@misc{SchieferdeckerWendler2019,
  author    = {Schieferdecker, Anne and Wendler, Petra},
  title     = {Structural mapping of missense mutations in the Pex1/Pex6 complex},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {1072},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-47284},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-472843},
  pages     = {27},
  year      = {2019},
  abstract  = {Peroxisome biogenesis disorders (PBDs) are nontreatable hereditary diseases with a broad range of severity. Approximately 65\% of patients are affected by mutations in the peroxins Pex1 and Pex6. The proteins form the heteromeric Pex1/Pex6 complex, which is important for protein import into peroxisomes. To date, no structural data are available for this AAA+ ATPase complex. However, a wealth of information can be transferred from low-resolution structures of the yeast scPex1/scPex6 complex and homologous, well-characterized AAA+ ATPases. We review the abundant records of missense mutations described in PBD patients with the aim to classify and rationalize them by mapping them onto a homology model of the human Pex1/Pex6 complex. Several mutations concern functionally conserved residues that are implied in ATP hydrolysis and substrate processing. Contrary to fold destabilizing mutations, patients suffering from function-impairing mutations may not benefit from stabilizing agents, which have been reported as potential therapeutics for PBD patients.},
  language  = {en}
}
@article{SchieferdeckerWendler2019,
  author    = {Schieferdecker, Anne and Wendler, Petra},
  title     = {Structural Mapping of Missense Mutations in the Pex1/Pex6 Complex},
  series = {International journal of molecular sciences},
  volume    = {20},
  journal   = {International journal of molecular sciences},
  number    = {15},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms20153756},
  pages     = {25},
  year      = {2019},
  abstract  = {Peroxisome biogenesis disorders (PBDs) are nontreatable hereditary diseases with a broad range of severity. Approximately 65\% of patients are affected by mutations in the peroxins Pex1 and Pex6. The proteins form the heteromeric Pex1/Pex6 complex, which is important for protein import into peroxisomes. To date, no structural data are available for this AAA+ ATPase complex. However, a wealth of information can be transferred from low-resolution structures of the yeast scPex1/scPex6 complex and homologous, well-characterized AAA+ ATPases. We review the abundant records of missense mutations described in PBD patients with the aim to classify and rationalize them by mapping them onto a homology model of the human Pex1/Pex6 complex. Several mutations concern functionally conserved residues that are implied in ATP hydrolysis and substrate processing. Contrary to fold destabilizing mutations, patients suffering from function-impairing mutations may not benefit from stabilizing agents, which have been reported as potential therapeutics for PBD patients.},
  language  = {en}
}
@article{KoetzingLagodzinskiLengleretal.2020,
  author    = {K{\"o}tzing, Timo and Lagodzinski, Gregor J. A. and Lengler, Johannes and Melnichenko, Anna},
  title     = {Destructiveness of lexicographic parsimony pressure and alleviation by a concatenation crossover in genetic programming},
  series = {Theoretical computer science},
  volume    = {816},
  journal   = {Theoretical computer science},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0304-3975},
  doi       = {10.1016/j.tcs.2019.11.036},
  pages     = {96 -- 113},
  year      = {2020},
  abstract  = {For theoretical analyses there are two specifics distinguishing GP from many other areas of evolutionary computation: the variable size representations, in particular yielding a possible bloat (i.e. the growth of individuals with redundant parts); and also the role and the realization of crossover, which is particularly central in GP due to the tree-based representation. Whereas some theoretical work on GP has studied the effects of bloat, crossover had surprisingly little share in this work. <br /> We analyze a simple crossover operator in combination with randomized local search, where a preference for small solutions minimizes bloat (lexicographic parsimony pressure); we denote the resulting algorithm Concatenation Crossover GP. We consider three variants of the well-studied MAJORITY test function, adding large plateaus in different ways to the fitness landscape and thus giving a test bed for analyzing the interplay of variation operators and bloat control mechanisms in a setting with local optima. We show that the Concatenation Crossover GP can efficiently optimize these test functions, while local search cannot be efficient for all three variants independent of employing bloat control. (C) 2019 Elsevier B.V. All rights reserved.},
  language  = {en}
}