@article{JonscherFlemmingSchmittetal.2018,
  author    = {Jonscher, Ernst and Flemming, Sven and Schmitt, Marius and Sabitzki, Ricarda and Reichard, Nick and Birnbaum, Jakob and Bergmann, B{\"a}rbel and H{\"o}hn, Katharina and Spielmann, Tobias},
  title     = {PfVPS45 Is Required for Host Cell Cytosol Uptake by Malaria Blood Stage Parasites},
  series = {Cell host \& microbe},
  volume    = {25},
  journal   = {Cell host \& microbe},
  number    = {1},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {1931-3128},
  doi       = {10.1016/j.chom.2018.11.010},
  pages     = {166 -- 173},
  year      = {2018},
  abstract  = {During development in human erythrocytes, the malaria parasite Plasmodium falciparum internalizes a large part of the cellular content of the host cell. The internalized cytosol, consisting largely of hemoglobin, is transported to the parasite's food vacuole where it is degraded, providing nutrients and space for growth. This host cell cytosol uptake (HCCU) is crucial for parasite survival but the parasite proteins mediating this process remain obscure. Here, we identify P. falciparum VPS45 as an essential factor in HCCU. Conditional inactivation of PfVPS45 led to an accumulation of host cell cytosol-filled vesicles within the parasite and inhibited the delivery of hemoglobin to the parasite's digestive vacuole, resulting in arrested parasite growth. A proportion of these HCCU vesicle intermediates was positive for phosphatidylinositol 3-phosphate, suggesting endosomal characteristics. Thus PfVPS45 provides insight into the elusive machinery of the ingestion pathway in a parasite that contains an endolysosomal system heavily repurposed for protein secretion.},
  language  = {en}
}
@book{RehseRiemerMeijeretal.2020,
  author    = {Rehse, Jessica and Riemer, Nathanael and Meijer, Saskia and Neumann, Helmuth Emanuel and Gottschalk, Matthias and Buttig, Steve and Gander, Heiko and West, Thomas and Gustavs, Jakob and Lehr, Moritz and Tobe, Mascha and Wendorf, Daniel and Bach-Sliwinski, Greta C{\"a}cilie and Ernst, Sebastian and Meier, Jan-Niklas},
  title     = {„Wir alle treffen Entscheidungen im Leben, aber letztendlich treffen unsere Entscheidungen uns."},
  editor    = {Rehse, Jessica and Riemer, Nathanael},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  isbn      = {978-3-86956-489-0},
  doi       = {10.25932/publishup-46846},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-468467},
  publisher      = {Universit{\"a}t Potsdam},
  pages     = {424},
  year      = {2020},
  abstract  = {„Wir alle treffen Entscheidungen im Leben, aber letztendlich treffen unsere Entscheidungen uns." So erging es den Herausgebern, nachdem sie sich dazu entschlossen hatten, Lehrveranstaltungen an der Universit{\"a}t Potsdam anzubieten, die sich mit dem Medium „Computerspiel" besch{\"a}ftigen sollten - und damit auf {\"u}berraschend große Resonanz stießen. Das Resultat ist vorliegendes Handbuch. Es m{\"o}chte Eltern, LehrerInnen und MultiplikatorInnen exemplarische Einblicke in die vielschichtigen Welten dieses Ph{\"a}nomens vermitteln. Bei den AutorInnen der Beitr{\"a}ge handelt es sich um EnthusiastInnen aus der Computerspielbranche sowie um videospielbegeisterte SozialarbeiterInnen, KulturwissenschaftlerInnen und LehrerInnen.},
  language  = {de}
}
@article{KarlowatzScharhagRahnenfuehreretal.2011,
  author    = {Karlowatz, Ruth-Jessica and Scharhag, J{\"u}rgen and Rahnenfuehrer, J{\"o}rg and Schneider, Ulrich and Jakob, Ernst and Kindermann, Wilfried and Zang, Klaus Dieter},
  title     = {Polymorphisms in the IGF1 signalling pathway including the myostatin gene are associated with left ventricular mass in male athletes},
  series = {British journal of sports medicine : the journal of sport and exercise medicine},
  volume    = {45},
  journal   = {British journal of sports medicine : the journal of sport and exercise medicine},
  number    = {1},
  publisher = {BMJ Publ. Group},
  address   = {London},
  issn      = {0306-3674},
  doi       = {10.1136/bjsm.2008.050567},
  pages     = {36 -- 41},
  year      = {2011},
  abstract  = {Background Athlete's heart as an adaptation to long-time and intensive endurance training can vary considerably between individuals. Genetic polymorphisms in the cardiological relevant insulin-like growth factor 1 (IGF1) signalling pathway seem to have an essential influence on the extent of physiological hypertrophy. Objective Analysis of polymorphisms in the genes of IGF1, IGF1 receptor (IGF1R) and the negative regulator of the cardiac IGF1 signalling pathway, myostatin (MSTN), and their relation to left ventricular mass (LVM) of endurance athletes. Methods In 110 elite endurance athletes or athletes with a high amount of endurance training (75 males and 35 females) and 27 male controls, which were examined by echocardiographic imaging methods and ergometric exercise-testing, the genotypes of a cytosine-adenine repeat polymorphism in the promoter region of the IGF1 gene and a G/A substitution at position 3174 in the IGF1R gene were determined. Additionally, a mutation screen of the MSTN gene was performed. Results The polymorphisms in the IGF1 and the IGF1R gene showed a significant relation to the LVM for male (IGF1: p=0.003; IGF1R: p=0.01), but not for female athletes. The same applies to a previously unnoticed polymorphism in the 1 intron of the MSTN gene, whose deletion allele (AAA -> AA) appears to increase the myostatic effect (p=0.015). Moreover, combinations of the polymorphisms showed significant synergistic effects on the LVM of the male athletes. Conclusions The authors' results argue for the importance of polymorphisms in the IGF1 signalling pathway in combination with MSTN on the variant degree of physiological hypertrophy of male athletes.},
  language  = {en}
}