in cholesterol content. The patient's cells, during incubation with normal plasma, acquired morphologic features of spiculated spherocytes with an increase in osmotic fragility and a 21% decrease in cholesterol content. Chenodeoxycholate and lithocholate were present in markedly elevated concentrations in serum. These studies show that a process identical to spur cell anemia in alcoholic cirrhosis may accompany severe liver disease in children with intrahepatic cholestasis.

Acute Disease↗
PubMed1987

Distinctive populations of basement membrane and cell membrane heparan sulfate proteoglycans are produced by cultured cell lines.

We have investigated the nature and distribution of different populations of heparan sulfate proteoglycans (HSPGs) in several cell lines in culture. Clone 9 hepatocytes and NRK and CHO cells were biosynthetically labeled with 35SO4, and proteoglycans were isolated by DEAE-Sephacel chromatography. Heterogeneous populations of HSPGs and chondroitin/dermatan proteoglycans (CSPGs) were found in the media and cell layer extracts of all cultures. HSPGs were further purified from the media and cell layers and separated from CSPGs by ion exchange chromatography after chondroitinase ABC digestion. In all cell types, HSPGs were found both in the cell layers (20-70% of the total) as well as the medium. When the purified HSPG fractions were further separated by octyl-Sepharose chromatography, very little HSPG in the incubation media bound to the octyl-Sepharose, whereas 40-55% of that in the cell layers bound and could be eluted with 1% Triton X-100. This hydrophobic population most likely consists of membrane-intercalated HSPGs. Basement membrane-type HSPGs were identified by immunoprecipitation as a component (30-80%) of the unbound (nonhydrophobic) HSPG fraction. By immunofluorescence, basement membrane-type HSPGs were distributed in a reticular network in Clone 9 and NRK cell monolayers; by immunoelectron microscopy, these HSPGs were localized to irregular clumps of extracellular matrix located beneath and between cells. The cells did not produce a morphologically recognizable basement membrane layer under these culture conditions. When membrane-associated HSPGs were localized by immunoelectron microscopy, they were found in a continuous layer along the cell membrane of all cell types. The results demonstrate that two antigenically distinct populations of HSPG--an extracellular matrix and a membrane-intercalated population--are found at the surface of several different cultured cells lines; these populations can be distinguished from one another by differences in their distribution in the monolayers by immunocytochemistry and can be separated by hydrophobic chromatography; and basement membrane-type HSPGs are secreted and deposited in the extracellular matrix by cultured cells even though they do not produce a bona fide basement membrane-like layer.

Animals↗
PubMed1980

Localization of Na+, K+ -ATPase to the inside of the basolateral cell membranes of epithelial cells of proximal and distal tubules in rabbit kidney.

Cysteine-sensitive alkaline phosphatase and/or ouabain-sensitive Na+, K+ -ATPase were studied by ultrastructure cytochemistry in epithelial cells of proximal and distal kidney tubules. Alkaline phosphatase reactivity was confined to the surface of the microvillous luminal cell membrane of proximal tubule cells, whereas distal tubules and collecting ducts were unreactive. The Na+, K+- ATPase reactivity was localized evenly along the cytoplasmic side of the basolateral cell membrane of cells of proximal and distal tubules and in collecting ducts. In the proximal tubules, where the activity was strongest, the Na+, K+- ATPase deposits were also found in the 10--50 nm gap between the cell membrane and the cisternae of tubulo-cisternal endoplasmic reticulum (TER) underlying a major part of the basolateral cell membrane. The restriction of NA+, K+ -ATPase sites, which are involved in extrusion of Na+ from the cell, to a narrow cytoplasmic compartment located between the cell membrane and the cisternae of TER, is consistent with a transport role for the TER.

Animals↗
PubMed2005

Functional interrelationships between cell membrane and cell wall in antimicrobial peptide-mediated killing of Staphylococcus aureus.

Perturbation of the Staphylococcus aureus cytoplasmic membrane (CM) is felt to play a key role in the microbicidal mechanism of many antimicrobial peptides (APs). However, it is not established whether membrane permeabilization (MP) alone is sufficient to kill susceptible staphylococci or if the cell wall (CW) and/or intracellular targets contribute to AP-induced lethality. We hypothesized that the relationships between MP and killing may differ for distinct APs. In this study, we investigated the association between AP-induced MP and lethality in S. aureus whole cells versus CW-free protoplasts, and in comparison to the MP of liposomes modeled after whole CMs in terms of phospholipid composition, fluidity and charge. Four APs with different structure-activity relationships were examined: thrombin-induced platelet microbicidal protein 1 (tPMP-1), human neutrophil protein 1 (hNP-1), gramicidin D, and polymyxin B. MP was quantified fluorometrically by calcein release. All APs tested, except polymyxin B, caused concentration-dependent MP and killing of whole cells, but not of protoplasts. The reduced AP susceptibility of protoplasts was associated with increased cardiolipin and lysyl-phosphatidylglycerol content and reduced fluidity of their CMs. However, liposomal MP induced by tPMP-1, hNP-1, and gramicidin D paralleled that of whole cells. Collectively, these results indicate that (i) structurally distinct APs likely exert their staphylocidal effects by differing mechanisms, (ii) MP is not the sole event leading to AP-induced staphylocidal activity, (iii) a complex interrelationship exists between the CM and CW in AP-induced killing, and (iv) liposomes modeled upon whole cell or protoplast CMs can recapitulate the respective susceptibilities to killing by distinct APs.

Anti-Bacterial Agents↗