Otto Barblan, Brustbild - Hymne aus der Calvenfeier, Liedanfang, Noten und Text

Signatur des Originals: S 36/F02685

Wilhelm Baumgartner, Brustbild - Baumgartner, Mein Heimatland, Liedanfang in Text und Noten

Signatur des Originals: S 36/F02829

Johannes Brahms, Brustbild - Ständchen, Liedanfang in Noten und Text

Signatur des Originals: S 36/F03148

Thomas Koschat, Brustbild - Liedanfang in Text und Noten: Verlassen verlassen; verlassen bin i!

Signatur des Originals: S 36/F05009

Fragm. lat. VII 61 - Kanonistischer Text

Trägerband: Inc. qu. 873; Vorbesitzer: Dominikanerkloster Frankfurt am Main

Samuel Hassel als Aschemann, Rollenbild, in: Ferdinand Raimund: Der Bauer als Millionär, nebst Liedauszug in Text und Noten

Signatur des Originals: S 36/G03140

Costume Bild zur Theaterzeitung : Die Spinn Scene aus der Oper "Martha", Text von Friedrich, Musik von Flotow

Signatur des Originals: S 36/G14524

Der Tosephtatraktat Roš Haššana : in vokalisiertem Text mit sprachlichen, textkritischen und sachlichen Bemerkungen

von Paul Fiebig

Sayings of the Jewish Fathers : comprising Pirqe Aboth and Pereq R. Meir ; ... with ... specimen pages of the Cambridge University manuscript of the Mishnah 'Jerushalmith' from which the text of Aboth is taken

by Charles Taylor

Deutsches Kolonialrecht : eine orientierende Schilderung der außereuropäischen Erwerbungen des Deutschen Reiches und Darstellung ihrer Rechtsordnung ; nebst dem Text und Erläuterungen der diese Schutzgebiete betreffenden Gesetze und kaiserlichen Verordnungen

von Karl Gareis

Fragm. lat. VIII 84 - Grammatischer Text

Trägerband: 15/481; Vorbesitzer: Dominikanerkloster Frankfurt am Main

Kritischer Commentar zu den Psalmen : nebst Text und Uebersetzung

von H. Graetz

Biographische Skizzen berühmter Feldherren des k. k. österreichischen Heeres von den ältesten bis auf die neuesten Zeiten : in kurzem Auszuge nach Nekrologen der österreichischen Militär-Zeitschrift, und des neuen Archivs für Geschichte, Staatenkunde, Literatur und Kunst ... und mehreren andern gedruckten und ungedruckten Quellen ; als Text zu den in 18 Heften enthaltenen 72 Abbildungen der k. k. österreichischen Generalität

hrsg. von Johann Ritter von Rittersberg

The p120-catenin/Kaiso signaling pathway

The canonical and non-canonical Wnt signaling pathways appear to interact with one another as a network in development, or when hyper-activated, in the progression of disease. A much studied key mediator of the canonical Wnt pathway, β-catenin, is characterized by a central armadillo-repeat domain that engages in multiple protein-protein interactions, such as those with cadherins functioning at cell-cell contact regions. In the nucleus, β-catenin forms a complex with the repressor TCF/LEF, promoting the activation of genes participating in processes such as proliferation, differentiation and stem cell survival. Somewhat similarly, the p120-catenin binds the distinct transcriptional repressor Kaiso, relieving Kaiso-mediated repression to promote gene activation. Here, employing Xenopus laevis, I report upon both downstream and upstream aspects of the p120-catenin/Kaiso pathway which was previously poorly understood. I first show that Kaiso, a BTB/POZ zinc-finger family member, directly represses canonical Wnt gene targets (Siamois, c-Fos, Cyclin-D1 and c-Myc) in conjunction with TCF. Depletion or dominant-negative inhibition of xKaiso results in Siamois de-repression, while xKaiso over-expression induces additional Siamois repression through recruitment of N-CoR co-repressor and chromatin modifications. Functional interdependencies are further corroborated by the capacity of Kaiso to suppress β-catenin-induced axis duplication. Thus, my work inter-relates the p120-catenin/Kaiso and β-catenin/TCF pathways at the level of specific gene promoters important in development and cancer progression. Regarding upstream aspects of the p120-catenin/Kaiso pathway, I collaboratively identified p120 in association with Frodo, a protein previously identified as a component of the canonical (β-catenin dependent) Wnt pathway. I determined that canonical Wnt signals result in Frodo-mediated stabilization of p120-catenin, resulting in the sequestration of Kaiso to the cytoplasm and thereby the activation (relief of repression) of gene targets. Developmental evidence supporting this view included findings that Frodo has the capacity to partially rescue Kaiso over-expression phenotypes in early Xenopus embryos. Taken together, my studies point to the convergence of p120-catenin/Kaiso and β-catenin/TCF signaling pathways at the level of gene transcription as well as at more upstream points during vertebrate development. ^

The low molecular weight (LMW) isoforms of cyclin E provide a novel mechanism of cell cycle deregulation

Cyclin E, in complex with cyclin dependent kinase 2 (CDK2), is a positive regulator of G1 to S phase progression of the cell cycle. Deregulation of G1/S phase transition occurs in the majority of tumors. Cyclin E is overexpressed and post-translationally generates low molecular weight (LMW) isoforms in breast cancer, but not normal cells. Such alteration of cyclin E is linked to poor prognosis. Therefore, we hypothesized that the LMW isoforms of cyclin E provide a novel mechanism of cell cycle de-regulation in cancer cells. Insect cell expression system was used to explore the biochemical properties of the cyclin E isoforms. Non-tumorigenic (76NE6) and tumorigenic (T47D) mammary epithelial cells transfected with the cyclin E isoforms and breast tumor tissue endogenously expressing the LMW isoforms were used to study the biologic consequences of the LMW isoforms of cyclin E. All model systems studied show that the LMW forms (compared to full-length cyclin E) have increased kinase activity when partnered with CDK2. Increases in the percentage of cells in S phase and colony formation were also observed after overexpression of LMW compared to full-length cyclin E. The LMW isoforms of cyclin E utilize several mechanisms to attain their hyper-activity. They bind CDK2 more efficiently, and are resistant to inhibition by cyclin dependent kinase inhibitors (CKIs) as compared to full-length cyclin E. In addition, the LMW isoforms sequester the CKIs from full-length cyclin E abrogating the overall negative regulation of cyclin E. Despite their correlation with adverse biological consequences, the direct role of the LMW isoforms of cyclin E in mediating tumorigenesis remained unanswered. Subsequent to LMW cyclin E expression in 76NE6 cells, they lose their ability to enter quiescence and exhibit genomic instability, both characteristic of a tumor cell phenotype. Furthermore, injection of 76NE6 cells overexpressing each of the cyclin E isoforms into the mammary fat pad of nude mice revealed that the LMW isoforms of cyclin E yield tumors, whereas the full-length cyclin E does not. In conclusion, the LMW isoforms of cyclin E utilize several mechanisms to acquire a hyperactive phenotype that results in deregulation of the cell cycle and initiates the tumorigenic process in otherwise non-transformed mammary epithelial cells. ^