Search Results - (Author, Cooperation:A. Strasser)

2014-02-28

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Female ; Humans ; Male ; Necrosis/*enzymology ; Sirtuin 2/*genetics/*metabolism

2012-08-24

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; BH3 Interacting Domain Death Agonist Protein/*immunology ; Epithelial Cells/*immunology ; Humans ; Immunity, Innate/*genetics ; Inflammation/*genetics ; Intestinal Mucosa/*immunology

2013-09-13

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Antigens, CD95/deficiency/metabolism ; Caspase 8/metabolism ; Cell Death ; Citrobacter rodentium/pathogenicity/physiology ; Enteropathogenic Escherichia coli/*metabolism/pathogenicity ; Enzyme Activation ; Escherichia coli Infections/*metabolism/*microbiology/pathology ; Escherichia coli Proteins/*metabolism ; Fas Ligand Protein/antagonists & inhibitors/metabolism ; Fas-Associated Death Domain Protein/chemistry/metabolism ; Female ; Gastrointestinal Tract/*microbiology ; HEK293 Cells ; HeLa Cells ; Humans ; Male ; Mice ; N-Acetylglucosaminyltransferases/metabolism ; Protein Structure, Tertiary ; Receptor-Interacting Protein Serine-Threonine Kinases/chemistry/metabolism ; *Signal Transduction ; TNF Receptor-Associated Death Domain Protein/chemistry/metabolism ; Virulence Factors/*metabolism

2018-11-02

Cold Spring Harbor Laboratory Press

0890-9369

Biology

2018-10-12

American Society of Hematology (ASH)

0006-4971

1528-0020

Biology

Medicine

Lymphoid Neoplasia

0168-583X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

1432-1459

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1440

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

0168-583X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

1432-0614

Springer Online Journal Archives 1860-2000

Biology

Process Engineering, Biotechnology, Nutrition Technology

Abstract Two non-Saccharomyces yeasts have been developed as hosts for heterologous gene expression. The celD gene from Clostridium thermocellum, encoding a heat-stable cellulase, served as the test sequence. The first system is based on the amylolytic species Schwanniomyces occidentalis, the second on the xylolytic species Pichia stipitis. The systems comprise auxotrophic host strains (trp5 in the case of S. occidentalis; trp5–10, his3 in the case of P. stipitis) and suitable transformation vectors. Vector components consist of an S. occidentalis-derived autonomously replicating sequence (SwARS) and the Saccharomyces cerevisiae-derived TRP5 sequence for plasmid propagation and selection in the yeast hosts, an ori and an ampicillin-resistance sequence for propagation and selection in a bacterial host. A range of vectors has been engineered employing different promoter elements for heterologous gene expression control in both species. Homologous elements derived from highly expressed genes of the respective hosts appeared to be of superior quality: in the case of S. occidentalis that of the GAM1 gene, in the case of P. stipitis that of the XYL1 gene. Further elements tested are the S. cerevisiae-derived ADH1 and PDC1 promoter sequences.

Electronic Resource

1432-0614

Springer Online Journal Archives 1860-2000

Biology

Process Engineering, Biotechnology, Nutrition Technology

Abstract  A DNA sequence coding for a subtype of the hirudin variant HV1 was expressed in the methylotrophic yeast Hansenula polymorpha from a strongly inducible promoter element derived from a gene of the methanol metabolism pathway. For secretion, the coding sequence was fused to the KEX2 recognition site of three different prepro segments engineered from the MFα1 gene of Saccharomyces cerevisiae, the glucoamylase (GAM1) gene of Schwanniomyces occidentalis and the gene for a crustacean hyperglycemic hormone from the shore crab Carcinus maenas. In all three cases, correct processing of the precursor molecule and efficient secretion of the mature protein were observed. In fermentations on a 10-l scale of a transformant strain harbouring a MFα1/hirudin-gene fusion yields in the range of grams per litre could be obtained. The majority of the secreted product was identified as the full-length 65-amino-acid hirudin. Only small amounts of a truncated 63-amino- acid product, frequently observed in S. cerevisiae-based expression systems, could be detected.

Electronic Resource

1432-0614

Springer Online Journal Archives 1860-2000

Biology

Process Engineering, Biotechnology, Nutrition Technology

Abstract A DNA sequence coding for a subtype of the hirudin variant HV1 was expressed in the methylotrophic yeast Hansenula polymorpha from a strongly inducible promoter element derived from a gene of the inducible promoter element derived from a gene of the methanol metabolism pathway. For secretion, the coding sequence was fused to the KEX2 recognition site of three different prepro segments engineered from the MFα1 gene of Saccharomyces cerevisiae, the gluco-amylase (GAM1) gene of Schwanniomyces occidentalis and the gene for a crustacean hyperglycemic hormone from the shore crab Carcinus maenas. In all three cases, correct processing of the precursor molecule and efficient secretion of the mature protein were observed. In fermentations on a 10-1 scale of a transformant strain harbouring a MFα1/hirudin-gene fusion yields in the range of grams per litre could be obtained. The majority of the secreted product was identified as the full-length 65-amino-acid hirudin. Only small amounts of a truncated 63-amino- acid product, frequently observed in S. cerevisiae-based expression systems, could be detected.

Electronic Resource

1420-908X

Key words: Cell death — Apoptosis — Autoimmunity — Bcl-2 — Fas (Apo-1, CD95)

Springer Online Journal Archives 1860-2000

Medicine

Abstract. The process of programmed cell death or apoptosis was already noted in 1842 by Vogt [1], but it was not until the more recent studies of Kerr et al. 1972 [2] that an explosion of interest in apoptosis research occurred. Genetic, biochemical and cellular analysis in certain mammals, in the nematode Caenorhabditis elegans and in the fruitfly Drosophila melanogaster have identified several apoptosis regulating genes. This indicates that programmed cell death is an active, genetically controlled process. Many of the known cell death regulators are homologous in mammals, nematodes and insects, indicating that apoptosis is an evolutionarily conserved process. Apoptosis can be induced via multiple independent signalling pathways which converge upon a common final effector machinery. This stimulates activation of latent cysteine proteases (caspases), which cleave vital cellular substrates and thereby lead to the death of cells. The regulatory pathways of apoptosis are becoming clear with the discovery of specific signalling molecules. It has become evident that many disease processes including autoimmunity and cancer can be caused by deregulation of the apoptotic process. With the discovery of novel cell surface-bound death receptors, their ligands and further insight into the apoptotic machinery within the cell, research may ultimately lead to the design of therapies that allow intervention in the apoptotic process. The aims of such strategies would be to turn on apoptosis in neoplastic cells or in lymphocytes that are causing autoimmune disease or to prevent cell death in degenerative disorders. This review describes current understanding of the molecular regulation of apoptosis, and focuses on issues relating to possible roles of defective cell death control in autoimmunity.

Electronic Resource

1432-2013

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1912

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

0044-281X

Schlüsselwörter Stickoxid – Endothelin – Gehirn – Ischämie –Ödem ; Key words Nitric oxide – endothelin-1 – ischemia – brain – edema

Springer Online Journal Archives 1860-2000

Medicine

Summary These studies were performed in an attempt to clarify some of the pathophysiologic mechanisms which occur during and after global ischemia. Both nitric oxide and endothelin were demonstrated in gerbils to participate in responses to ischemia. It was shown that endogenous nitric oxide influences early postischemic reperfusion, systemic blood pressure and postischemic dopamine metabolism. Furthermore, the results indicated that nitric oxide played a role in dopamine release and that preischemic intracerebral nitric oxide formation significantly decreased ischemic dopamine release. In addition, ischemic release of endothelin-1 was detected; participation of nitric oxide in this release was observed. Further indication of functional interactions between nitric oxide and endothelin-1 in postischemic reperfusion were indicated by observations that endothelin-1 antagonists inhibited early hypoperfusion caused by Nitro-L-arginin and late hypoperfusion caused by endogenous endothelin-1. Nitric oxide was shown to decrease edema formation during the early postischemic period but contribute to edema formation during the late postischemic period. The findings indicate the importance of nitric oxide in stroke and ischemia.

Zusammenfassung Diese Untersuchungen sollten zur Klärung verschiedener pathophysiologischer Mechanismen während und nach Ischämie beitragen und demonstrierten im Tiermodell (Gerbil) eine Beteiligung von sowohl Stickoxid als auch Endothelin beim ischämischen Geschehen. Es wurde nachgewiesen, daß endogenes Stickoxid die Phase der frühen postischämischen Reperfusion, den systemischen Blutdruck und den postischämischen Dopaminstoffwechsel beeinflußt, auch bei der Dopaminfreisetzung eine Rolle spielt, und eine intrazerebrale präischämische Stickoxidbildung die ischämische Dopaminfreisetzung stark vermindert. Zusätzlich konnte eine ischämische Endothelinfreisetzung sowie eine Einflußnahme von Stickoxid nachgewiesen werden. Als weiterer Hinweis auf eine funktionelle Interaktion zwischen Stickoxid und Endothelin bei der postischämischen Reperfusion konnte demonstriert werden, daß Endothelinantagonisten sowohl die frühe, durch Nitro-L-Arginin, wie auch die späte, durch endogenes Endothelin verursachte, postischämische Hypoperfusion verhindern. Beim postischämischen Gehirnödem vermindert Stickoxid anfänglich die Ödembildung, trägt jedoch in weiterer Folge zur Entwicklung des Gehirnödems bei. Die beschriebenen Untersuchungen weisen auf die Bedeutung von Stickoxid bei Schlaganfall und Ischämie hin.

Electronic Resource

0016-7835

Key words Oxfordian ; Sequence stratigraphy ; Cyclostratigraphy ; Stratigraphic correlation ; Swiss Jura ; Spain ; Normandy

Springer Online Journal Archives 1860-2000

Geosciences

Abstract  The Oxfordian sedimentary successions studied in the Swiss Jura, in Normandy, and in the Soria and Cazorla regions of Spain display complex facies evolution and stacking patterns. Based on biostratigraphy and absolute age dating, it is suggested that the shallow-water depositional settings in the Jura, Normandy, and the Soria region as well as the deeper-water environments in the Cazorla region, recorded climatic and sea-level fluctuations in the Milankovitch frequency band. Beds and bedsets corresponding to 20-, 100-, and 400-ka cyclicities can be identified. Facies evolution inside such small-scale sequences and also in the larger sequences of million-year scale is interpreted in terms of sequence stratigraphy. Superposition of high-frequency cyclicity on a longer-term sea-level trend led to multiplication of diagnostic surfaces: sequence-boundary and maximum-flooding zones in the large-scale sequences can thus be defined. These zones are correlated between closely spaced sections, but also from the Swiss Jura to Normandy and to Spain. The narrow time lines given by Milankovitch cyclicity then allow comparison of facies evolution in the different regions on a scale of 100 ka or less. By filtering out local effects of differential subsidence and sediment supply, a long-term sea-level curve valid for the northwestern margin of the Tethys ocean can be reconstructed for the Middle to Late Oxfordian. Differential subsidence is implied from varying thicknesses of the sequences as well as from the distribution of siliciclastics which have been channelized through depressions. Tilted blocks, reduced sedimentation, or increased input of siliciclastics appearing at the same time in all study areas point to a widespread regional tectonic event. Distribution through the sequences of climate-dependent facies components such as corals, ooids, palynomorphs, and siliciclastics indicates that climate changes were dependent on atmospheric circulation patterns and thus on paleolatitude. Rainy periods and related increase of siliciclastics in the Swiss Jura were more abundant during low sea-level stands, whereas in the Soria region they coincided with sea-level highs. Through the combination of high-resolution sequence stratigraphy and cyclostratigraphy, and supported by biostratigraphy and absolute dating, it becomes possible to analyze paleoenvironmental changes in a very narrow time framework.

Electronic Resource