bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracellular localization and degradation of diphtheria toxin
Authors: Fedde Kenton N. , Sly William S. 
Published: December 2004

AbstractThe internalization of surface‐bound diphtheria toxin (DT) in BS‐C‐1 cells correlated with its appearance in intracellular endosomal vesicles; essentially no toxin appeared within secondary lysosomal vesicles. In contrast, internalized epidermal growth factor (EGF) was localized within both endosomal and lysosomal vesicles. Upon prein‐cubation of cells with leupeptin, a lysosomal protease inhibitor, a threefold increase in the accumulation of EGF into lysosomes was observed. Under identical conditions, essentially all of the diphtheria toxin remained within endosomes (less than 2% of the intracellular diphtheria toxin accumulated in the lysosomaJ fraction), indicating that the inability to detect diphtheria toxin in lysosomes was not due to its rapid turnover within this vesicle. Following internalization of EGF or DT, up to 40% of the lgand appeared in the medium as TCA‐soluble radioactivity. EGF degradation was partially leupeptin‐sensitive and markedly NH4Cl‐sensitive, indicating lysosomal degradation. In contrast, DT A‐fragment degradation was resistant to these inhibitors, while B‐fragment showed only partial sensitivity. These data suggest that the bulk of endocytosed diphtheria toxin is localized within endosomes and degraded by a pathway essentially independent of lysosomes.
Membrane association of the hyaluronate stimulatory factor from LX‐1 human lung carcinoma cells
Authors: Knudson Warren , Toole Bryan P. 
Published: December 2004

AbstractLX‐1 human lung carcinoma cells interact with human fibroblasts in culture to cause an increase in hyaluronate production (Knudson et al: Proceedings of the National Academy of Sciences of the United States of America 81:6767, 1984). It is shown here that a similar increase in hyaluronate production also occurs when membranes derived from LX‐1 cells, or detergent extracts thereof, are added to cultures of the human fibroblasts. However, no stimulation occurs when membranes or extracts from fibroblasts are added to cultures of the LX‐1 cells. The hyaluronate stimulatory factor present in the detergent extracts is a heat‐ and trypsin‐sensitive protein, requires more than 12 h for its action on fibroblasts, causes an elevation in hyaluronate synthetase activity in membranes derived from the fibroblasts, and can be reconstituted into artificial lipid vesicles. Thus, it is concluded that the stimulatory factor is a membrane‐bound protein present on the surface of the LX‐1 cells and that it interacts with fibroblasts to induce increased hyaluronate synthesis.
Distinct mechanisms of interferon‐gamma and tumor necrosis factor‐alpha action in oncogene‐transformed mouse fibroblasts
Authors: Seliger Barbara , Killian Marion , Pfizenmaier Klaus 
Published: December 2004

AbstractThe potential mechanisms of interferon (IFN)‐gamma and tumor necrosis factor (TNF)‐alpha action on tumor cells have been investigated in a model of mouse fibroblasts transformed by distinct retroviral vectors carrying the v‐mos, c‐myc, and v‐Ha‐ras oncogene, respectively. Treatment with both cytokines not only caused growth inhibition of v‐mos‐ and c‐myc‐transformants, but also a reversion of transformation‐induced suppression of major histocompatibility complex (MHC) class I antigen expression in all transformed cell lines. The phenotypical reversion of transformants was preceded by a selective modulation of LTR‐controlled oncogene expression. TNF‐alpha primarily affected stability of oncogene‐specific RNAs without influencing the activity of retroviral promoters. In contrast, IFN‐gamma was effective at the transcriptional level, apparently due to inhibition of LTR activity as revealed from reduced CAT activity in IFN‐gamma‐treated LTR‐CAT transformants. This IFN‐gamma‐mediated down‐regulation of retroviral promoter activity seemed to be selective for Moloney‐virus‐derived promoters, since the activity of other viral and cellular promoters was not suppressed by IFN‐gamma.
Studies on the human retinoblastoma susceptibility gene
Authors: Lee Wen‐Hwa , Bookstein Robert , Lee Eva Y‐H. P. 
Published: December 2004

AbstractThe retinoblastoma susceptibility (RB) gene is unique among other cloned cancer genes because its causal role in a human cancer, retinoblastoma, was established by classical genetic methods before its isolation. Earlier hypotheses and experimental data suggested that inactivation of a gene in chromosome band 13q14 resulted in retinoblastoma formation. A gene in this region was identified as the RB gene on the basis of mutations found specifically in retinoblastoma tumors; however, its proposed biological activity in suppressing neoplasia has yet to be demonstrated. The RB gene product was identified as a nuclear phosphoprotein of 110 kD associated with DNA binding activity, suggesting that the RB protein may regulate other genes. Probes for the RB gene and gene product will be useful for genetic diagnosis of retinoblastoma susceptibility in affected families; for direct detection of mutant RB alleles; and, potentially, for genetic diagnosis of susceptibility to osteosarcoma and other tumors tentatively linked to RB‐gene dysfunction. Continued study of the RB gene should yield further insight into mechanisms of oncogenesis, development, and gene regulation.
Evidence for autocrine activation of a tyrosine kinase in a human gastric carcinoma cell line
Authors: Giordano Silvia , Renzo Maria Flavia Di , Narsimhan Radha P. , Tamagnone Luca , Gerbaudo Elena V. , Chiadó‐Piat Loredana , Comoglio Paolo M. 
Published: December 2004

AbstractPhosphotyrosine (P‐Tyr) antibodies have been used to identify the phosphorylated forms of growth factor receptors and oncogene‐coded tyrosine kinases. Western blot analysis of a gastric carcinoma cell line with P‐Tyr antibodies revealed a tyrosine‐phosphorylated protein of Mr 145,000 (P145). In addition, in vitro phosphorylation with (γ‐32P)ATP of P‐Tyr immunoprecipitates of the same cells resulted in labelling of this protein on tyrosine. P145 appears to be a transmembrane glycoprotein, with features suggestive of a growth factor receptor. However, the in vivo or in vitro addition of known growth factors did not affect P145 tyrosine phosphorylation. We now report that P145 is rapidly dephosphorylated in vivo when cells are exposed to low pH, a condition known to dissociate ligands from their receptors. The addition of serum‐free medium, conditioned by the gastric carcinoma cells, fully restores the tyrosine phosphorylation lost with acid treatment. These data suggest that the activity responsible for P145 phosphorylation on tyrosine, whether intrinsic to P145 itself or due to an associated kinase, is stimulated by a factor secreted by the tumor cells themselves.
Selective expression of mRNA encoding platelet‐derived growth factor B chain following transfection of foreign genes into cell lines derived from baby hamster kidney
Authors: Sakariassen Kjell S. , Powell Jerry S. , Raines Elaine W. , Ross Russell 
Published: December 2004

AbstractThe genes for platelet‐derived growth factor (PDGF) A and PDGF B chains are expressed in a variety of biological situations. Active PDGF consists of two distinct but homologous polypeptide chains, PDGF A and PDGF B, which are found as heterodimers or homodimers. We report a novel situation in which there is selective expression of mRNA encoding PDGF B in cell lines derived from baby hamster kidney (BHK) following transfection with various gene/cDNA constructs and following growth selection with methotrexate. The process of transfection itself, and not expression of the proteins encoded by the transfected genes/cDNAs (hormones, enzymes, and structural proteins), induces expression of PDGF B. No PDGF B mRNA is detectable in control cell lines. Low levels of mRNA encoding PDGF A are constitutively present and are not changed by transfection and/or growth selection. PDGF‐like activity is present in the medium whenever PDGF B mRNA is detected. The composition of the secreted PDGF dimer cannot be established from our data, but quantitative analysis of mRNA suggests that the PDGF is a B‐B dimer. However, the data show that transcription of the PDGF A and PDGF B genes in BHK cells is regulated independently, similar to that reported for some human tumor cells. Furthermore, the selective expression of PDGF B in response to the introduction of foreign genes and to growth selection may be an important aspect of the reaction of these cells to nonoptimal growth conditions, allowing survival and growth of the cells that express PDGF B.
Expression of enzymatically active enkephalinase (neutral endopeptidase) in mammalian cells
Authors: Gorman Cornelia M. , Gies David , Schofield Peter R. , Kado‐Fong Helen , Malfroy Bernard 
Published: December 2004

AbstractA cDNA encoding the rat enkephalinase protein (neutral endopeptidase; EC 3.4.24.11) has been constructed from overlapping > 10 cDNA clones. This cDNA was inserted into an expression plasmid containing the cytomegalovirus enhancer and promoter. When transfected with this plasmid, Cos 7 cells transiently expressed the enkephalinase protein in a membrane‐bound state. Recombinant enkephalinase recovered in solubilized extracts from transfected Cos 7 cells was enzymatically active and displayed properties similar to those of the native enzyme with respect to sensitivity to classical enkephalinase inhibitors.
Cholera toxin inhibits the increase in cytoplasmic free calcium induced via the CD2 pathway of human T‐lymphocyte activation
Authors: Nunes Jacques , Bagnasco Marcello , Lopez Marc , Olive Daniel , Mawas Claude 
Published: December 2004

AbstractWe investigated the action of cholera toxin on the intracellular ionized calcium [Ca2+]i increase induced by anti‐CD2 and anti‐CD3 monoclonal antibodies in the leukemic human T‐cell line Jurkat. Cholera toxin inhibits in a dose‐dependent manner these two pathways of human T‐lymphocyte activation but with different half maximal inhibition doses (75 ng/ml for CD3, 30 ng/ml for CD2). This effect cannot be accounted for only by the increase in cAMP induced by cholera toxin because forskolin, which raises cellular cyclic adenosine monophosphate (cAMP) to the same levels, induced only a small inhibition of the [Ca2+]i increase in similar conditions. Cholera toxin induced a decrease in the surface expression of the CD3 molecule, suggesting a down‐regulation of the CD3 molecules. On the other hand, the expression of CD2 remained unchanged. Cell surface disappearance of the CD3 molecule cannot account for all the inhibitory effects of cholera toxin because CD2 molecule expression was not affected (no modifications in the half maximal binding of anti‐CD2 monoclonal antibodies). All together, these results suggest that cholera toxin acts on substrates, possibly G proteins, that could regulate the [Ca2+]i increase induced by anti‐CD2 and anti‐CD3 mAbs in Jurkat cells. In addition, the present study demonstrated that the rise in cellular cAMP partially inhibits the [Ca2+]i increase induced by anti‐CD2 and anti‐CD3 mAbs.
Glucocorticoid dexamethasone reversibly complements EJ‐ras oncogene to transform mouse embryo BALB‐3T3 cells
Authors: Kovary Karla , Armelin Mari C. S. , Armelin Hugo A. 
Published: December 2004

AbstractEJ‐A is a Balb‐3T3 transfectant cell line that bears a small number of EJ‐ras oncogene copies/cell, has low EJ‐ras expression, and resembles the parental cell line in displaying a non‐transformed phenotype. The glucocorticoid hormone dexamethasone reversibly induces transformation traits in EJ‐A cells, namely: (1) morphological transformation; (2) increased growth rate and saturation density; (3) reduced G1 length; and (4) independence of the FGF requirement to initiate DNA synthesis. Western blot analysis revealed that dexamethasone does not increase the p21ras protein intracellular level. β‐IFN, added to the culture medium, does not suppress the dexamethasone‐induced growth stimulation and morphological transformation. Therefore, glucocorticoid hormones can complement low EJ‐ras expression to transform Balb‐3T3 cells, by a mechanism that is likely to be independent of p21ras increase and β‐IFN decrease.
Differential growth factor expression in transformed mouse NIH‐3T3 cells
Authors: Ciardiello Fortunato , Valverius Eva M. , Colucci‐D'Amato G. Luca , Kim Nancy , Bassin Robert H. , S.Salomon David 
Published: December 2004

AbstractThe expression of growth factor‐specific mRNA transcripts and the presence of biologically active growth factors in the conditioned medium and in the cell extracts from mouse NIH‐3T3 cells transformed by different oncogences (Ki‐ras, mos, src, fms, fes, met, and trk), by DNA tumor virus (SV40), or by a chemical carcinogen (N‐nitrosomethylurea) were studied. In contrast to NIH‐3T3 cells or simain virus 40 (SV40)‐transformed 3T3 cells, all the other transformed NIH‐3T3 cell lines express a 4.5 kb transforming growth factor‐α (TGFα)‐specific mRNA transcript and secreted immunoreactive and biologically active TGFα ranging from 100 to 225 ng/108 cell/48 h. In addition, in the transformed cell lines that were secreting elevated levels of biologically active TGFα, there was a 75–95% reduction in the total number of epidermal growth factor receptors on these cells. A 2.6 kb TGFβ mRNA transcript and TGFβ protein in the conditioned medium (30–140ng/108 cells/48h) was also detected in those lines expressing TGFα. Basic fibroblast growth factor‐like activity (11–50 ng/108 cells) was detected in the cell lysates from NIH‐3T3 cells transformed with N‐nitrosomethylurea or with trk, where expression of specific 6.9 and 3.9 kb mRNA transcripts for basic fibroblast growth factor could also be found. B chain (c‐sis) expression of platelet‐derived growth factor was present only in trk‐transformed NIH‐3T3 cells in which specific c‐sis 6.5 and 4.6 kb transcripts were identified. In contrast, platelet‐derived growth factor A chain expression of 2.9 and 2.3 kb transcripts was found in ras‐, met‐, mos‐, and fms‐transformed NIH‐3T3 cells. These results suggest that the expression of different sets of growth factors is controlled in part by structurally distinct groups of transforming genes.
Transfer of a normal human chromosome 11 suppresses tumorigenicity of some but not all tumor cell lines
Authors: Oshimura Mitsuo , Kugoh Hiroyuki , Koi Minoru , Shimizu Motoyuki , Yamada Hideto , Satoh Hitoshi , Barrett J. Carl 
Published: December 2004

AbstractThe complete suppression of tumorigenicity of a human cervical cancer cell (HeLa) and a Wilms' tumor cell line (G401) following the introduction via microcell fusion of a single chromosome t(X;11) has been demonstrated by Stanbridge and co‐workers. To determine whether other tumor cell lines are suppressed by chromosome 11, we performed chromosome transfer experiments via microcell fusion into various human tumor cell lines, including a uterine cervical carcinoma (SiHa), a rhabdomyosarcoma (A204), a uterine endometrial carcinoma (HHUA), a renal cell carcinoma (YCR‐1), and a rat ENU‐induced nephroblastoma (ENU‐T1). We first isolated a mouse A9 cell containing a single human chromosome 11 with integratedp SV2‐neo plasmid DNA. Following microcell fusion of the neo‐marked chromosome 11 with the various tumors mentioned above, we isolated clones that were resistant to G418 and performed karyotypic analyses and chromosomal in situ hybridization to ensure the transfer of the marked chromosome. Whereas the parental cell of each cell line were highly tumorigenic, SiHa and A204 microcell hybrid clones at early passages were nontumorigenic in nude mice and HHUA was moderately tumorigenic. On the other hand, YCR‐1 and ENU‐T1 microcell hybrid clones were still highy tumorigenic following the introduction of chromosome 11. Thus, the introduction of a normal chromosome 11 suppresses the tumorigenicity of some but not all tumors, suggesting that the function of the putative suppressor gene(s) on chromosome 11 is effective only in specific tumors.
Cautionary note on the use of the B subunit of cholera toxin as a ganglioside GM1 probe: Detection of cholera toxin A subunit in B subunit preparations by a sensitive adenylate cyclase assay
Authors: Spiegel Sarah 
Published: December 2004

AbstractThe Use of the B subunit of cholera toxin, a protein that binds specifically to ganglioside GM1, has provided a new paradigm for studying physiological functions of ganglioside GM1. The B subunit inhibited the growth of rat glioma C6 cells that had been pretreated with ganglioside GM1. In some preparations of the B subunit, the inhibition was endependent of adenylate cyclase activation and was due to the binding of the B subunit to ganglioside GM1 inserted onto the cell surface. However, in other preparations of the B subunit, there was an additional inhibitory effect due to small contaminations with the A subunit, which caused increases in intracellular cyclic adenosine monophosphate (cAMP) levels and concomittant growth inhibition. This vanishingly small contamination with the A subunit could not be detected by conventional protein sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDSPAGE) analysis but could be measured utilizing a sensitive adenylate cyclase activation assay. Thus caution must be used to ensure that any biological effects of the B subunit are not due to contaminating A subunit and are due solely to the binding of the B subunit to ganglioside GM1 exposed on the cell surface. This is especially important in cyclic nucleotide‐sensitive systems.
DNA‐binding activity of jun is increased through its interaction with Fos
Authors: Allegretto Elizabeth A. , Smeal Tod , Angel Peter , Spiegelman Bruce M. , Karin Michael 
Published: December 2004

AbstractTranscription factor AP‐1 mediates induction of a set of genes in response to the phorbol ester tumor promoter TPA. Recently, AP‐I preparations from HeLa cells were shown to contain a product of the c‐JUN protooncogene (Jun/AP‐l) which forms a tight complex with the Fos protein. In this paper, we examine the role of the Fos protein in the DNA‐binding activity of the AP‐I complex. We show that the DNA‐binding activity of bacterially expressed trpE‐Jun fusion proteins is increased many‐fold upon their interaction with Fos (or a Fos‐relaied antigen) expressed from a baculovirus vector. The site of Fos interaction is within the DNA‐binding domain of Jun/AP‐l, and anti‐Fos antibodies interfere with the binding of affinity purified AP‐1 to DNA. These results suggest that, by associating with Jun/AP‐l, Fos is responsible for the formation of a multimeric protein complex that has greater affinity for the target sequence than does Jun/AP‐l alone.
Die durch Sauerstoffzufuhr verursachte Stromlieferung galvanischer Elemente als Maß für die Oxydation und Anfangskorrosion von Metallen
Authors: Tödt F. 
Published: December 2004

AbstractDie aus einer wässerigen Lösung an eine Platinoberfläche gelangende Sauerstoffmenge kann durch die Strommenge in Coulombs gemessen werden, welche die Platinoberfläche als Kathode in Verbindung mit einer unpolarisierbaren Anode liefern kann. Durch zeitlich abgestuftes Abschalten dieses galvanischen Elementes in Lösungen mit verschiedenen Sauerstoffgehalten wird die Metalloberfläche mit Sauerstoffmengen beladen, welche zwischen 10−9 und 10−12 Grammäquivalent je cm2 liegen, entsprechend einer Bedeckung mit mehreren Atmoschichten bis zum tausendsten Teil einer monomolekularen Bedeckung. Auch diese geringe Sauerstoffbedeckung bzw. Oxydation kann noch als Strommenge von etwa 0,2 × 10−6 Coulomb/cm2 gemessen werden. Die Übertragung dieser Ergebnisse auf die Korrosionserscheinungen ergibt wesentlich vereinfachte Vorstellungen über die Grundvorgänge. Die beobachtete Anfangskorrosion von Eisen, Kupfer und Nickel zeigt den gleichen Verlauf wie die Strommengenmessung der galvanischen Metallelemente.
Spezifische ätzfärbungen an Eisen‐Siliziumlegierungen Eine neue Schnellmethode zum Erkennen hochprozentiger Eisen‐Siliziumlegierungen
Authors: Fitzer E. 
Published: December 2004

AbstractNach Besprechung der im Schrifttum verzeichneten Methoden zur Farbätzung von Fe‐Si‐Legierungen wird über eine neue elektrographische Methode berichtet, die gestattet, F‐Si‐Mischkristalle mit mindestens 8 % Si am Schliff zu identifizieren. Die Methode besteht in einer anodischen Oxydation der Legierung und darauf‐folgender Anfärbung mit Methylenblau. Sie ist spezifisch für Silizium in Eisen und ist neben ihrer Anwendung in der Metallographie zur Entwicklung des Feingefüges von Fe‐Si‐Legierungen auch als zerstörungsfreie Schnell‐methode zur Identifizierung von säurebeständigem Fe‐Si‐Guß geeignet.
Zur Wirkungsweise von Beizinhibitoren
Authors: Willems F. 
Published: December 2004

AbstractAus den durchgeführten Versuchen geht hervor, daß bei den 7 untersuchten Sparbeizen bereits bei Raumtemperatur ein Angriff auf das blanke Metall stattfindet. Unterschiedlich ist dabei Art und Stärke des Angriffs und weiter seine Wirkung auf das Metall im Langzeitversuch. Dabei kann man die benutzten Beizen in 4 Gruppen unterteilen, und zwar:1. in Beizen, die das blanke Beizgut ohne erkennbare Schutzwirkung auf der gesamten Oberfläche schnell und gleichmäßig abtragen, aber weder Lochfraß noch Blasenbildung sichtbar zur Folge haben. Dazu würden in unserem Fall die Beizen 1 und 2 (Abb. 6, 6a, 16 und 17) zählen;.
Graphit als Werkstoff im chemischen Apparatebau
Authors: Schmidt A. 
Published: December 2004

AbstractAllgemeine Eignung von Graphit als Apparatewerkstoff — Entwicklung von Graphitwärmeaustauschern durch die I. G. Farbenindustrie, Bitterfeld — Imprägniermittel und ‐verfahren zur Verringerung der Porosität des Graphits — Verbindung von Bauelementen aus Graphit.
Zur Theorie der Oxydation von Metallen und Metall‐Legierungen
Authors: Hauffe K. 
Published: December 2004

AbstractFehlordnungserscheinungen in festen Ionenkristallen — Wesen der Anlauf‐ und Zundersysteme — Ausbildung dicker Zunderschichten auf reinen Metallen (Theorie der Oxydation reiner Metalle von Wagner; Zundersysteme mit ionenleitenden bzw. mit elektronenleitenden Zunderschichten) — Ausbildung dünner Anlaufschichten auf reinen Metallen (Theorie von Mott‐Cabrera) — Theorie der Zundervorgänge an Metallegierungen von Hauffe und Wagner (Zundersysteme mit ionenleitenden bzw. mit elektronenleitenden Zunderschichten) — Über die Mitwirkung von Phasengrenzreaktionen während der Oxydation und des Aufbaus von Deckschichten — Theorie der inneren Oxydation von Metallegierungen nach Rhines — Über die Möglichkeit der Entwicklung zunderfester Metallegierungen — Zusammenfassung.