Aspects of the Production and Reception of Female Writers in an International Context

Als roter Faden dieses Sammelbandes internationaler Wissenschaftler/innen wirkt die 1997 veröffentlichte niederländische Anthologie Met en zonder lauwerkrans von Autorinnen zwischen 1550 und 1850. Der Leser/die Leserin erhält Gelegenheit, die Probleme, Theorien, Möglichkeiten und Übereinstimmungen feministischer Literaturwissenschaft zu verfolgen und dabei Autorinnen und ihre Themen in Literaturen kennenzulernen, die, wiewohl zueinander benachbart, sonst kaum vermittelt werden. Vergleiche können gezogen, Anregungen zu neuen Ansätzen gegeben werden.The topic of this collection of essays of international scholars is the anthology Met en zonder lauwerkrans of Dutch and Flemish female authors between 1550 and 1850, published in 1997. Readers are offered the possibility to follow up as well re-appraise problems, theories, possibilities and conventions of the historiography of feminist approaches to literature. The essays introduce women authors, their genres in languages and literatures, many of which are geographically close but also virtually unknown. Comparisons are made, and the question of how to write the history of women’s literature is posed again

Review of: Monika Kubrova: Vom guten Leben. Adelige Frauen im 19. Jahrhundert. Berlin: Akademie Verlag 2011.

Monika Kubrova hinterfragt konsequent ideologische Konstrukte und bürgerliche Kategorien wie die einer Geschlechterpolarität im Hinblick auf die Lebenswelt adliger Frauen. Ihr methodischer Ansatz ist der der Relationalität des Geschlechterbegriffs, der sich aus dem jeweiligen Kontext entschlüsselt, wobei die Konzepte von Adeligkeit, Familie, Geschlecht und Autobiographik die Forschungsansätze bilden. Es finden sich vielfältige weibliche Lebensgeschichten zu Ende des 19. Jahrhunderts, sowohl in einer Art von Normalbiographie im Familien- und gesellschaftlichen Rahmen als auch in einer beruflichen Bindung, wie es für ledige Frauen möglich schien. Erst mit biographischen Konflikten, also mit dem Verlassen des Schutzraums des Adels, wurde das Geschlecht an sich zu einer Kategorie von Benachteiligung.Monika Kubrova examines ideological constructs and bourgeois categories, such as gender polarity, with regards to the environment of aristocratic women. Her methodological approach is the relationality of the notion of gender, which depends on the particular context, while the concepts of aristocracy, family, gender, and autobiography provide the basic research approaches. There are manifold female life stories at the end of the 19th century, both as a type of normal biography in the framework of family and society as well as in professional relations, which seemed possible for single women. Not until the appearance of biographical conflicts, i.e. with leaving the safe haven of nobility, did gender in itself become a category of disadvantage

Deep proteome of human nNOS/NOS1-positive versus MOCK SH-SY5Y neuroblastoma cells under full nutrition, serum free starvation and rapamycin treatment

Upregulations of neuronal nitric oxide synthase (nNOS/NOS1) in the mouse brain upon aging suggest a role in age-associated changes of protein homeostasis. We generated a cell model, in which constitutive expression of nNOS in SH-SY5Y cells at a level comparable to mouse brain replicates the aging phenotype i.e. slowing of cell proliferation, cell enlargement and expression of senescence markers. nNOS+ and MOCK cells were exposed to proteostasis stress by treatment with rapamycin or serum-free starvation. The proteomes were analyzed per SILAC or label-free using hybrid liquid chromatography/mass spectrometry (LC/MS). Full scan MS-data were acquired using Xcalibur, and raw mass spectra were analyzed using the proteomics software MaxQuant. The human reference proteome from uniprot was used as template to identify peptides and proteins and quantify protein expression. The DiB data file contains essential MaxQuant output tables and includes peptide and protein identification, accession numbers, protein and gene names, sequence coverage and quantification values of each sample. Differences in protein expression in MOCK versus nNOS+ SH-SY5Y cells and interpretation of results are presented in Valek et al. (2018). Raw mass spectra and MaxQuant output files have been deposited to the ProteomeXchange Consortium (Vizcaino et al., 2014) via the PRIDE partner repository with the dataset identifier PRIDE: PXD010538

Redox-proteomes of human NOS1-transduced versus MOCK SH-SY5Y neuroblastoma cells under full nutrition, serum-free starvation, and rapamycin treatment

Upregulations of neuronal nitric oxide synthase (nNOS/NOS1) in the mouse brain upon aging and stress suggest a role of NO-dependent redox protein modifications for age-associated protein imbalances or dysfunctions. We generated a cell model, in which constitutive expression of nNOS in SH-SY5Y cells at a level comparable with mouse brain replicates the aging phenotype, that is, slowing of cell proliferation, cell enlargement, and expression of senescence markers. nNOS+ and MOCK cells were exposed to proteostasis stress by the treatment with rapamycin or serum-free starvation versus control conditions. To analyze NO-mediated S-nitrosylations (SNO) and other reversible protein modifications including disulfides and sulfoxides, we used complimentary proteomic approaches encompassing 2D-SNO-DIGE (differential gel electrophoresis), SNO-site identification (SNOSID), SNO Super-SILAC, SNO BIAM-Switch, and Redox-BIAM switch. The redox proteomes were analyzed using hybrid liquid chromatography/mass spectrometry (LC/MS). Full scan MS-data were acquired using Xcalibur, and raw mass spectra were analyzed using the proteomics software MaxQuant. The human reference proteome sets from uniprot were used as templates to identify peptides and proteins and quantify protein expression. The DiB data file contains MaxQuant output tables of the redox-modified proteins.The tables include peptide and protein identification, accession numbers, protein, and gene names, sequence coverage and quantification values of each sample. Differences in protein redox modifications in MOCK versus nNOS+ SH-SY5Y cells and interpretation of results are presented in (Valek et al., 2018)

Redox-proteomes of human NOS1-transduced versus MOCK SH-SY5Y neuroblastoma cells under full nutrition, serum-free starvation, and rapamycin treatment

Upregulations of neuronal nitric oxide synthase (nNOS/NOS1) in the mouse brain upon aging and stress suggest a role of NO-dependent redox protein modifications for age-associated protein imbalances or dysfunctions. We generated a cell model, in which constitutive expression of nNOS in SH-SY5Y cells at a level comparable with mouse brain replicates the aging phenotype, that is, slowing of cell proliferation, cell enlargement, and expression of senescence markers. nNOS+ and MOCK cells were exposed to proteostasis stress by the treatment with rapamycin or serum-free starvation versus control conditions. To analyze NO-mediated S-nitrosylations (SNO) and other reversible protein modifications including disulfides and sulfoxides, we used complimentary proteomic approaches encompassing 2D-SNO-DIGE (differential gel electrophoresis), SNO-site identification (SNOSID), SNO Super-SILAC, SNO BIAM-Switch, and Redox-BIAM switch. The redox proteomes were analyzed using hybrid liquid chromatography/mass spectrometry (LC/MS). Full scan MS-data were acquired using Xcalibur, and raw mass spectra were analyzed using the proteomics software MaxQuant. The human reference proteome sets from uniprot were used as templates to identify peptides and proteins and quantify protein expression. The DiB data file contains MaxQuant output tables of the redox-modified proteins.The tables include peptide and protein identification, accession numbers, protein, and gene names, sequence coverage and quantification values of each sample. Differences in protein redox modifications in MOCK versus nNOS+ SH-SY5Y cells and interpretation of results are presented in (Valek et al., 2018)

Data file of a deep proteome analysis of the prefrontal cortex in aged mice with progranulin deficiency or neuronal overexpression of progranulin

AbstractProgranulin deficiency is associated with neurodegeneration in humans and in mice. The mechanisms likely involve progranulin-promoted removal of protein waste via autophagy. We performed a deep proteomic screen of the pre-frontal cortex in aged (13–15 months) female progranulin-deficient mice (GRN−/−) and mice with inducible neuron-specific overexpression of progranulin (SLICK-GRN-OE) versus the respective control mice. Proteins were extracted and analyzed per liquid chromatography/mass spectrometry (LC/MS) on a Thermo Scientific™ Q Exactive Plus equipped with an ultra-high performance liquid chromatography unit and a Nanospray Flex Ion-Source. Full Scan MS-data were acquired using Xcalibur and raw files were analyzed using the proteomics software Max Quant. The mouse reference proteome set from uniprot (June 2015) was used to identify peptides and proteins. The DiB data file is a reduced MaxQuant output and includes peptide and protein identification, accession numbers, protein and gene names, sequence coverage and label free quantification (LFQ) values of each sample. Differences in protein expression in genotypes are presented in "Progranulin overexpression in sensory neurons attenuates neuropathic pain in mice: Role of autophagy" (C. Altmann, S. Hardt, C. Fischer, J. Heidler, H.Y. Lim, A. Haussler, B. Albuquerque, B. Zimmer, C. Moser, C. Behrends, F. Koentgen, I. Wittig, M.H. Schmidt, A.M. Clement, T. Deller, I. Tegeder, 2016) [1]

Nitric oxide contributes to protein homeostasis by S-nitrosylations of the chaperone HSPA8 and the ubiquitin ligase UBE2D

Upregulations of neuronal nitric oxide synthase (nNOS) in the rodent brain have been associated with neuronal aging. To address underlying mechanisms we generated SH-SY5Y neuronal cells constitutively expressing nNOS at a level similar to mouse brain (nNOS+ versus MOCK). Initial experiments revealed S-nitrosylations (SNO) of key players of protein homeostasis: heat shock cognate HSC70/HSPA8 within its nucleotide-binding site, and UBE2D ubiquitin conjugating enzymes at the catalytic site cysteine. HSPA8 is involved in protein folding, organelle import/export and chaperone-mediated LAMP2a-dependent autophagy (CMA). A set of deep redox and full proteome analyses, plus analysis of autophagy, CMA and ubiquitination with rapamycin and starvation as stimuli confirmed the initial observations and revealed a substantial increase of SNO modifications in nNOS+ cells, in particular targeting protein networks involved in protein catabolism, ubiquitination, carbohydrate metabolism and cell cycle control. Importantly, NO-independent reversible oxidations similarly occurred in both cell lines. Functionally, nNOS caused an accumulation of proteins, including CMA substrates and loss of LAMP2a. UBE2D activity and proteasome activity were impaired, resulting in dysregulations of cell cycle checkpoint proteins. The observed changes of protein degradation pathways caused an expansion of the cytoplasm, large lysosomes, slowing of the cell cycle and suppression of proliferation suggesting a switch of the phenotype towards aging, supported by downregulations of neuronal progenitor markers but increase of senescence-associated proteins. Hence, upregulation of nNOS in neuronal cells imposes aging by SNOing of key players of ubiquitination, chaperones and of substrate proteins leading to interference with crucial steps of protein homeostasis. Keywords: Redox modification, Nitric oxide, Autophagy, Ubiquitin, Chaperone, Lysosome, Posttranslational modification, Starvation, Rapamycin, Senescenc