@article{BreitenbachHelfrichFoersterDandekar2021,
  author    = {Breitenbach, Tim and Helfrich-F{\"o}rster, Charlotte and Dandekar, Thomas},
  title     = {An effective model of endogenous clocks and external stimuli determining circadian rhythms},
  series = {Scientific Reports},
  volume    = {11},
  journal   = {Scientific Reports},
  number    = {1},
  doi       = {10.1038/s41598-021-95391-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-261655},
  pages     = {16165},
  year      = {2021},
  abstract  = {Circadian endogenous clocks of eukaryotic organisms are an established and rapidly developing research field. To investigate and simulate in an effective model the effect of external stimuli on such clocks and their components we developed a software framework for download and simulation. The application is useful to understand the different involved effects in a mathematical simple and effective model. This concerns the effects of Zeitgebers, feedback loops and further modifying components. We start from a known mathematical oscillator model, which is based on experimental molecular findings. This is extended with an effective framework that includes the impact of external stimuli on the circadian oscillations including high dose pharmacological treatment. In particular, the external stimuli framework defines a systematic procedure by input-output-interfaces to couple different oscillators. The framework is validated by providing phase response curves and ranges of entrainment. Furthermore, Aschoffs rule is computationally investigated. It is shown how the external stimuli framework can be used to study biological effects like points of singularity or oscillators integrating different signals at once. The mathematical framework and formalism is generic and allows to study in general the effect of external stimuli on oscillators and other biological processes. For an easy replication of each numerical experiment presented in this work and an easy implementation of the framework the corresponding Mathematica files are fully made available. They can be downloaded at the following link: https://www.biozentrum.uni-wuerzburg.de/bioinfo/computing/circadian/.},
  language  = {en}
}
@article{DandekarArgos1994,
  author    = {Dandekar, Thomas and Argos, Patrick},
  title     = {Amiloride-sensitive epithelial Na\(^+\) channel is made of three homologous subunits},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-29734},
  year      = {1994},
  abstract  = {No abstract available},
  language  = {en}
}
@article{GuptaSrivastavaMinochaetal.2021,
  author    = {Gupta, Shishir K. and Srivastava, Mugdha and Minocha, Rashmi and Akash, Aman and Dangwal, Seema and Dandekar, Thomas},
  title     = {Alveolar regeneration in COVID-19 patients: a network perspective},
  series = {International Journal of Molecular Sciences},
  volume    = {22},
  journal   = {International Journal of Molecular Sciences},
  number    = {20},
  issn      = {1422-0067},
  doi       = {10.3390/ijms222011279},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-284307},
  year      = {2021},
  abstract  = {A viral infection involves entry and replication of viral nucleic acid in a host organism, subsequently leading to biochemical and structural alterations in the host cell. In the case of SARS-CoV-2 viral infection, over-activation of the host immune system may lead to lung damage. Albeit the regeneration and fibrotic repair processes being the two protective host responses, prolonged injury may lead to excessive fibrosis, a pathological state that can result in lung collapse. In this review, we discuss regeneration and fibrosis processes in response to SARS-CoV-2 and provide our viewpoint on the triggering of alveolar regeneration in coronavirus disease 2019 (COVID-19) patients.},
  language  = {en}
}
@article{DandekarGramschHoughtonetal.1985,
  author    = {Dandekar, Thomas and Gramsch, Christian and Houghton, Richard A. and Schultz, R{\"u}diger},
  title     = {Affinity purification of \(\beta\)-endorphin-like material from NG108CC15 cells by means of the monoclonal \(\beta\)-endorphin antibody 3-E7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-29896},
  year      = {1985},
  abstract  = {No abstract available},
  language  = {en}
}
@article{RackeveiBorgesEngstleretal.2022,
  author    = {Rackevei, Antonia S. and Borges, Alyssa and Engstler, Markus and Dandekar, Thomas and Wolf, Matthias},
  title     = {About the analysis of 18S rDNA sequence data from trypanosomes in barcoding and phylogenetics: tracing a continuation error occurring in the literature},
  series = {Biology},
  volume    = {11},
  journal   = {Biology},
  number    = {11},
  issn      = {2079-7737},
  doi       = {10.3390/biology11111612},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-297562},
  year      = {2022},
  abstract  = {The variable regions (V1-V9) of the 18S rDNA are routinely used in barcoding and phylogenetics. In handling these data for trypanosomes, we have noticed a misunderstanding that has apparently taken a life of its own in the literature over the years. In particular, in recent years, when studying the phylogenetic relationship of trypanosomes, the use of V7/V8 was systematically established. However, considering the current numbering system for all other organisms (including other Euglenozoa), V7/V8 was never used. In Maia da Silva et al. [Parasitology 2004, 129, 549-561], V7/V8 was promoted for the first time for trypanosome phylogenetics, and since then, more than 70 publications have replicated this nomenclature and even discussed the benefits of the use of this region in comparison to V4. However, the primers used to amplify the variable region of trypanosomes have actually amplified V4 (concerning the current 18S rDNA numbering system).},
  language  = {en}
}