{ "types" : { "Bookmark" : { "pluralLabel" : "Bookmarks" }, "Publication" : { "pluralLabel" : "Publications" }, "GoldStandardPublication" : { "pluralLabel" : "GoldStandardPublications" }, "GoldStandardBookmark" : { "pluralLabel" : "GoldStandardBookmarks" }, "Tag" : { "pluralLabel" : "Tags" }, "User" : { "pluralLabel" : "Users" }, "Group" : { "pluralLabel" : "Groups" }, "Sphere" : { "pluralLabel" : "Spheres" } }, "properties" : { "count" : { "valueType" : "number" }, "date" : { "valueType" : "date" }, "changeDate" : { "valueType" : "date" }, "url" : { "valueType" : "url" }, "id" : { "valueType" : "url" }, "tags" : { "valueType" : "item" }, "user" : { "valueType" : "item" } }, "items" : [ { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2b7b46f23342a8502e56e4b49ab73cd6b/pumaizi", "tags" : [ "izi","2011","hausser" ], "intraHash" : "b7b46f23342a8502e56e4b49ab73cd6b", "interHash" : "8d1e7bd28ea0fea95f0da4dd7fcf54da", "label" : "A novel protein kinase D phosphorylation site in the tumor suppressor Rab interactor 1 is critical for coordination of cell migration", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Molecular Biology of the Cell", "year": "2011", "url": "http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E10-05-0427", "author": [ "S. Ziegler","T. Eiseler","R.-P. Scholz","A. Beck","G. Link","A. Hausser" ], "authors": [ {"first" : "S.", "last" : "Ziegler"}, {"first" : "T.", "last" : "Eiseler"}, {"first" : "R.-P.", "last" : "Scholz"}, {"first" : "A.", "last" : "Beck"}, {"first" : "G.", "last" : "Link"}, {"first" : "A.", "last" : "Hausser"} ], "volume": "22","number": "5","pages": "570--580","abstract": "The multifunctional signal adapter protein Ras and Rab interactor 1 (RIN1) is a Ras effector protein involved in the regulation of epithelial cell processes such as cell migration and endocytosis. RIN1 signals via two downstream pathways, namely the activation of Rab5 and Abl family kinases. Protein kinase D (PKD) phosphorylates RIN1 at serine 351 in vitro, thereby regulating interaction with 14-3-3 proteins. Here, we report the identification of serine 292 in RIN1 as an in vivo PKD phosphorylation site. PKD-mediated phosphorylation at this site was confirmed with a phospho-specific antibody and by mass spectrometry. We demonstrate that phosphorylation at serine 292 controls RIN1-mediated inhibition of cell migration by modulating the activation of Abl kinases. We further provide evidence that RIN1 in vivo phosphorylation at serine 351 occurs independently of PKD. Collectively, our data identify a novel PKD signaling pathway through RIN1 and Abl kinases that is involved in the regulation of actin remodeling and cell migration.", "isbn" : "1939-4586 (Electronic)$\\backslash$n1059-1524 (Linking)", "pmid" : "21209314", "issn" : "1059-1524", "doi" : "10.1091/mbc.E10-05-0427", "bibtexKey": "Ziegler2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2836a77bb0abc210beb7e5184837b22a2/pumaizi", "tags" : [ "boettinger","izi","2011" ], "intraHash" : "836a77bb0abc210beb7e5184837b22a2", "interHash" : "9e48e448e75575d525cf2694217d4b90", "label" : "Aldehyde PEGylation kinetics: A standard protein versus a pharmaceutically relevant single chain variable fragment", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Bioconjugate Chemistry", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21780828", "author": [ "Anna Moosmann","Jessica Blath","Robert Lindner","Egbert Müller","Heiner Böttinger" ], "authors": [ {"first" : "Anna", "last" : "Moosmann"}, {"first" : "Jessica", "last" : "Blath"}, {"first" : "Robert", "last" : "Lindner"}, {"first" : "Egbert", "last" : "Müller"}, {"first" : "Heiner", "last" : "Böttinger"} ], "volume": "22","number": "8","pages": "1545--1558","abstract": "The mPEG-aldehyde PEGylation with two different PEG sizes and two proteins was experimentally determined with respect to yield, conversion, and selectivity. The kinetic behavior of these PEGylation reactions was simulated using a numerically solved set of differential equations. We show that the assumption of an inactivation of mPEG-aldehyde is crucial for the simulation of the overall PEGylation and that the inactivation is pH-dependent. We further demonstrate that ideal PEGylation parameters such as pH, temperature, reaction time, and protein concentration need to be chosen carefully depending on the protein and PEG size. In terms of selectivity and yield, we show that the reaction should be stopped before the highest mono-PEG concentration is reached. Moreover, room temperature and a slightly acidic pH of approximately 6 are good starting points. In conclusion, selectivity can be optimized choosing a shorter reaction time and a reduced reaction temperature.", "isbn" : "0086222740", "pmid" : "21780828", "issn" : "10431802", "doi" : "10.1021/bc200090x", "bibtexKey": "Moosmann2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2137acc942a2bed5b959cc024609cbf9e/pumaizi", "tags" : [ "izi","2011","kontermann" ], "intraHash" : "137acc942a2bed5b959cc024609cbf9e", "interHash" : "0e6526909181a7f5888436e5fc213694", "label" : "Strategies for extended serum half-life of protein therapeutics", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Current Opinion in Biotechnology", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21862310", "author": [ "Roland E. Kontermann" ], "authors": [ {"first" : "Roland E.", "last" : "Kontermann"} ], "volume": "22","number": "6","pages": "868--876","abstract": "With a growing number of protein therapeutics being developed, many of them exhibiting a short plasma half-life, half-life extension strategies find increasing attention by the biotech and pharmaceutical industry. Extension of the half-life can help to reduce the number of applications and to lower doses, thus are beneficial for therapeutic but also economic reasons. Here, a comprehensive overview of currently developed half-life extension strategies is provided including those aiming at increasing the hydrodynamic volume of a protein drug but also those implementing recycling processes mediated by the neonatal Fc receptor. © 2011 Elsevier Ltd.", "isbn" : "0958-1669", "pmid" : "21862310", "issn" : "09581669", "doi" : "10.1016/j.copbio.2011.06.012", "bibtexKey": "Kontermann2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/28094e00d7baa3373d91c2f9f72aa904b/pumaizi", "tags" : [ "izi","2011","hausser" ], "intraHash" : "8094e00d7baa3373d91c2f9f72aa904b", "interHash" : "452e1e485fd32951a1a7b1be2d45136a", "label" : "Phosphorylation of ser 402 impedes phosphatase activity of slingshot 1", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "EMBO Reports", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21525957", "author": [ "Sandra Barisić","Anja C. Nagel","Mirita Franz-Wachtel","Boris MacEk","Anette Preiss","Gisela Link","Dieter Maier","Angelika Hausser" ], "authors": [ {"first" : "Sandra", "last" : "Barisić"}, {"first" : "Anja C.", "last" : "Nagel"}, {"first" : "Mirita", "last" : "Franz-Wachtel"}, {"first" : "Boris", "last" : "MacEk"}, {"first" : "Anette", "last" : "Preiss"}, {"first" : "Gisela", "last" : "Link"}, {"first" : "Dieter", "last" : "Maier"}, {"first" : "Angelika", "last" : "Hausser"} ], "volume": "12","number": "6","pages": "527--533","abstract": "By using mass spectrometry, we have identified Ser 402 as a new phosphorylation site within the catalytic domain of human slingshot 1 (SSH1). Phosphorylation at this site inhibits substrate binding and, thus, phosphatase activity in vitro, resulting in enrichment of phosphorylated cofilin in monolayer cell culture. We further demonstrate that protein kinase D (PKD) is upstream from Ser 402 phosphorylation. Accordingly, expression of active PKD in Drosophila phenotypically mimics the loss of SSH activity by inducing accumulation of phosphorylated cofilin and filamentous actin. We thus identify a universal mechanism by which PKD controls SSH1 phosphatase activity.", "isbn" : "1469-3178 (Electronic)$\\backslash$r1469-221X (Linking)", "pmid" : "21525957", "issn" : "1469221X", "doi" : "10.1038/embor.2011.53", "bibtexKey": "Barisic2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/28b83434ecc5452f6b7c052ac101593b4/pumaizi", "tags" : [ "izi","2011","pfizenmaier" ], "intraHash" : "8b83434ecc5452f6b7c052ac101593b4", "interHash" : "dc34d6971a21bb0257a17bb2bbea1202", "label" : "Ligand-induced internalization of TNF receptor 2 mediated by a di-leucin motif is dispensable for activation of the NFκB pathway", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Cellular Signalling", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/20807567", "author": [ "Roman Fischer","Olaf Maier","Matthias Naumer","Anja Krippner-Heidenreich","Peter Scheurich","Klaus Pfizenmaier" ], "authors": [ {"first" : "Roman", "last" : "Fischer"}, {"first" : "Olaf", "last" : "Maier"}, {"first" : "Matthias", "last" : "Naumer"}, {"first" : "Anja", "last" : "Krippner-Heidenreich"}, {"first" : "Peter", "last" : "Scheurich"}, {"first" : "Klaus", "last" : "Pfizenmaier"} ], "volume": "23","number": "1","pages": "161--170","abstract": "Endocytosis is an important mechanism to regulate tumor necrosis factor (TNF) signaling. In contrast to TNF receptor 1 (TNFR1; CD120a), the relevance of receptor internalization for signaling as well as the fate and route of internalized TNF receptor 2 (TNFR2; CD120b) is poorly understood. To analyze the dynamics of TNFR2 signaling and turnover at the plasma membrane we established a human TNFR2 expressing mouse embryonic fibroblast cell line in a TNFR1-/-/TNFR2-/- background. TNF stimulation resulted in a decrease of constitutive TNFR2 ectodomain shedding. We hypothesized that reduced ectodomain release is a result of TNF/TNFR2 complex internalization. Indeed, we could demonstrate that TNFR2 was internalized together with its ligand and cytoplasmic binding partners. Upon endocytosis the TNFR2 signaling complex colocalized with late endosome/lysosome marker Rab7 and entered the lysosomal degradation pathway. Furthermore, we identified a di-leucin motif in the cytoplasmic part of TNFR2 suggesting clathrin-dependent internalization of TNFR2. Internalization defective TNFR2 mutants are capable to signal, i.e. activate NF??B, demonstrating that the di-leucin motif dependent internalization is dispensable for this response. We therefore propose that receptor internalization primarily serves as a negative feed-back to limit TNF responses via TNFR2. ?? 2010 Elsevier Inc.", "isbn" : "1873-3913 (Electronic)$\\backslash$r0898-6568 (Linking)", "pmid" : "20807567", "issn" : "08986568", "doi" : "10.1016/j.cellsig.2010.08.016", "bibtexKey": "Fischer2011a" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2b4186f12063f4d91c36243786ff879d2/pumaizi", "tags" : [ "izi","2011" ], "intraHash" : "b4186f12063f4d91c36243786ff879d2", "interHash" : "8b1767162b0cbe125dcde3b4dc3b78c4", "label" : "Caspase-3 cleaves XIAP in a positive feedback loop to sensitize melanoma cells to TRAIL-induced apoptosis", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Oncogene", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/20856198", "author": [ "M. Hörnle","N. Peters","B. Thayaparasingham","H. Vörsmann","H. Kashkar","D. Kulms" ], "authors": [ {"first" : "M.", "last" : "Hörnle"}, {"first" : "N.", "last" : "Peters"}, {"first" : "B.", "last" : "Thayaparasingham"}, {"first" : "H.", "last" : "Vörsmann"}, {"first" : "H.", "last" : "Kashkar"}, {"first" : "D.", "last" : "Kulms"} ], "volume": "30","number": "5","pages": "575--587","abstract": "Successful treatment of melanoma is still challenging, because metastasis remain chemoresistant and radioresistant. Accordingly, combinational treatments involving death ligands are mandatory. In a recent study from our lab, the majority out of 18 melanoma cell lines remained resistant against treatment with the death ligand TRAIL (tumor necrosis factor related apoptosis inducing ligand). Resistance was shown to be mainly due to incomplete processing of caspase-3 into catalytically inactive p21 by binding of the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP). Co-irradiation with sub-lethal ultraviolet (UV) B caused depletion of XIAP resulting in synergistic sensitization of all but two melanoma cell lines to TRAIL. We show here the XIAP depletion to essentially require initial caspase-mediated cleavage, which promotes proteasomal degradation of XIAP. Utilizing specific caspase inhibitors and small interfering RNA-mediated knockdown, we further identified caspase-3 to be responsible for performing the initial cleavage of XIAP after UVB treatment. Additional evidence suggests an accelerated mitochondrial outer membrane permeabilization in response to co-treatment with TRAIL and UVB, which directs the release of XIAP antagonizing factors including Smac. Distraction of XIAP consequently liberates caspase-3 to autocatalytically process into active p17. Activated caspase-3 cleaves XIAP and further enhances its activation in a positive regulatory feedback loop. The molecular mechanism discovered here appears to have broader implications, because cleavage of XIAP was also shown to accompany cisplatin-induced sensitization of melanoma cells to TRAIL.", "isbn" : "1476-5594 (Electronic)$\\backslash$r0950-9232 (Linking)", "pmid" : "20856198", "issn" : "09509232", "doi" : "10.1038/onc.2010.434", "bibtexKey": "Hornle2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/26db7f9a3df78160b8be5f6f35e69dbb3/pumaizi", "tags" : [ "izi","2011","pfizenmaier" ], "intraHash" : "6db7f9a3df78160b8be5f6f35e69dbb3", "interHash" : "31cec666650161c6087134e937f10f3f", "label" : "Therapeutic Targeting of CD95 and the TRAIL Death Receptors", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Recent Patents on Anti-Cancer Drug Discovery", "year": "2011", "url": "https://doi.org/10.2174/157489211796957739", "author": [ "Jeannette Gerspach","Klaus Pfizenmaier","Harald Wajant" ], "authors": [ {"first" : "Jeannette", "last" : "Gerspach"}, {"first" : "Klaus", "last" : "Pfizenmaier"}, {"first" : "Harald", "last" : "Wajant"} ], "volume": "6","number": "3","pages": "294--310","abstract": "The death receptors CD95, TRAILR1 and TRAILR2 induce cell death in many types of tumor cells. Activation of these receptors has received considerable interest due to its potential use in cancer therapy. In particular the observation that most primary cells are not or only barely TRAIL-sensitive resulted in the development of targeted therapy concepts that base on activation of the TRAIL death receptors by recombinant TRAIL or agonistic antibodies. Indeed, a variety of preclinical studies and several phase I and II clinical trials show that activation of TRAIL death receptors effectively induces apoptosis in cancer cells in vivo without therapy-limiting toxicity on normal cells. Primary tumor cells are often sparsely sensitive for TRAIL death receptor-mediated apoptosis or acquire resistance during therapy. Sensitization/resensitization of tumor cells by chemotherapeutic drugs or radiation can therefore be necessary for TRAIL-based therapies, but this involves the danger of triggering side effects related to the breakage of apoptosis resistance of non-transformed cells. Thus, there is a foreseeable need to develop optimized combination therapies or to locally restrict TRAIL receptor activation to fully exploit the antitumoral potential of TRAIL death receptors in the clinic. Although the high sensitivity of hepatocytes for CD95-mediated apoptosis prohibits therapies resulting in systemic activation of CD95, several studies have shown that this limitation can be overcome by ex vivo treatment regimes or by CD95 activating agonists with cell type-specific activity. This patent review is focused on the death receptor agonists currently under consideration in clinical trials, but also addresses the hurdles that have to be cleared to broaden and to improve the applicability of the currently used clinical concepts related to death receptor activation.", "isbn" : "2212-3970 (Electronic)\n1574-8928 (Linking)", "pmid" : "21762072", "issn" : "15748928", "doi" : "10.2174/157489211796957739", "bibtexKey": "Gerspach2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/240d54da4856f59188505f32030d3146d/pumaizi", "tags" : [ "sauter","izi","2011","kulms" ], "intraHash" : "40d54da4856f59188505f32030d3146d", "interHash" : "d379f97cd4eeef3fb0d5b3afce25df1a", "label" : "Modeling time delay in the NFκB signaling pathway following low dose IL-1 stimulation.", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 7, "pub-type": "article", "journal": "EURASIP journal on bioinformatics & systems biology", "year": "2011", "url": "https://doi.org/10.1186/1687-4153-2011-3", "author": [ "Johannes Witt","Sandra Barisic","Oliver Sawodny","Michael Ederer","Dagmar Kulms","Thomas Sauter" ], "authors": [ {"first" : "Johannes", "last" : "Witt"}, {"first" : "Sandra", "last" : "Barisic"}, {"first" : "Oliver", "last" : "Sawodny"}, {"first" : "Michael", "last" : "Ederer"}, {"first" : "Dagmar", "last" : "Kulms"}, {"first" : "Thomas", "last" : "Sauter"} ], "volume": "2011","number": "1","pages": "3","abstract": "Stimulation of human epithelial cells with IL-1 (10 ng/ml) + UVB radiation results in sustained NF$\\kappa$B activation caused by continuous IKK$\\beta$ phosphorylation. We have recently published a strictly reduced ordinary differential equation model elucidating the involved mechanisms. Here, we compare model extensions for low IL-1 doses (0.5 ng/ml), where delayed IKK$\\beta$ phosphorylation is observed. The extended model including a positive regulatory element, most likely auto-ubiquitination of TRAF6, reproduces the observed experimental data most convincingly. The extension is shown to be consistent with the original model and contains very sensitive processes which may serve as potential intervention targets.", "isbn" : "9783540752097", "pmid" : "21910922", "issn" : "1687-4153", "doi" : "10.1186/1687-4153-2011-3", "bibtexKey": "Witt2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2feb4ef63f990ed469250271bc0cabcaf/pumaizi", "tags" : [ "izi","2011","scheuric" ], "intraHash" : "feb4ef63f990ed469250271bc0cabcaf", "interHash" : "a581258b47f38b8c7d608594368e2d2d", "label" : "Identification of models of heterogeneous cell populations from population snapshot data", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 7, "pub-type": "article", "journal": "BMC Bioinformatics", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21527025", "author": [ "Jan Hasenauer","Steffen Waldherr","Malgorzata Doszczak","Nicole Radde","Peter Scheurich","Frank Allgöwer" ], "authors": [ {"first" : "Jan", "last" : "Hasenauer"}, {"first" : "Steffen", "last" : "Waldherr"}, {"first" : "Malgorzata", "last" : "Doszczak"}, {"first" : "Nicole", "last" : "Radde"}, {"first" : "Peter", "last" : "Scheurich"}, {"first" : "Frank", "last" : "Allgöwer"} ], "volume": "12","pages": "125","abstract": "Most of the modeling performed in the area of systems biology aims at achieving a quantitative description of the intracellular pathways within a \"typical cell\". However, in many biologically important situations even clonal cell populations can show a heterogeneous response. These situations require study of cell-to-cell variability and the development of models for heterogeneous cell populations.", "isbn" : "7116856773", "pmid" : "21527025", "issn" : "14712105", "doi" : "10.1186/1471-2105-12-125", "bibtexKey": "Hasenauer2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/23e47b14cdfd127a8a5b3c7a104442bce/pumaizi", "tags" : [ "izi","2011","scheuric" ], "intraHash" : "3e47b14cdfd127a8a5b3c7a104442bce", "interHash" : "6bf6a6d4992f721385fd181ffe0d45e0", "label" : "TNFR1-induced activation of the classical NF-κB pathway", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "FEBS Journal", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21232017", "author": [ "Harald Wajant","Peter Scheurich" ], "authors": [ {"first" : "Harald", "last" : "Wajant"}, {"first" : "Peter", "last" : "Scheurich"} ], "volume": "278","number": "6","pages": "862--876","abstract": "The molecular mechanisms underlying activation of the I$\\kappa$B kinase (IKK) complex are presumably best understood in the context of tumor necrosis factor (TNF) receptor-1 (TNFR1) signaling. In fact, it seems that most, if not all, proteins relevant for this process have been identified and extensive biochemical and genetic data are available for the role of these factors in TNF-induced IKK activation. There is evidence that protein modification-independent assembly of a core TNFR1 signaling complex containing TNFR1-associated death domain, receptor interacting kinase 1, TNF receptor-associated factor 2 and cellular inhibitor of apoptosis protein 1 and 2 starts a chain of nondegrading ubiquitination events that culminate in the recruitment and activation of IKK complex-stimulating kinases and the IKK complex itself. Here, we sum up the known details of TNFR1-induced IKK activation, address arising contradictions and discuss possible explanations resolving the apparent discrepancies.", "isbn" : "1742-4658 (Electronic)$\\backslash$r1742-464X (Linking)", "pmid" : "21232017", "issn" : "1742464X", "doi" : "10.1111/j.1742-4658.2011.08015.x", "bibtexKey": "Wajant2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/23b9f0967438e22c6855e7c4b3e645681/pumaizi", "tags" : [ "izi","2011","scheuric" ], "intraHash" : "3b9f0967438e22c6855e7c4b3e645681", "interHash" : "4721a47c0ad608d7759743082cee304a", "label" : "Heterogeneity reduces sensitivity of cell death for TNF-Stimuli", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "BMC Systems Biology", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/22204418", "author": [ "Monica Schliemann","Eric Bullinger","Steffen Borchers","Frank Allgöwer","Rolf Findeisen","Peter Scheurich" ], "authors": [ {"first" : "Monica", "last" : "Schliemann"}, {"first" : "Eric", "last" : "Bullinger"}, {"first" : "Steffen", "last" : "Borchers"}, {"first" : "Frank", "last" : "Allgöwer"}, {"first" : "Rolf", "last" : "Findeisen"}, {"first" : "Peter", "last" : "Scheurich"} ], "volume": "5","pages": "204","abstract": "BACKGROUND: Apoptosis is a form of programmed cell death essential for the maintenance of homeostasis and the removal of potentially damaged cells in multicellular organisms. By binding its cognate membrane receptor, TNF receptor type 1 (TNF-R1), the proinflammatory cytokine Tumor Necrosis Factor (TNF) activates pro-apoptotic signaling via caspase activation, but at the same time also stimulates nuclear factor $\\kappa$B (NF-$\\kappa$B)-mediated survival pathways. Differential dose-response relationships of these two major TNF signaling pathways have been described experimentally and using mathematical modeling. However, the quantitative analysis of the complex interplay between pro- and anti-apoptotic signaling pathways is an open question as it is challenging for several reasons: the overall signaling network is complex, various time scales are present, and cells respond quantitatively and qualitatively in a heterogeneous manner.$\\backslash$n$\\backslash$nRESULTS: This study analyzes the complex interplay of the crosstalk of TNF-R1 induced pro- and anti-apoptotic signaling pathways based on an experimentally validated mathematical model. The mathematical model describes the temporal responses on both the single cell level as well as the level of a heterogeneous cell population, as observed in the respective quantitative experiments using TNF-R1 stimuli of different strengths and durations. Global sensitivity of the heterogeneous population was quantified by measuring the average gradient of time of death versus each population parameter. This global sensitivity analysis uncovers the concentrations of Caspase-8 and Caspase-3, and their respective inhibitors BAR and XIAP, as key elements for deciding the cell's fate. A simulated knockout of the NF-$\\kappa$B-mediated anti-apoptotic signaling reveals the importance of this pathway for delaying the time of death, reducing the death rate in the case of pulse stimulation and significantly increasing cell-to-cell variability.$\\backslash$n$\\backslash$nCONCLUSIONS: Cell ensemble modeling of a heterogeneous cell population including a global sensitivity analysis presented here allowed us to illuminate the role of the different elements and parameters on apoptotic signaling. The receptors serve to transmit the external stimulus; procaspases and their inhibitors control the switching from life to death, while NF-$\\kappa$B enhances the heterogeneity of the cell population. The global sensitivity analysis of the cell population model further revealed an unexpected impact of heterogeneity, i.e. the reduction of parametric sensitivity.", "isbn" : "1752-0509 (Electronic)$\\backslash$r1752-0509 (Linking)", "pmid" : "22204418", "issn" : "17520509", "doi" : "10.1186/1752-0509-5-204", "bibtexKey": "Schliemann2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2e3342accca96c0996810d38de3daffdd/pumaizi", "tags" : [ "izi","2011","pfizenmaier" ], "intraHash" : "e3342accca96c0996810d38de3daffdd", "interHash" : "4324a09532d41fc10adc7de00154c55b", "label" : "Workshop Summary: Introduction to Rational Design of New Means for Therapeutic Modulation of Function of the TNF Family", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Adv Exp Med Biol", "year": "2011", "url": "http://link.springer.com/10.1007/978-1-4419-6612-4_50", "author": [ "Klaus Pfizenmaier","David E. Szymkowski" ], "authors": [ {"first" : "Klaus", "last" : "Pfizenmaier"}, {"first" : "David E.", "last" : "Szymkowski"} ], "volume": "691","pages": "487--491", "isbn" : "0065-2598 (Print)\n0065-2598 (Linking)", "pmid" : "21153353", "doi" : "10.1007/978-1-4419-6612-4_50", "bibtexKey": "Pfizenmaier2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2e2d33dda0164ca0eb7883552bc173c97/pumaizi", "tags" : [ "izi","2011","pfizenmaier" ], "intraHash" : "e2d33dda0164ca0eb7883552bc173c97", "interHash" : "5672b4a984f513a765bac2ea40f4d6cd", "label" : "Genetic engineering of death ligands for improvement of therapeutic activity", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Advances in Experimental Medicine and Biology", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21153356", "author": [ "Jeannette Gerspach","Britta Schneider","Nicole Müller","Tina Otz","Harald Wajant","Klaus Pfizenmaier" ], "authors": [ {"first" : "Jeannette", "last" : "Gerspach"}, {"first" : "Britta", "last" : "Schneider"}, {"first" : "Nicole", "last" : "Müller"}, {"first" : "Tina", "last" : "Otz"}, {"first" : "Harald", "last" : "Wajant"}, {"first" : "Klaus", "last" : "Pfizenmaier"} ], "volume": "691","pages": "507--519","abstract": "The death ligands TRAIL, FasL/CD95L, and TNF are in the focus of intense preclinical and clinical research efforts having the aim to exploit these molecules as new anticancer drugs. A common feature of these ligands is that their transmembrane form displays higher and/or broader activity than their soluble counterpart. Accordingly, the bioactivity of the soluble form of these ligands ranges from being poorly active (FasL/CD95L) to displaying a receptor type-selective signaling capacity (TNF, TRAIL). The presently approved or clinically exploited recombinant variants of TNF and TRAIL correspond to the soluble trimeric form of these proteins. In order to increase their intrinsic and tumor-selective bioactivity, we modified these ligands by genetic engineering to reach two aims: (i) stabilization of their trimeric organization and/or (ii) directing ligand action to the diseased tissue. Here, we summarize our concepts and show recent data on improving death ligand activity by intramolecular stabilization and/or membrane ligand mimicking activity through cell surface presentation. © 2011 Springer Science+Business Media, LLC.", "isbn" : "9781441966117", "pmid" : "21153356", "issn" : "00652598", "doi" : "10.1007/978-1-4419-6612-4_53", "bibtexKey": "Gerspach2011a" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/20afad721e56e20c3a0b41ffe8be87f4e/pumaizi", "tags" : [ "izi","2011","kulms" ], "intraHash" : "0afad721e56e20c3a0b41ffe8be87f4e", "interHash" : "ce33786d895142a454e242b693ff541e", "label" : "The farnesyl transferase inhibitor lonafarnib inhibits mTOR signaling and enforces sorafenib-induced apoptosis in melanoma cells", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Journal of Investigative Dermatology", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/20944654", "author": [ "Heike Niessner","Daniela Beck","Tobias Sinnberg","Konstantinos Lasithiotakis","Evelyn MacZey","Jeannette Gogel","Sascha Venturelli","Alexander Berger","Mario Mauthe","Mahmoud Toulany","Keith Flaherty","Martin Schaller","Dirk Schadendorf","Tassula Proikas-Cezanne","Birgit Schittek","Claus Garbe","Dagmar Kulms","Friedegund Meier" ], "authors": [ {"first" : "Heike", "last" : "Niessner"}, {"first" : "Daniela", "last" : "Beck"}, {"first" : "Tobias", "last" : "Sinnberg"}, {"first" : "Konstantinos", "last" : "Lasithiotakis"}, {"first" : "Evelyn", "last" : "MacZey"}, {"first" : "Jeannette", "last" : "Gogel"}, {"first" : "Sascha", "last" : "Venturelli"}, {"first" : "Alexander", "last" : "Berger"}, {"first" : "Mario", "last" : "Mauthe"}, {"first" : "Mahmoud", "last" : "Toulany"}, {"first" : "Keith", "last" : "Flaherty"}, {"first" : "Martin", "last" : "Schaller"}, {"first" : "Dirk", "last" : "Schadendorf"}, {"first" : "Tassula", "last" : "Proikas-Cezanne"}, {"first" : "Birgit", "last" : "Schittek"}, {"first" : "Claus", "last" : "Garbe"}, {"first" : "Dagmar", "last" : "Kulms"}, {"first" : "Friedegund", "last" : "Meier"} ], "volume": "131","number": "2","pages": "468--479","abstract": "Farnesyl transferase inhibitors (FTIs) inhibit the farnesylation of proteins, including RAS and RHEB (Ras homolog enriched in brain). RAS signals to the RAF-MEK-ERK (MAPK) and PI3K-AKT-mTOR (AKT) signaling pathways, which have a major role in melanoma progression. RHEB positively regulates mammalian target of rapamycin (mTOR). We investigated the effects of the FTI lonafarnib alone and in combination with MAPK (mitogen-activated protein kinase) or AKT (acutely transforming retrovirus AKT8 in rodent T-cell lymphoma) pathway inhibitors on proliferation, survival, and invasive tumor growth of melanoma cells. Lonafarnib alone did not sufficiently inhibit melanoma cell growth. Combinations of lonafarnib with AKT pathway inhibitors did not significantly increase melanoma cell growth inhibition. In contrast, combinations of lonafarnib with MAPK pathway inhibitors yielded additional growth-inhibiting effects. In particular, the combination of the FTI lonafarnib with the pan-RAF inhibitor sorafenib synergistically inhibited melanoma cell growth, significantly enhanced sorafenib-induced apoptosis, and completely suppressed invasive tumor growth in monolayer and organotypic cultures, respectively. Apoptosis induction was associated with upregulation of the endoplasmic reticulum stress-related transcription factors p8 and CHOP (CAAT/enhancer binding protein (C/EBP) homologous protein), and downregulation of the antiapoptotic Bcl-2 (B-cell lymphoma-2) family protein Mcl-1(myeloid cell leukemia 1). Lonafarnib did not affect MAPK and AKT but did affect mTOR signaling. Together, these findings suggest that the FTI lonafarnib inhibits mTOR signaling and enforces sorafenib-induced apoptosis in melanoma cells and may therefore represent an effective alternative for melanoma treatment.", "isbn" : "1523-1747 (Electronic)$\\backslash$n0022-202X (Linking)", "pmid" : "20944654", "issn" : "0022202X", "doi" : "10.1038/jid.2010.297", "bibtexKey": "Niessner2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/23d35b256f68387179a616dcbcd5ed549/pumaizi", "tags" : [ "izi","2011","pfizenmaier" ], "intraHash" : "3d35b256f68387179a616dcbcd5ed549", "interHash" : "d397b09c495bcefb2b6a78d063613bdb", "label" : "A TNF receptor 2 selective agonist rescues human neurons from oxidative stress-induced cell death", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "PLoS ONE", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/22110694", "author": [ "Roman Fischer","Olaf Maier","Martin Siegemund","Harald Wajant","Peter Scheurich","Klaus Pfizenmaier" ], "authors": [ {"first" : "Roman", "last" : "Fischer"}, {"first" : "Olaf", "last" : "Maier"}, {"first" : "Martin", "last" : "Siegemund"}, {"first" : "Harald", "last" : "Wajant"}, {"first" : "Peter", "last" : "Scheurich"}, {"first" : "Klaus", "last" : "Pfizenmaier"} ], "volume": "6","number": "11","pages": "e27621","abstract": "Tumor necrosis factor (TNF) plays a dual role in neurodegenerative diseases. Whereas TNF receptor (TNFR) 1 is predominantly associated with neurodegeneration, TNFR2 is involved in tissue regeneration and neuroprotection. Accordingly, the availability of TNFR2-selective agonists could allow the development of new therapeutic treatments of neurodegenerative diseases. We constructed a soluble, human TNFR2 agonist (TNC-scTNF(R2)) by genetic fusion of the trimerization domain of tenascin C to a TNFR2-selective single-chain TNF molecule, which is comprised of three TNF domains connected by short peptide linkers. TNC-scTNF(R2) specifically activated TNFR2 and possessed membrane-TNF mimetic activity, resulting in TNFR2 signaling complex formation and activation of downstream signaling pathways. Protection from neurodegeneration was assessed using the human dopaminergic neuronal cell line LUHMES. First we show that TNC-scTNF(R2) interfered with cell death pathways subsequent to H(2)O(2) exposure. Protection from cell death was dependent on TNFR2 activation of the PI3K-PKB/Akt pathway, evident from restoration of H(2)O(2) sensitivity in the presence of PI3K inhibitor LY294002. Second, in an in vitro model of Parkinson disease, TNC-scTNF(R2) rescues neurons after induction of cell death by 6-OHDA. Since TNFR2 is not only promoting anti-apoptotic responses but also plays an important role in tissue regeneration, activation of TNFR2 signaling by TNC-scTNF(R2) appears a promising strategy to ameliorate neurodegenerative processes.", "isbn" : "1932-6203", "pmid" : "22110694", "issn" : "19326203", "doi" : "10.1371/journal.pone.0027621", "bibtexKey": "Fischer2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2cc25b0c9f100a19ceab332b71631a67d/pumaizi", "tags" : [ "izi","2011","scheuric" ], "intraHash" : "cc25b0c9f100a19ceab332b71631a67d", "interHash" : "94ac91bea7c111d25d3c3079ad4fb898", "label" : "Nanotube action between human mesothelial cells reveals novel aspects of inflammatory responses", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "PLoS ONE", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/22216308", "author": [ "Julia Ranzinger","Amin Rustom","Marcus Abel","Julia Leyh","Lars Kihm","Margarete Witkowski","Peter Scheurich","Martin Zeier","Vedat Schwenger" ], "authors": [ {"first" : "Julia", "last" : "Ranzinger"}, {"first" : "Amin", "last" : "Rustom"}, {"first" : "Marcus", "last" : "Abel"}, {"first" : "Julia", "last" : "Leyh"}, {"first" : "Lars", "last" : "Kihm"}, {"first" : "Margarete", "last" : "Witkowski"}, {"first" : "Peter", "last" : "Scheurich"}, {"first" : "Martin", "last" : "Zeier"}, {"first" : "Vedat", "last" : "Schwenger"} ], "volume": "6","number": "12","pages": "e29537","abstract": "A well-known role of human peritoneal mesothelial cells (HPMCs), the resident cells of the peritoneal cavity, is the generation of an immune response during peritonitis by activation of T-cells via antigen presentation. Recent findings have shown that intercellular nanotubes (NTs) mediate functional connectivity between various cell types including immune cells - such as T-cells, natural killer (NK) cells or macrophages - by facilitating a spectrum of long range cell-cell interactions. Although of medical interest, the relevance of NT-related findings for human medical conditions and treatment, e.g. in relation to inflammatory processes, remains elusive, particularly due to a lack of appropriate in vivo data. Here, we show for the first time that primary cultures of patient derived HPMCs are functionally connected via membranous nanotubes. NT formation appears to be actin cytoskeleton dependent, mediated by the action of filopodia. Importantly, significant variances in NT numbers between different donors as a consequence of pathophysiological alterations were observable. Furthermore, we show that TNF-$\\alpha$ induces nanotube formation and demonstrate a strong correlation of NT connectivity in accordance with the cellular cholesterol level and distribution, pointing to a complex involvement of NTs in inflammatory processes with potential impact for clinical treatment.", "isbn" : "1932-6203 (Electronic) 1932-6203 (Linking)", "pmid" : "22216308", "issn" : "19326203", "doi" : "10.1371/journal.pone.0029537", "bibtexKey": "Ranzinger2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/22807e16313accd04d3cedd71fa742f04/pumaizi", "tags" : [ "izi","2011" ], "intraHash" : "2807e16313accd04d3cedd71fa742f04", "interHash" : "07c560c04027fa0e64e67d8c9b6d04e5", "label" : "Self-interaction of Abutilon mosaic virus replication initiator protein (Rep) in plant cell nuclei", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 4, "pub-type": "article", "journal": "Virus Research", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21840354", "author": [ "Björn Krenz","Felix Neugart","Tatjana Kleinow","Holger Jeske" ], "authors": [ {"first" : "Björn", "last" : "Krenz"}, {"first" : "Felix", "last" : "Neugart"}, {"first" : "Tatjana", "last" : "Kleinow"}, {"first" : "Holger", "last" : "Jeske"} ], "volume": "161","number": "2","pages": "194--197","abstract": "Geminiviruses replicate their circular single-stranded DNA genome in nuclei of infected plant cells. Their replication initiator proteins (Reps) possess interaction domains for homo- and hetero-oligomerization as shown previously by in vitro studies and yeast two hybrid assays. Here, homo-oligomerization and cellular localization of the Abutilon mosaic virus (AbMV) Rep was analysed with bimolecular fluorescence complementation (BiFC) in epidermal tissues of Nicotiana benthamiana. BiFC revealed that Rep oligomers accumulated within the nucleoplasm, but were excluded from nucleoli as indicated by a nucleoli/cajal body marker. A similar subcellular distribution was observed for Rep fused to full-length cyan fluorescent protein. To examine whether tagged Reps were functionally active, N. benthamiana plants transgenic for a dimeric AbMV DNA B were inoculated with the BiFC expression constructs and nucleic acids were analysed by rolling circle amplification/restriction fragment length polymorphism as well as Southern blot hybridization. The results confirmed that the modified AbMV Rep was able to transreplicate DNA B. © 2011 Elsevier B.V.", "isbn" : "1872-7492 (Electronic)$\\backslash$r0168-1702 (Linking)", "pmid" : "21840354", "issn" : "01681702", "doi" : "10.1016/j.virusres.2011.07.020", "bibtexKey": "Krenz2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/24b2f5f10c4b8f040a9e8c16b1f439c47/pumaizi", "tags" : [ "izi","2011","pfizenmaier","hausser" ], "intraHash" : "4b2f5f10c4b8f040a9e8c16b1f439c47", "interHash" : "f7051b02ac865835cca90369362b9e0c", "label" : "Protein kinase D controls voluntary-running-induced skeletal muscle remodelling", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Biochemical Journal", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21848513", "author": [ "Kornelia Ellwanger","Christine Kienzle","Sylke Lutz","Zheng\u2011Gen Jin","Maria T. Wiekowski","Klaus Pfizenmaier","Angelika Hausser" ], "authors": [ {"first" : "Kornelia", "last" : "Ellwanger"}, {"first" : "Christine", "last" : "Kienzle"}, {"first" : "Sylke", "last" : "Lutz"}, {"first" : "Zheng\u2011Gen", "last" : "Jin"}, {"first" : "Maria T.", "last" : "Wiekowski"}, {"first" : "Klaus", "last" : "Pfizenmaier"}, {"first" : "Angelika", "last" : "Hausser"} ], "volume": "440","number": "3","pages": "327--324","abstract": "Skeletal muscle responds to exercise by activation of signalling pathways that co-ordinate gene expression to sustain muscle performance. MEF2 (myocyte enhancer factor 2)-dependent transcriptional activation of MHC (myosin heavy chain) genes promotes the transformation from fast-twitch into slow-twitch fibres, with MEF2 activity being tightly regulated by interaction with class IIa HDACs (histone deacetylases). PKD (protein kinase D) is known to directly phosphorylate skeletal muscle class IIa HDACs, mediating their nuclear export and thus derepression of MEF2. In the present study, we report the generation of transgenic mice with inducible conditional expression of a dominant-negative PKD1kd (kinase-dead PKD1) protein in skeletal muscle to assess the role of PKD in muscle function. In control mice, long-term voluntary running experiments resulted in a switch from type IIb+IId/x to type IIa plantaris muscle fibres as measured by indirect immunofluorescence of MHCs isoforms. In mice expressing PKD1kd, this fibre type switch was significantly impaired. These mice exhibited altered muscle fibre composition and decreased running performance compared with control mice. Our findings thus indicate that PKD activity is essential for exercise-induced MEF2-dependent skeletal muscle remodelling in vivo.", "isbn" : "1470-8728", "pmid" : "21848513", "issn" : "0264-6021", "doi" : "10.1042/BJ20101980", "bibtexKey": "Ellwanger2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/22003d5413fadf339c69f5bb2b7e7ec58/pumaizi", "tags" : [ "olayioye","izi","2011","hausser" ], "intraHash" : "2003d5413fadf339c69f5bb2b7e7ec58", "interHash" : "662b199abb2329400f6b9cdc3941c86d", "label" : "The tumor suppressor protein DLC1 is regulated by PKD-mediated GAP domain phosphorylation", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Experimental Cell Research", "year": "2011", "url": "https://www.ncbi.nlm.nih.gov/pubmed/21087603", "author": [ "Rolf Peter Scholz","Johan O.R. Gustafsson","Peter Hoffmann","Mamta Jaiswal","Mohammed Reza Ahmadian","Stephan A. Eisler","Patrik Erlmann","Simone Schmid","Angelika Hausser","Monilola A. Olayioye" ], "authors": [ {"first" : "Rolf Peter", "last" : "Scholz"}, {"first" : "Johan O.R.", "last" : "Gustafsson"}, {"first" : "Peter", "last" : "Hoffmann"}, {"first" : "Mamta", "last" : "Jaiswal"}, {"first" : "Mohammed Reza", "last" : "Ahmadian"}, {"first" : "Stephan A.", "last" : "Eisler"}, {"first" : "Patrik", "last" : "Erlmann"}, {"first" : "Simone", "last" : "Schmid"}, {"first" : "Angelika", "last" : "Hausser"}, {"first" : "Monilola A.", "last" : "Olayioye"} ], "volume": "317","number": "4","pages": "496--503","abstract": "Deleted in liver cancer 1 (DLC1) is a tumor suppressor protein that is frequently downregulated in various tumor types. DLC1 contains a Rho GTPase activating protein (GAP) domain that appears to be required for its tumor suppressive functions. Little is known about the molecular mechanisms that regulate DLC1. By mass spectrometry we have mapped a novel phosphorylation site within the DLC1 GAP domain on serine 807. Using a phospho-S807-specific antibody, our results identify protein kinase D (PKD) to phosphorylate this site in DLC1 in intact cells. Although phosphorylation on serine 807 did not directly impact on in vitro GAP activity, a DLC1 serine-to-alanine exchange mutant inhibited colony formation more potently than the wild type protein. Our results thus show that PKD-mediated phosphorylation of DLC1 on serine 807 negatively regulates DLC1 cellular function. © 2010 Elsevier Inc.", "isbn" : "1090-2422 (Electronic)$\\backslash$r0014-4827 (Linking)", "pmid" : "21087603", "issn" : "10902422", "doi" : "10.1016/j.yexcr.2010.11.003", "bibtexKey": "Scholz2011" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/203360d9e2cd713cf83095e13413576f4/pumaizi", "tags" : [ "izi","2011","pfizenmaier" ], "intraHash" : "03360d9e2cd713cf83095e13413576f4", "interHash" : "46d1ebbbd12250a64c62a0a9b7157804", "label" : "Neuroprotective and neurodegenerative effects of the chronic expression of tumor necrosis factor α in the nigrostriatal dopaminergic circuit of adult mice", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 3, "pub-type": "article", "journal": "Experimental Neurology","publisher":"Elsevier BV", "year": "2011", "url": "https://doi.org/10.1016%2Fj.expneurol.2010.11.010", "author": [ "M. Chertoff","N. Di Paolo","A. Schoeneberg","A. Depino","C. Ferrari","W. Wurst","K. Pfizenmaier","U. Eisel","F. Pitossi" ], "authors": [ {"first" : "M.", "last" : "Chertoff"}, {"first" : "N. Di", "last" : "Paolo"}, {"first" : "A.", "last" : "Schoeneberg"}, {"first" : "A.", "last" : "Depino"}, {"first" : "C.", "last" : "Ferrari"}, {"first" : "W.", "last" : "Wurst"}, {"first" : "K.", "last" : "Pfizenmaier"}, {"first" : "U.", "last" : "Eisel"}, {"first" : "F.", "last" : "Pitossi"} ], "volume": "227","number": "2","pages": "237--251", "doi" : "10.1016/j.expneurol.2010.11.010", "bibtexKey": "Chertoff_2011" } ] }