@article{PehlivanogluWuertzKozakHeideretal.2019, author = {Pehlivanoglu, Tuna and W{\"u}rtz-Kozak, Karin and Heider, Franziska and Sauer, Daniel and Wanke-Jellinek, Lorenz and Mayer, Michael and Mehren, Christoph}, title = {Clinical and Radiographic Outcome of Patients With Cervical Spondylotic Myelopathy Undergoing Total Disc Replacement}, series = {SPINE}, volume = {44}, journal = {SPINE}, number = {20}, publisher = {Lippincott Williams \& Wilkins}, address = {Philadelphia}, issn = {0362-2436}, doi = {10.1097/BRS.0000000000003079}, pages = {1403 -- 1411}, year = {2019}, abstract = {Study Design. A nonrandomized, prospective, and single-center clinical trial. Objective. The aim of this study was to investigate the clinical and radiographic efficacy of ProDisc Vivo cervical total disc replacement (cTDR) in patients with clinical and radiographic documented cervical spondylotic myelopathy (CSM), due to degenerative changes at the index level. Summary of Background Data. Decompression and fusion is still the gold standard in patients with cervical myelopathy. Very limited data are available regarding the application of cTDR in patients with clinical and radiological documented CSM in context of clinical and radiographic outcomes. Methods. Clinical outcome scores included the Neck Disability Index (NDI), Visual Analogue Scale (VAS), arm and neck pain self-assessment questionnaires as well as the Nurick grade and the Japanese Orthopaedic Association (JOA) score. The radiological outcome included the range of motion (ROM), the segmental and global (C2-C7) lordosis, and the occurrence of heterotopic ossifications. Results. Eighteen consecutive patients (10 males, 8 females) with documented clinical and radiological signs of myelopathy were included in this investigation. The study population had a mean age of 52.4 years and a follow-up period of 20.3 months in average (range 3-48 months). The mean range ROM of the index level stayed consistent with 6.8 degrees preoperatively and 7.2 degrees (P = 0.578) at the last follow-up; the global lordosis in neutral position changed from 3.5 degrees to 14.2 degrees significantly (P = 0.005) in mean. The JOA score improved from 11.3 to 16.6 (P < 0.001) as well as the NDI 36.7 to 10.3 (P < 0.001) and the VAS score from 5.7/6.1 (arm/neck) to 1.3/2.0 (P P < 0.001). The mean Nurick grade was 1.33 preoperatively and dropped down in all cases to Nurick grade of 0 (P < 0.001). Conclusion. cTDR (with ProDisc Vivio) in patients with CSM yielded good clinical and radiographic outcomes and found as a reliable, safe, and motion-preserving surgical treatment option, although its indication is very limited due to numerous exclusion criteria.}, language = {en} } @article{SauerKleineVehn2019, author = {Sauer, Michael and Kleine-Vehn, J{\"u}rgen}, title = {PIN-FORMED and PIN-LIKES auxin transport facilitators}, series = {Development : Company of Biologists}, volume = {146}, journal = {Development : Company of Biologists}, number = {15}, publisher = {Company biologists ltd}, address = {Cambridge}, issn = {0950-1991}, doi = {10.1242/dev.168088}, pages = {5}, year = {2019}, abstract = {The phytohormone auxin influences virtually all aspects of plant growth and development. Auxin transport across membranes is facilitated by, among other proteins, members of the PIN-FORMED (PIN) and the structurally similar PIN-LIKES (PILS) families, which together govern directional cell-to-cell transport and intracellular accumulation of auxin. Canonical PIN proteins, which exhibit a polar localization in the plasma membrane, determine many patterning and directional growth responses. Conversely, the less-studied noncanonical PINs and PILS proteins, which mostly localize to the endoplasmic reticulum, attenuate cellular auxin responses. Here, and in the accompanying poster, we provide a brief summary of current knowledge of the structure, evolution, function and regulation of these auxin transport facilitators.}, language = {en} } @article{SauerGrebe2021, author = {Sauer, Michael and Grebe, Markus}, title = {Plant cell biology}, series = {Current biology : CB}, volume = {31}, journal = {Current biology : CB}, number = {9}, publisher = {Cell Press}, address = {Cambridge}, issn = {0960-9822}, doi = {10.1016/j.cub.2021.03.070}, pages = {R449 -- R451}, year = {2021}, abstract = {PIN-FORMED (PIN) polar protein localization directs transport of the growth and developmental regulator auxin in plants. Once established after cytokinesis, PIN polarity requires maintenance. Now, direct interactions between PIN, MAB4/MEL and PID proteins suggest self-reinforced maintenance of PIN polarity through limiting lateral diffusion.}, language = {en} } @article{KellerSauerStraussetal.2005, author = {Keller, S. and Sauer, I. and Strauss, H. and Gast, Klaus and Dathe, M. and Bienert, Michael C.}, title = {Membrane-mimetic nanocarriers formed by a dipalmitoylated cell-penetrating peptide}, year = {2005}, language = {en} } @misc{PratHajnýGrunewaldetal.2018, author = {Pr{\´a}t, Tom{\´a}š and Hajny', Jakub and Grunewald, Wim and Vasileva, Mina and Moln{\´a}r, Gergely and Tejos, Ricardo and Schmid, Markus and Sauer, Michael and Friml, Jiř{\´i}}, title = {WRKY23 is a component of the transcriptional network mediating auxin feedback on PIN polarity}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {1123}, issn = {1866-8372}, doi = {10.25932/publishup-44633}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-446331}, pages = {20}, year = {2018}, abstract = {Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17-and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain-and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development.}, language = {en} } @article{MunozManganoPazGonzalezGarciaetal.2017, author = {Mu{\~n}oz, Alfonso and Mangano, Silvina and Paz Gonzalez-Garcia, Mary and Contreras, Ramon and Sauer, Michael and De Rybel, Bert and Weijers, Dolf and Juan Sanchez-Serrano, Jose and Sanmartin, Maite and Rojo, Enrique}, title = {RIMA-Dependent Nuclear Accumulation of IYO Triggers Auxin-Irreversible Cell Differentiation in Arabidopsis}, series = {The plant cell}, volume = {29}, journal = {The plant cell}, number = {3}, publisher = {American Society of Plant Physiologists}, address = {Rockville}, issn = {1040-4651}, doi = {10.1105/tpc.16.00791}, pages = {575 -- 588}, year = {2017}, abstract = {The transcriptional regulator MINIYO (IYO) is essential and rate-limiting for initiating cell differentiation in Arabidopsis thaliana. Moreover, IYO moves from the cytosol into the nucleus in cells at the meristem periphery, possibly triggering their differentiation. However, the genetic mechanisms controlling IYO nuclear accumulation were unknown, and the evidence that increased nuclear IYO levels trigger differentiation remained correlative. Searching for IYO interactors, we identified RPAP2 IYO Mate (RIMA), a homolog of yeast and human proteins linked to nuclear import of selective cargo. Knockdown of RIMA causes delayed onset of cell differentiation, phenocopying the effects of IYO knockdown at the transcriptomic and developmental levels. Moreover, differentiation is completely blocked when IYO and RIMA activities are simultaneously reduced and is synergistically accelerated when IYO and RIMA are concurrently overexpressed, confirming their functional interaction. Indeed, RIMA knockdown reduces the nuclear levels of IYO and prevents its prodifferentiation activity, supporting the conclusion that RIMA-dependent nuclear IYO accumulation triggers cell differentiation in Arabidopsis. Importantly, by analyzing the effect of the IYO/RIMA pathway on xylem pole pericycle cells, we provide compelling evidence reinforcing the view that the capacity for de novo organogenesis and regeneration from mature plant tissues can reside in stem cell reservoirs.}, language = {en} } @article{FagesHanghojKhanetal.2019, author = {Fages, Antoine and Hanghoj, Kristian and Khan, Naveed and Gaunitz, Charleen and Seguin-Orlando, Andaine and Leonardi, Michela and Constantz, Christian McCrory and Gamba, Cristina and Al-Rasheid, Khaled A. S. and Albizuri, Silvia and Alfarhan, Ahmed H. and Allentoft, Morten and Alquraishi, Saleh and Anthony, David and Baimukhanov, Nurbol and Barrett, James H. and Bayarsaikhan, Jamsranjav and Benecke, Norbert and Bernaldez-Sanchez, Eloisa and Berrocal-Rangel, Luis and Biglari, Fereidoun and Boessenkool, Sanne and Boldgiv, Bazartseren and Brem, Gottfried and Brown, Dorcas and Burger, Joachim and Crubezy, Eric and Daugnora, Linas and Davoudi, Hossein and Damgaard, Peter de Barros and de Chorro y de Villa-Ceballos, Maria de los Angeles and Deschler-Erb, Sabine and Detry, Cleia and Dill, Nadine and Oom, Maria do Mar and Dohr, Anna and Ellingvag, Sturla and Erdenebaatar, Diimaajav and Fathi, Homa and Felkel, Sabine and Fernandez-Rodriguez, Carlos and Garcia-Vinas, Esteban and Germonpre, Mietje and Granado, Jose D. and Hallsson, Jon H. and Hemmer, Helmut and Hofreiter, Michael and Kasparov, Aleksei and Khasanov, Mutalib and Khazaeli, Roya and Kosintsev, Pavel and Kristiansen, Kristian and Kubatbek, Tabaldiev and Kuderna, Lukas and Kuznetsov, Pavel and Laleh, Haeedeh and Leonard, Jennifer A. and Lhuillier, Johanna and von Lettow-Vorbeck, Corina Liesau and Logvin, Andrey and Lougas, Lembi and Ludwig, Arne and Luis, Cristina and Arruda, Ana Margarida and Marques-Bonet, Tomas and Silva, Raquel Matoso and Merz, Victor and Mijiddorj, Enkhbayar and Miller, Bryan K. and Monchalov, Oleg and Mohaseb, Fatemeh A. and Morales, Arturo and Nieto-Espinet, Ariadna and Nistelberger, Heidi and Onar, Vedat and Palsdottir, Albina H. and Pitulko, Vladimir and Pitskhelauri, Konstantin and Pruvost, Melanie and Sikanjic, Petra Rajic and Papesa, Anita Rapan and Roslyakova, Natalia and Sardari, Alireza and Sauer, Eberhard and Schafberg, Renate and Scheu, Amelie and Schibler, Jorg and Schlumbaum, Angela and Serrand, Nathalie and Serres-Armero, Aitor and Shapiro, Beth and Seno, Shiva Sheikhi and Shevnina, Irina and Shidrang, Sonia and Southon, John and Star, Bastiaan and Sykes, Naomi and Taheri, Kamal and Taylor, William and Teegen, Wolf-Rudiger and Vukicevic, Tajana Trbojevic and Trixl, Simon and Tumen, Dashzeveg and Undrakhbold, Sainbileg and Usmanova, Emma and Vahdati, Ali and Valenzuela-Lamas, Silvia and Viegas, Catarina and Wallner, Barbara and Weinstock, Jaco and Zaibert, Victor and Clavel, Benoit and Lepetz, Sebastien and Mashkour, Marjan and Helgason, Agnar and Stefansson, Kari and Barrey, Eric and Willerslev, Eske and Outram, Alan K. and Librado, Pablo and Orlando, Ludovic}, title = {Tracking five millennia of horse management with extensive ancient genome time series}, series = {Cell}, volume = {177}, journal = {Cell}, number = {6}, publisher = {Cell Press}, address = {Cambridge}, issn = {0092-8674}, doi = {10.1016/j.cell.2019.03.049}, pages = {1419 -- 1435}, year = {2019}, abstract = {Horse domestication revolutionized warfare and accelerated travel, trade, and the geographic expansion of languages. Here, we present the largest DNA time series for a non-human organism to date, including genome-scale data from 149 ancient animals and 129 ancient genomes (>= 1-fold coverage), 87 of which are new. This extensive dataset allows us to assess the modem legacy of past equestrian civilisations. We find that two extinct horse lineages existed during early domestication, one at the far western (Iberia) and the other at the far eastern range (Siberia) of Eurasia. None of these contributed significantly to modern diversity. We show that the influence of Persian-related horse lineages increased following the Islamic conquests in Europe and Asia. Multiple alleles associated with elite-racing, including at the MSTN "speed gene," only rose in popularity within the last millennium. Finally, the development of modem breeding impacted genetic diversity more dramatically than the previous millennia of human management.}, language = {en} } @article{PratHajnyGrunewaldetal.2018, author = {Prat, Tomas and Hajny, Jakub and Grunewald, Wim and Vasileva, Mina and Molnar, Gergely and Tejos, Ricardo and Schmid, Markus and Sauer, Michael and Friml, Jiř{\´i}}, title = {WRKY23 is a component of the transcriptional network mediating auxin feedback on PIN polarity}, series = {PLoS Genetics : a peer-reviewed, open-access journal}, volume = {14}, journal = {PLoS Genetics : a peer-reviewed, open-access journal}, number = {1}, publisher = {PLoS}, address = {San Fransisco}, issn = {1553-7404}, doi = {10.1371/journal.pgen.1007177}, pages = {18}, year = {2018}, abstract = {Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17-and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain-and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development.}, language = {en} } @article{TejosRodriguezFurlanAdamowskietal.2018, author = {Tejos, Ricardo and Rodriguez-Furlan, Cecilia and Adamowski, Maciej and Sauer, Michael and Norambuena, Lorena and Friml, Jiri}, title = {PATELLINS are regulators of auxin-mediated PIN1 relocation and plant development in Arabidopsis thaliana}, series = {Journal of cell science}, volume = {131}, journal = {Journal of cell science}, number = {2}, publisher = {Company of Biologists Limited}, address = {Cambridge}, issn = {0021-9533}, doi = {10.1242/jcs.204198}, pages = {10}, year = {2018}, abstract = {Coordinated cell polarization in developing tissues is a recurrent theme in multicellular organisms. In plants, a directional distribution of the plant hormone auxin is at the core of many developmental programs. A feedback regulation of auxin on the polarized localization of PIN auxin transporters in individual cells has been proposed as a self-organizing mechanism for coordinated tissue polarization, but the molecular mechanisms linking auxin signalling to PIN-dependent auxin transport remain unknown. We used a microarray-based approach to find regulators of the auxin-induced PIN relocation in Arabidopsis thaliana root, and identified a subset of a family of phosphatidylinositol transfer proteins (PITPs), the PATELLINs (PATLs). Here, we show that PATLs are expressed in partially overlapping cell types in different tissues going through mitosis or initiating differentiation programs. PATLs are plasma membrane-associated proteins accumulated in Arabidopsis embryos, primary roots, lateral root primordia and developing stomata. Higher order patl mutants display reduced PIN1 repolarization in response to auxin, shorter root apical meristem, and drastic defects in embryo and seedling development. This suggests that PATLs play a redundant and crucial role in polarity and patterning in Arabidopsis.}, language = {en} } @misc{TenFreyhausHuntgeburthWingleretal.2006, author = {Ten Freyhaus, Henrik and Huntgeburth, Michael and Wingler, Kirstin and Baeumer, A. T. and Wartenberg, Maria and Sauer, H. and Bekhite, Mohamed M. and Rosenkranz, S.}, title = {Inhibition of ROS liberation by the novel nox inhibitor VAS2870 attenuates PDGF-dependent src activation and chemotaxis, but not proliferation in vascular smooth muscle cells}, series = {European heart journal}, volume = {27}, journal = {European heart journal}, publisher = {Oxford University Press}, address = {Oxford}, issn = {0195-668X}, pages = {965 -- 965}, year = {2006}, language = {en} } @misc{KleineVehnSauer2017, author = {Kleine-Vehn, J{\"u}rgen and Sauer, Michael}, title = {Preface}, series = {Plant Hormones: Methods and Protocols}, volume = {1497}, journal = {Plant Hormones: Methods and Protocols}, editor = {Kleine-Vehn, J{\"u}rgen and Sauer, Michael}, edition = {3}, publisher = {Springer}, address = {New York}, isbn = {978-1-4939-6469-7}, issn = {1064-3745}, doi = {10.1007/978-1-4939-6469-7}, pages = {V -- V}, year = {2017}, language = {en} } @misc{ZouharSauer2014, author = {Zouhar, Jan and Sauer, Michael}, title = {Helping hands for budding prospects: ENTH/ANTH/VHS accessory proteins in endocytosis, vacuolar transport, and secretion}, series = {The plant cell}, volume = {26}, journal = {The plant cell}, number = {11}, publisher = {American Society of Plant Physiologists}, address = {Rockville}, issn = {1040-4651}, doi = {10.1105/tpc.114.131680}, pages = {4232 -- 4244}, year = {2014}, abstract = {Coated vesicles provide a major mechanism for the transport of proteins through the endomembrane system of plants. Transport between the endoplasmic reticulum and the Golgi involves vesicles with COPI and COPII coats, whereas clathrin is the predominant coat in endocytosis and post-Golgi trafficking. Sorting of cargo, coat assembly, budding, and fission are all complex and tightly regulated processes that involve many proteins. The mechanisms and responsible factors are largely conserved in eukaryotes, and increasing organismal complexity tends to be associated with a greater numbers of individual family members. Among the key factors is the class of ENTH/ANTH/VHS domain-containing proteins, which link membrane subdomains, clathrin, and other adapter proteins involved in early steps of clathrin coated vesicle formation. More than 30 Arabidopsis thaliana proteins contain this domain, but their generally low sequence conservation has made functional classification difficult. Reports from the last two years have greatly expanded our knowledge of these proteins and suggest that ENTH/ANTH/VHS domain proteins are involved in various instances of clathrin-related endomembrane trafficking in plants. This review aims to summarize these new findings and discuss the broader context of clathrin-dependent plant vesicular transport.}, language = {en} } @misc{LechonSanzPollmannetal.2016, author = {Lechon, Tamara and Sanz, Luis and Pollmann, Stephan and Sauer, Michael and Sandalio, Luisa and Lorenzo, Oscar}, title = {Nitric oxide modification of plant endocytosis and PIN1 localization}, series = {New biotechnology}, volume = {33}, journal = {New biotechnology}, publisher = {Elsevier}, address = {Amsterdam}, issn = {1871-6784}, doi = {10.1016/j.nbt.2015.10.028}, pages = {424 -- 424}, year = {2016}, language = {en} } @article{RobertGrunewaldSaueretal.2015, author = {Robert, Helene S. and Grunewald, Wim and Sauer, Michael and Cannoot, Bernard and Soriano, Mercedes and Swarup, Ranjan and Weijers, Dolf and Bennett, Malcolm and Boutilier, Kim and Friml, Jiri}, title = {Plant embryogenesis requires AUX/LAX-mediated auxin influx}, series = {Development : Company of Biologists}, volume = {142}, journal = {Development : Company of Biologists}, number = {4}, publisher = {Company of Biologists Limited}, address = {Cambridge}, issn = {0950-1991}, doi = {10.1242/dev.115832}, pages = {702 -- 711}, year = {2015}, abstract = {The plant hormone auxin and its directional transport are known to play a crucial role in defining the embryonic axis and subsequent development of the body plan. Although the role of PIN auxin efflux transporters has been clearly assigned during embryonic shoot and root specification, the role of the auxin influx carriers AUX1 and LIKE-AUX1 (LAX) proteins is not well established. Here, we used chemical and genetic tools on Brassica napus microspore-derived embryos and Arabidopsis thaliana zygotic embryos, and demonstrate that AUX1, LAX1 and LAX2 are required for both shoot and root pole formation, in concert with PIN efflux carriers. Furthermore, we uncovered a positive-feedback loop between MONOPTEROS-(ARF5)dependent auxin signalling and auxin transport. This MONOPTEROS dependent transcriptional regulation of auxin influx (AUX1, LAX1 and LAX2) and auxin efflux (PIN1 and PIN4) carriers by MONOPTEROS helps to maintain proper auxin transport to the root tip. These results indicate that auxin-dependent cell specification during embryo development requires balanced auxin transport involving both influx and efflux mechanisms, and that this transport is maintained by a positive transcriptional feedback on auxin signalling.}, language = {en} } @misc{tenFreyhausHuntgeburthWingeretal.2006, author = {ten Freyhaus, Henrik and Huntgeburth, Michael and Winger, Kirstin and B{\"a}umer, Anselm T. and Vantler, Marius and Bekhite, Mohamed M. and Wartenberg, Maria and Sauer, Heinrich and Sparwel, Jan and Rosenkranz, Stephan}, title = {Inhibition of ROS liberation attenuates PDGF-Dependent chemotaxis, but not proliferation in vascular smooth muscle cells - Critical role of Src kinase}, series = {Circulation : an American Heart Association journal}, volume = {114}, journal = {Circulation : an American Heart Association journal}, publisher = {Lippincott Williams \& Wilkins}, address = {Philadelphia}, issn = {0009-7322}, pages = {296 -- 297}, year = {2006}, language = {en} } @article{CuiSchlesingerSchoenhalsetal.2016, author = {Cui, Huanhuan and Schlesinger, Jenny and Schoenhals, Sophia and Toenjes, Martje and Dunkel, Ilona and Meierhofer, David and Cano, Elena and Schulz, Kerstin and Berger, Michael F. and Haack, Timm and Abdelilah-Seyfried, Salim and Bulyk, Martha L. and Sauer, Sascha and Sperling, Silke R.}, title = {Phosphorylation of the chromatin remodeling factor DPF3a induces cardiac hypertrophy through releasing HEY repressors from DNA}, series = {Nucleic acids research}, volume = {44}, journal = {Nucleic acids research}, publisher = {Oxford Univ. Press}, address = {Oxford}, issn = {0305-1048}, doi = {10.1093/nar/gkv1244}, pages = {2538 -- 2553}, year = {2016}, abstract = {DPF3 (BAF45c) is a member of the BAF chromatin remodeling complex. Two isoforms have been described, namely DPF3a and DPF3b. The latter binds to acetylated and methylated lysine residues of histones. Here, we elaborate on the role of DPF3a and describe a novel pathway of cardiac gene transcription leading to pathological cardiac hypertrophy. Upon hypertrophic stimuli, casein kinase 2 phosphorylates DPF3a at serine 348. This initiates the interaction of DPF3a with the transcriptional repressors HEY, followed by the release of HEY from the DNA. Moreover, BRG1 is bound by DPF3a, and is thus recruited to HEY genomic targets upon interaction of the two components. Consequently, the transcription of downstream targets such as NPPA and GATA4 is initiated and pathological cardiac hypertrophy is established. In human, DPF3a is significantly up-regulated in hypertrophic hearts of patients with hypertrophic cardiomyopathy or aortic stenosis. Taken together, we show that activation of DPF3a upon hypertrophic stimuli switches cardiac fetal gene expression from being silenced by HEY to being activated by BRG1. Thus, we present a novel pathway for pathological cardiac hypertrophy, whose inhibition is a long-term therapeutic goal for the treatment of the course of heart failure.}, language = {en} } @article{ToySutherlandTownendetal.2017, author = {Toy, Virginia Gail and Sutherland, Rupert and Townend, John and Allen, Michael J. and Becroft, Leeza and Boles, Austin and Boulton, Carolyn and Carpenter, Brett and Cooper, Alan and Cox, Simon C. and Daube, Christopher and Faulkner, D. R. and Halfpenny, Angela and Kato, Naoki and Keys, Stephen and Kirilova, Martina and Kometani, Yusuke and Little, Timothy and Mariani, Elisabetta and Melosh, Benjamin and Menzies, Catriona D. and Morales, Luiz and Morgan, Chance and Mori, Hiroshi and Niemeijer, Andre and Norris, Richard and Prior, David and Sauer, Katrina and Schleicher, Anja Maria and Shigematsu, Norio and Teagle, Damon A. H. and Tobin, Harold and Valdez, Robert and Williams, Jack and Yeo, Samantha and Baratin, Laura-May and Barth, Nicolas and Benson, Adrian and Boese, Carolin and C{\´e}l{\´e}rier, Bernard and Chamberlain, Calum J. and Conze, Ronald and Coussens, Jamie and Craw, Lisa and Doan, Mai-Linh and Eccles, Jennifer and Grieve, Jason and Grochowski, Julia and Gulley, Anton and Howarth, Jamie and Jacobs, Katrina and Janku-Capova, Lucie and Jeppson, Tamara and Langridge, Robert and Mallyon, Deirdre and Marx, Ray and Massiot, C{\´e}cile and Mathewson, Loren and Moore, Josephine and Nishikawa, Osamu and Pooley, Brent and Pyne, Alex and Savage, Martha K. and Schmitt, Doug and Taylor-Offord, Sam and Upton, Phaedra and Weaver, Konrad C. and Wiersberg, Thomas and Zimmer, Martin}, title = {Bedrock geology of DFDP-2B, central Alpine Fault, New Zealand}, series = {New Zealand journal of geology and geophysics : an international journal of the geoscience of New Zealand, the Pacific Rim, and Antarctica ; NZJG}, volume = {60}, journal = {New Zealand journal of geology and geophysics : an international journal of the geoscience of New Zealand, the Pacific Rim, and Antarctica ; NZJG}, number = {4}, publisher = {Taylor \& Francis}, address = {Abingdon}, organization = {DFDP-2 Sci Team}, issn = {0028-8306}, doi = {10.1080/00288306.2017.1375533}, pages = {497 -- 518}, year = {2017}, abstract = {During the second phase of the Alpine Fault, Deep Fault Drilling Project (DFDP) in the Whataroa River, South Westland, New Zealand, bedrock was encountered in the DFDP-2B borehole from 238.5-893.2 m Measured Depth (MD). Continuous sampling and meso- to microscale characterisation of whole rock cuttings established that, in sequence, the borehole sampled amphibolite facies, Torlesse Composite Terrane-derived schists, protomylonites and mylonites, terminating 200-400 m above an Alpine Fault Principal Slip Zone (PSZ) with a maximum dip of 62°. The most diagnostic structural features of increasing PSZ proximity were the occurrence of shear bands and reduction in mean quartz grain sizes. A change in composition to greater mica:quartz + feldspar, most markedly below c. 700 m MD, is inferred to result from either heterogeneous sampling or a change in lithology related to alteration. Major oxide variations suggest the fault-proximal Alpine Fault alteration zone, as previously defined in DFDP-1 core, was not sampled.}, language = {en} } @inproceedings{KurbelNowakAzodietal.2015, author = {Kurbel, Karl and Nowak, Dawid and Azodi, Amir and Jaeger, David and Meinel, Christoph and Cheng, Feng and Sapegin, Andrey and Gawron, Marian and Morelli, Frank and Stahl, Lukas and Kerl, Stefan and Janz, Mariska and Hadaya, Abdulmasih and Ivanov, Ivaylo and Wiese, Lena and Neves, Mariana and Schapranow, Matthieu-Patrick and F{\"a}hnrich, Cindy and Feinbube, Frank and Eberhardt, Felix and Hagen, Wieland and Plauth, Max and Herscheid, Lena and Polze, Andreas and Barkowsky, Matthias and Dinger, Henriette and Faber, Lukas and Montenegro, Felix and Czach{\´o}rski, Tadeusz and Nycz, Monika and Nycz, Tomasz and Baader, Galina and Besner, Veronika and Hecht, Sonja and Schermann, Michael and Krcmar, Helmut and Wiradarma, Timur Pratama and Hentschel, Christian and Sack, Harald and Abramowicz, Witold and Sokolowska, Wioletta and Hossa, Tymoteusz and Opalka, Jakub and Fabisz, Karol and Kubaczyk, Mateusz and Cmil, Milena and Meng, Tianhui and Dadashnia, Sharam and Niesen, Tim and Fettke, Peter and Loos, Peter and Perscheid, Cindy and Schwarz, Christian and Schmidt, Christopher and Scholz, Matthias and Bock, Nikolai and Piller, Gunther and B{\"o}hm, Klaus and Norkus, Oliver and Clark, Brian and Friedrich, Bj{\"o}rn and Izadpanah, Babak and Merkel, Florian and Schweer, Ilias and Zimak, Alexander and Sauer, J{\"u}rgen and Fabian, Benjamin and Tilch, Georg and M{\"u}ller, David and Pl{\"o}ger, Sabrina and Friedrich, Christoph M. and Engels, Christoph and Amirkhanyan, Aragats and van der Walt, Est{\´e}e and Eloff, J. H. P. and Scheuermann, Bernd and Weinknecht, Elisa}, title = {HPI Future SOC Lab}, editor = {Meinel, Christoph and Polze, Andreas and Oswald, Gerhard and Strotmann, Rolf and Seibold, Ulrich and Schulzki, Bernhard}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-102516}, pages = {iii, 154}, year = {2015}, abstract = {Das Future SOC Lab am HPI ist eine Kooperation des Hasso-Plattner-Instituts mit verschiedenen Industriepartnern. Seine Aufgabe ist die Erm{\"o}glichung und F{\"o}rderung des Austausches zwischen Forschungsgemeinschaft und Industrie. Am Lab wird interessierten Wissenschaftlern eine Infrastruktur von neuester Hard- und Software kostenfrei f{\"u}r Forschungszwecke zur Verf{\"u}gung gestellt. Dazu z{\"a}hlen teilweise noch nicht am Markt verf{\"u}gbare Technologien, die im normalen Hochschulbereich in der Regel nicht zu finanzieren w{\"a}ren, bspw. Server mit bis zu 64 Cores und 2 TB Hauptspeicher. Diese Angebote richten sich insbesondere an Wissenschaftler in den Gebieten Informatik und Wirtschaftsinformatik. Einige der Schwerpunkte sind Cloud Computing, Parallelisierung und In-Memory Technologien. In diesem Technischen Bericht werden die Ergebnisse der Forschungsprojekte des Jahres 2015 vorgestellt. Ausgew{\"a}hlte Projekte stellten ihre Ergebnisse am 15. April 2015 und 4. November 2015 im Rahmen der Future SOC Lab Tag Veranstaltungen vor.}, language = {en} }