@phdthesis{Vetter2012,
  author    = {Vetter, Sebastian},
  title     = {Elektrophysiologische Charakterisierung von STIM2-Knock-Out-M{\"a}usen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77005},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2012},
  abstract  = {Um eine m{\"o}gliche elektrophysiologische, kardiale Ursache f{\"u}r den pl{\"o}tzlichen Tod von STIM2 Knock-Out M{\"a}usen zu pr{\"u}fen, wurde eine elektrophysiologische Charakterisierung mittels Ruhe- und Stress-EKG, telemetrischem Langzeit-EKG sowie Elektrophysiologischer Untersuchung durchgef{\"u}hrt. Hierbei konnte keine kardial-elektrophysiologische Grundlage f{\"u}r den pl{\"o}tzlichen Tod dieser Tiere gefunden werden.},
  subject      = {Knock-Out <Druckschrift>},
  language  = {de}
}
@phdthesis{Erro2009,
  author    = {Erro, Alejandro Berna},
  title     = {Generation and Characterization of Stromal Interaction Molecule 2 (STIM2)-deficient Mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47301},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2009},
  abstract  = {An increase in cytosolic Ca2+ levels ([Ca2+]i) is a key event that occurs downstream of many signaling cascades in response to an external stimulus and regulates a wide range of cellular processes, including platelet activation. Eukaryotic cells increase their basal [Ca2+]i allowing extracellular Ca2+ influx into the cell, which involves different mechanisms. Store-operated Ca2+ entry (SOCE) is considered the main mechanism of extracellular Ca2+ influx in electrically non-excitable cells and platelets, and comprises an initial Ca2+ depletion from intracellular Ca2+ stores prior to activation of extracellular Ca2+ influx. Although the close relation between Ca2+ release from intracellular stores and extracellular Ca2+ influx was clear, the nature of the signal that linked both events remained elusive until 2005, when Stromal Interaction Molecule 1 (STIM1) was identified as an endoplasmic reticulum (ER) Ca2+ sensor essential for inositol (1,4,5)-trisphosphate (IP3)-mediated SOCE in vitro. However, the function of its homologue STIM2 in Ca2+ homeostasis was in general unknown. Therefore, mice lacking STIM2 (Stim2-/-) were generated in this work to study initially STIM2 function in platelets and in cells of the immune system. Stim2-/- mice developed normally in size and weight to adulthood and were fertile. However, for unknown reasons, they started to die spontaneously at the age of 8 weeks. Unexpectedly, Stim2-/- mice did not show relevant differences in platelets, revealing that STIM2 function is not essential in these cells. However, STIM2 seems to be involved in mammary gland development during pregnancy and is essential for mammary gland function during lactation. CD4+ T cells lacking STIM2 showed decreased SOCE. Our data suggest that STIM2 has a very specific function in the immune system and is involved in Experimental Autoimmune Encephalomyelitis (EAE) at early stages of the disease progression. Stim2-/- neurons were also defective in SOCE. Surprisingly, our results evidenced that STIM2 participates in mechanisms of neuronal damage after ischemic events in brain. This is the first time that the involvement of SOCE in ischemic neuronal damage has been reported. This finding may serve as a basis for the development of novel neuroprotective agents for the treatment of ischemic stroke, and possibly other neurodegenerative disorders in which disturbances in cellular Ca2+ homeostasis are considered a major pathophysiological component.},
  subject      = {Calcium-bindende Proteine},
  language  = {en}
}
@article{SaintFleurLominyMausVaethetal.2018,
  author    = {Saint Fleur-Lominy, Shella and Maus, Mate and Vaeth, Martin and Lange, Ingo and Zee, Isabelle and Suh, David and Liu, Cynthia and Wu, Xiaojun and Tikhonova, Anastasia and Aifantis, Iannis and Feske, Stefan},
  title     = {STIM1 and STIM2 Mediate Cancer-Induced Inflammation in T Cell Acute Lymphoblastic Leukemia},
  series = {Cell Reports},
  volume    = {24},
  journal   = {Cell Reports},
  number    = {11},
  doi       = {10.1016/j.celrep.2018.08.030},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227259},
  pages     = {3045-3060},
  year      = {2018},
  abstract  = {T cell acute lymphoblastic leukemia (T-ALL) is commonly associated with activating mutations in the NOTCH1 pathway. Recent reports have shown a link between NOTCH1 signaling and intracellular Ca2+ homeostasis in T-ALL. Here, we investigate the role of store-operated Ca2+ entry (SOCE) mediated by the Ca2+ channel ORAI1 and its activators STIM1 and STIM2 in T-ALL. Deletion of STIM1 and STIM2 in leukemic cells abolishes SOCE and significantly prolongs the survival of mice in a NOTCH1-dependent model of T-ALL. The survival advantage is unrelated to the leukemic cell burden but is associated with the SOCE-dependent ability of malignant T lymphoblasts to cause inflammation in leukemia-infiltrated organs. Mice with STIM1/STIM2-deficient T-ALL show a markedly reduced necroinflammatory response in leukemia-infiltrated organs and downregulation of signaling pathways previously linked to cancer-induced inflammation. Our study shows that leukemic T lymphoblasts cause inflammation of leukemia-infiltrated organs that is dependent on SOCE.},
  language  = {en}
}