Emmy Hainmüller als Ninabella, Herbert Hesse als Kaspar, Szenenfoto, Doppelbildnis, in: Werner Egk: Die Zaubergeige

Signatur des Originals: S 36/F10745

Heinz Werner Zimmermann, Brustbild

Signatur des Originals: S 36/F11311

Wolf Dieter Tropf als Macheath, Karin Werner als Spelunken-Jenny, Szenenfoto, in: Kurt Weill: Die Dreigroschenoper, Frankfurt a. M.: Schauspielhaus, 1979

Signatur des Originals: S 36/F11320

Elste Wilfried als Quaste, Heinz Werner Kraehkamp als Wiesel, Barbara Sukowa als Karfunkel, Ingo Lampe als Schmaltz, Szenenfoto, Gruppenbildnis, Kniestück, in: Friedrich Carl Waechter: Schule mit Clowns, 1977

Signatur des Originals: S 36/F11343

Ingo Lampe als Schmaltz, Wilfried Elste als Quaste, Michael Altmann als Dr. Sinn, Heinz Werner Kraehkamp als Wiesel, Barbara Sukowa als Karfunkel, Szenenfoto, Gruppenbildnis, in: Friedrich Carl Waechter: Schule mit Clowns, 1977

Signatur des Originals: S 36/F11345

Werner Siedhoff als Urosch, Szenenfoto, Brustbild, in: Rudolf Perak: Verliebte Frauen

Signatur des Originals: S 36/F11801

Hans Baur, Werner Siedhoff, Szenenfoto, in: Gerhard Schumann: Gudruns Tod

Signatur des Originals: S 36/F12032

Ilse Werner, Rollenbild, Brustbild

Signatur des Originals: S 36/F11918

Werner Alberti, Brustbild

Signatur des Originals: S 36/G00232

Werner Alberti, Brustbild

Signatur des Originals: S 36/G00233

Anton von Werner beim Cellospiel

Signatur des Originals: S 36/G13733

Worte der Erinnerung an den am 22. Juni 1918 aus dem Leben geschiedenen Rabbiner der Israelitischen Kultusgemeinde München Professor Dr. Cossmann Werner : gesprochen bei den am 25. Juni 1918 stattgefundenen Trauerfeierlichkeiten

Aus der Sammlung des Leo Baeck Institute, digitalisiert in Kooperation mit dem Center for Jewish History, NY

Werner Beierwaltes, Eriúgena. Rasgos fundamentales de su pensamiento, Colección de Pensamiento medieval y renacentista, Eunsa, Pamplona, 2009, 347 p., ISBN 978-84- 313-2598-5

Fil: Peretó Rivas, Rubén. Consejo Nacional de Investigaciones Científicas y Técnicas

Nucleolar localization of the Werner syndrome protein in human cells

Werner Syndrome (WS) is a human genetic disorder with many features of premature aging. The gene defective in WS (WRN) has been cloned and encodes a protein homologous to several helicases, including Escherichia coli RecQ, the human Bloom syndrome protein (BLM), and Saccharomyces cerevisiae Sgs1p. To better define the function of WRN protein we have determined its subcellular localization. Indirect immunofluorescence using polyclonal anti-human WRN shows a predominant nucleolar localization. Studies of WRN mutant cells lines confirmed the specificity of antibody recognition. No difference was seen in the subcellular localization of the WRN protein in a variety of normal and transformed human cell lines, including both carcinomas and sarcomas. The nucleolar localization of human WRN protein was supported by the finding that upon biochemical subcellular fractionation, WRN protein is present in an increased concentration in a subnuclear fraction enriched for nucleolar proteins. We have also determined the subcellular localization of the mouse WRN homologue (mWRN). In contrast to human WRN protein, mWRN protein is present diffusely throughout the nucleus. Understanding the function of WRN in these organisms of vastly differing lifespan may yield new insights into the mechanisms of lifespan determination.

A deletion within the murine Werner syndrome helicase induces sensitivity to inhibitors of topoisomerase and loss of cellular proliferative capacity

Werner syndrome (WS) is an autosomal recessive disorder characterized by genomic instability and the premature onset of a number of age-related diseases. The gene responsible for WS encodes a member of the RecQ-like subfamily of DNA helicases. Here we show that its murine homologue maps to murine chromosome 8 in a region syntenic with the human WRN gene. We have deleted a segment of this gene and created Wrn-deficient embryonic stem (ES) cells and WS mice. While displaying reduced embryonic survival, live-born WS mice otherwise appear normal during their first year of life. Nonetheless, although several DNA repair systems are apparently intact in homozygous WS ES cells, such cells display a higher mutation rate and are significantly more sensitive to topoisomerase inhibitors (especially camptothecin) than are wild-type ES cells. Furthermore, mouse embryo fibroblasts derived from homozygous WS embryos show premature loss of proliferative capacity. At the molecular level, wild-type, but not mutant, WS protein copurifies through a series of centrifugation and chromatography steps with a multiprotein DNA replication complex.