@article{GoetzSendtner2014,
  author    = {G{\"o}tz, Rudolf and Sendtner, Michael},
  title     = {Cooperation of Tyrosine Kinase Receptor TrkB and Epidermal Growth Factor Receptor Signaling Enhances Migration and Dispersal of Lung Tumor Cells},
  series = {PLoS ONE},
  volume    = {9},
  journal   = {PLoS ONE},
  number    = {6},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0100944},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119578},
  pages     = {e100944},
  year      = {2014},
  abstract  = {TrkB mediates the effects of brain-derived neurotrophic factor (BDNF) in neuronal and nonnneuronal cells. Based on recent reports that TrkB can also be transactivated through epidermal growth-factor receptor (EGFR) signaling and thus regulates migration of early neurons, we investigated the role of TrkB in migration of lung tumor cells. Early metastasis remains a major challenge in the clinical management of non-small cell lung cancer (NSCLC). TrkB receptor signaling is associated with metastasis and poor patient prognosis in NSCLC. Expression of this receptor in A549 cells and in another adenocarcinoma cell line, NCI-H441, promoted enhanced migratory capacity in wound healing assays in the presence of the TrkB ligand BDNF. Furthermore, TrkB expression in A549 cells potentiated the stimulatory effect of EGF in wound healing and in Boyden chamber migration experiments. Consistent with a potential loss of cell polarity upon TrkB expression, cell dispersal and de-clustering was induced in A549 cells independently of exogeneous BDNF. Morphological transformation involved extensive cytoskeletal changes, reduced E-cadherin expression and suppression of E-cadherin expression on the cell surface in TrkB expressing tumor cells. This function depended on MEK and Akt kinase activity but was independent of Src. These data indicate that TrkB expression in lung adenoma cells is an early step in tumor cell dissemination, and thus could represent a target for therapy development.},
  language  = {en}
}
@article{DusikSenthilanMentzeletal.2014,
  author    = {Dusik, Verena and Senthilan, Pingkalai R. and Mentzel, Benjamin and Hartlieb, Heiko and W{\"u}lbeck, Corina and Yoshii, Taishi and Raabe, Thomas and Helfrich-F{\"o}rster, Charlotte},
  title     = {The MAP Kinase p38 Is Part of Drosophila melanogaster's Circadian Clock},
  series = {PLoS Genetics},
  volume    = {10},
  journal   = {PLoS Genetics},
  number    = {8},
  issn      = {1553-7404},
  doi       = {10.1371/journal.pgen.1004565},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119433},
  pages     = {e1004565},
  year      = {2014},
  abstract  = {All organisms have to adapt to acute as well as to regularly occurring changes in the environment. To deal with these major challenges organisms evolved two fundamental mechanisms: the p38 mitogen-activated protein kinase (MAPK) pathway, a major stress pathway for signaling stressful events, and circadian clocks to prepare for the daily environmental changes. Both systems respond sensitively to light. Recent studies in vertebrates and fungi indicate that p38 is involved in light-signaling to the circadian clock providing an interesting link between stress-induced and regularly rhythmic adaptations of animals to the environment, but the molecular and cellular mechanisms remained largely unknown. Here, we demonstrate by immunocytochemical means that p38 is expressed in Drosophila melanogaster's clock neurons and that it is activated in a clock-dependent manner. Surprisingly, we found that p38 is most active under darkness and, besides its circadian activation, additionally gets inactivated by light. Moreover, locomotor activity recordings revealed that p38 is essential for a wild-type timing of evening activity and for maintaining ∼ 24 h behavioral rhythms under constant darkness: flies with reduced p38 activity in clock neurons, delayed evening activity and lengthened the period of their free-running rhythms. Furthermore, nuclear translocation of the clock protein Period was significantly delayed on the expression of a dominant-negative form of p38b in Drosophila's most important clock neurons. Western Blots revealed that p38 affects the phosphorylation degree of Period, what is likely the reason for its effects on nuclear entry of Period. In vitro kinase assays confirmed our Western Blot results and point to p38 as a potential "clock kinase" phosphorylating Period. Taken together, our findings indicate that the p38 MAP Kinase is an integral component of the core circadian clock of Drosophila in addition to playing a role in stress-input pathways.},
  language  = {en}
}
@article{CalebiroMaiellaro2014,
  author    = {Calebiro, Davide and Maiellaro, Isabella},
  title     = {cAMP signaling microdomains and their observation by optical methods},
  series = {Frontiers in Cellular Neuroscience},
  volume    = {8},
  journal   = {Frontiers in Cellular Neuroscience},
  issn      = {1662-5102},
  doi       = {10.3389/fncel.2014.00350},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-118252},
  pages     = {350},
  year      = {2014},
  abstract  = {The second messenger cyclic AMP (cAMP) is a major intracellular mediator of many hormones and neurotransmitters and regulates a myriad of cell functions, including synaptic plasticity in neurons. Whereas cAMP can freely diffuse in the cytosol, a growing body of evidence suggests the formation of cAMP gradients and microdomains near the sites of cAMP production, where cAMP signals remain apparently confined. The mechanisms responsible for the formation of such microdomains are subject of intensive investigation. The development of optical methods based on fluorescence resonance energy transfer (FRET), which allow a direct observation of cAMP signaling with high temporal and spatial resolution, is playing a fundamental role in elucidating the nature of such microdomains. Here, we will review the optical methods used for monitoring cAMP and protein kinase A (PKA) signaling in living cells, providing some examples of their application in neurons, and will discuss the major hypotheses on the formation of cAMP/PKA microdomains.},
  language  = {en}
}
@article{BuchnerBlancoRedondoBunzetal.2013,
  author    = {Buchner, Erich and Blanco Redondo, Beatriz and Bunz, Melanie and Halder, Partho and Sadanandappa, Madhumala K. and M{\"u}hlbauer, Barbara and Erwin, Felix and Hofbauer, Alois and Rodrigues, Veronica and VijayRaghavan, K. and Ramaswami, Mani and Rieger, Dirk and Wegener, Christian and F{\"o}rster, Charlotte},
  title     = {Identification and Structural Characterization of Interneurons of the Drosophila Brain by Monoclonal Antibodies of the W{\"u}rzburg Hybridoma Library},
  series = {PLoS ONE},
  journal   = {PLoS ONE},
  doi       = {10.1371/journal.pone.0075420},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-97109},
  year      = {2013},
  abstract  = {Several novel synaptic proteins have been identified by monoclonal antibodies (mAbs) of the W{\"u}rzburg hybridoma library generated against homogenized Drosophila brains, e.g. cysteine string protein, synapse-associated protein of 47 kDa, and Bruchpilot. However, at present no routine technique exists to identify the antigens of mAbs of our library that label only a small number of cells in the brain. Yet these antibodies can be used to reproducibly label and thereby identify these cells by immunohistochemical staining. Here we describe the staining patterns in the Drosophila brain for ten mAbs of the W{\"u}rzburg hybridoma library. Besides revealing the neuroanatomical structure and distribution of ten different sets of cells we compare the staining patterns with those of antibodies against known antigens and GFP expression patterns driven by selected Gal4 lines employing regulatory sequences of neuronal genes. We present examples where our antibodies apparently stain the same cells in different Gal4 lines suggesting that the corresponding regulatory sequences can be exploited by the split-Gal4 technique for transgene expression exclusively in these cells. The detection of Gal4 expression in cells labeled by mAbs may also help in the identification of the antigens recognized by the antibodies which then in addition to their value for neuroanatomy will represent important tools for the characterization of the antigens. Implications and future strategies for the identification of the antigens are discussed.},
  language  = {en}
}
@article{AlbertWeissenbergerVarrallyayRaslanetal.2012,
  author    = {Albert-Weißenberger, Christiane and V{\´a}rrallyay, Csan{\´a}d and Raslan, Furat and Kleinschnitz, Christoph and Sir{\´e}n, Anna-Leena},
  title     = {An experimental protocol for mimicking pathomechanisms of traumatic brain injury in mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75368},
  year      = {2012},
  abstract  = {Traumatic brain injury (TBI) is a result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events. In order to examine injury processes associated with TBI, a number of rodent models to induce brain trauma have been described. However, none of these models covers the entire spectrum of events that might occur in TBI. Here we provide a thorough methodological description of a straightforward closed head weight drop mouse model to assess brain injuries close to the clinical conditions of human TBI.},
  subject      = {Medizin},
  language  = {en}
}