@article{MikhailyukKnoxPaschenkoetal.2006,
  author    = {Mikhailyuk, Igor K. and Knox, Peter P. and Paschenko, Vladimir Z. and Razjivin, Andrej P. and Lokstein, Heiko},
  title     = {Analysis of absorption spectra of purple bacterial reaction centers in the near infrared region by higher order derivative spectroscopy},
  doi       = {10.1016/j.bpc.2006.02.002},
  year      = {2006},
  abstract  = {Reaction centers (RCs) of purple bacteria are uniquely suited objects to study the mechanisms of the photosynthetic conversion of light energy into chemical energy. A recently introduced method of higher order derivative spectroscopy [I.K. Mikhailyuk, H. Lokstein, A.P. Razjivin, A method of spectral subband decomposition by simultaneous fitting the initial spectrum and a set of its derivatives, J. Biochem. Biophys. Methods 63 (2005) 10-23] was used to analyze the NIR absorption spectra of RC preparations from Rhodobacter (R.) sphaeroides strain 2R and Blastochloris (B.) viridis strain KH, containing bacteriochlorophyll (BChl) a and b, respectively. Q(y) bands of individual RC porphyrin components (BChls and bacteriopheophytins, BPheo) were identified. The results indicate that the upper exciton level Py+ of the photo-active BChl dimer in RCs of R. sphaeroides has an absorption maximum of 810nm. The blue shift of a complex integral band at approximately 800nm upon oxidation of the RC is caused primarily by bleaching of Py+, rather than by an electrochromic shift of the absorption band(s) of the monomeric BChls. Likewise, the disappearance of a band peaking at 842 nm upon oxidation of RCs from B. viridis indicates that this band has to be assigned to Py+, A blue shift of an absorption band at approximately 830nm upon oxidation of RCs of B. viridis is also essentially caused by the disappearance of Py+, rather than by an electrochromic shift of the absorption bands of monomeric BChls. Absorption maxima of the monomeric BCHls, B-B and B-A are at 802 and 797nm, respectively, in RCs of R. sphaeroides at room temperature. BPheo co-factors H-B and HA peak at 748 and 758 nm, respectively, at room temperature. For B. viridis RCs the spectral positions of HB and HA were found to be 796 and 816nm, respectively, at room temperature.},
  language  = {en}
}
@article{OttenKnoxBouldayetal.2018,
  author    = {Otten, Cecile and Knox, Jessica and Boulday, Gwenola and Eymery, Mathias and Haniszewski, Marta and Neuenschwander, Martin and Radetzki, Silke and Vogt, Ingo and Haehn, Kristina and De Luca, Coralie and Cardoso, Cecile and Hamad, Sabri and Igual Gil, Carla and Roy, Peter and Albiges-Rizo, Corinne and Faurobert, Eva and von Kries, Jens P. and Campillos, Monica and Tournier-Lasserve, Elisabeth and Derry, William Brent and Abdelilah-Seyfried, Salim},
  title     = {Systematic pharmacological screens uncover novel pathways involved in cerebral cavernous malformations},
  series = {EMBO molecular medicine},
  volume    = {10},
  journal   = {EMBO molecular medicine},
  number    = {10},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {1757-4676},
  doi       = {10.15252/emmm.201809155},
  pages     = {17},
  year      = {2018},
  abstract  = {Cerebral cavernous malformations (CCMs) are vascular lesions in the central nervous system causing strokes and seizures which currently can only be treated through neurosurgery. The disease arises through changes in the regulatory networks of endothelial cells that must be comprehensively understood to develop alternative, non-invasive pharmacological therapies. Here, we present the results of several unbiased small-molecule suppression screens in which we applied a total of 5,268 unique substances to CCM mutant worm, zebrafish, mouse, or human endothelial cells. We used a systems biology-based target prediction tool to integrate the results with the whole-transcriptome profile of zebrafish CCM2 mutants, revealing signaling pathways relevant to the disease and potential targets for small-molecule-based therapies. We found indirubin-3-monoxime to alleviate the lesion burden in murine preclinical models of CCM2 and CCM3 and suppress the loss-of-CCM phenotypes in human endothelial cells. Our multi-organism-based approach reveals new components of the CCM regulatory network and foreshadows novel small-molecule-based therapeutic applications for suppressing this devastating disease in patients.},
  language  = {en}
}