@book{Herb2022,
  author    = {Herb, Christopher},
  title     = {Restrukturierung von Wertsch{\"o}pfungsketten in der Digitalisierung. Eine Analyse der deutschen Schuhbranche vom Hersteller bis zum Konsumenten},
  publisher = {W{\"u}rzburg University Press},
  address   = {W{\"u}rzburg},
  isbn      = {978-3-95826-186-0},
  issn      = {2626-8906},
  doi       = {10.25972/WUP-978-3-95826-187-7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-269564},
  publisher      = {W{\"u}rzburg University Press},
  pages     = {xii, 284},
  year      = {2022},
  abstract  = {Globale Wertsch{\"o}pfungsketten stellen nicht nur hochkomplexe Beziehungsgef{\"u}ge dar, sondern unterliegen auch einem st{\"a}ndigen Wandlungsprozess. Ein zentraler Treiber dieser Wandlungsprozesse ist der technologische Fortschritt. Moderne Informations- und Kommunikationstechnologien, insbesondere die Ph{\"a}nomene der Digitalisierung und des Online-Handels, sind derzeit von besonderer Bedeutung f{\"u}r Wertsch{\"o}pfungsketten, da unterschiedliche Fortschritte in der Digitalisierung nicht nur zu wirtschaftlichen Vor- und Nachteilen von Unternehmen f{\"u}hren k{\"o}nnen, sondern auch zu Up- bzw. Downgradingprozessen innerhalb der Wertsch{\"o}pfungsketten. In der vorliegenden Studie wird der Fokus auf den handels- bzw. konsumentennahen Teil von Wertsch{\"o}pfungsketten gelegt, um die Folgen der Digitalisierung f{\"u}r Hersteller, H{\"a}ndler und Konsumenten n{\"a}her zu betrachten. Als konkretes Forschungsbeispiel dient die deutsche Schuhbranche, da sich diese gegenw{\"a}rtig - von Industrie bis Handel - in einem umfassenden Strukturwandel befindet. Die Analyse zeigt, dass sich die Komplexit{\"a}t von Wertsch{\"o}pfungsketten im Zuge der Digitalisierung deutlich erh{\"o}ht (hat). In der Schuhbranche dr{\"a}ngen neue Akteure auf den Markt, bestehende Akteure m{\"u}ssen sich anpassen. Direkte Folgen sind nicht nur eine neue Akteurskonstellation, sondern auch ein sich neu bildendes Machtgef{\"u}ge. Es kommt somit zur Restrukturierung bisheriger Wertsch{\"o}pfungsketten.},
  subject      = {Wertsch{\"o}pfungskette},
  language  = {de}
}
@unpublished{HennigPrustyKauferetal.2021,
  author    = {Hennig, Thomas and Prusty, Archana B. and Kaufer, Benedikt and Whisnant, Adam W. and Lodha, Manivel and Enders, Antje and Thomas, Julius and Kasimir, Francesca and Grothey, Arnhild and Herb, Stefanie and J{\"u}rges, Christopher and Meister, Gunter and Erhard, Florian and D{\"o}lken, Lars and Prusty, Bhupesh K.},
  title     = {Selective inhibition of microRNA processing by a herpesvirus-encoded microRNA triggers virus reactivation from latency},
  edition   = {submitted version},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-267858},
  year      = {2021},
  abstract  = {Herpesviruses have mastered host cell modulation and immune evasion to augment productive infection, life-long latency and reactivation thereof 1,2. A long appreciated, yet elusively defined relationship exists between the lytic-latent switch and viral non-coding RNAs 3,4. Here, we identify miRNA-mediated inhibition of miRNA processing as a novel cellular mechanism that human herpesvirus 6A (HHV-6A) exploits to disrupt mitochondrial architecture, evade intrinsic host defense and drive the latent-lytic switch. We demonstrate that virus-encoded miR-aU14 selectively inhibits the processing of multiple miR-30 family members by direct interaction with the respective pri-miRNA hairpin loops. Subsequent loss of miR-30 and activation of miR-30/p53/Drp1 axis triggers a profound disruption of mitochondrial architecture, which impairs induction of type I interferons and is necessary for both productive infection and virus reactivation. Ectopic expression of miR-aU14 was sufficient to trigger virus reactivation from latency thereby identifying it as a readily drugable master regulator of the herpesvirus latent-lytic switch. Our results show that miRNA-mediated inhibition of miRNA processing represents a generalized cellular mechanism that can be exploited to selectively target individual members of miRNA families. We anticipate that targeting miR-aU14 provides exciting therapeutic options for preventing herpesvirus reactivations in HHV-6-associated disorders like myalgic encephalitis/chronic fatigue syndrome (ME/CFS) and Long-COVID.},
  language  = {en}
}
@unpublished{HennigPrustyKauferetal.2022,
  author    = {Hennig, Thomas and Prusty, Archana B. and Kaufer, Benedikt and Whisnant, Adam W. and Lodha, Manivel and Enders, Antje and Thomas, Julius and Kasimir, Francesca and Grothey, Arnhild and Herb, Stefanie and J{\"u}rges, Christopher and Meister, Gunter and Erhard, Florian and D{\"o}lken, Lars and Prusty, Bhupesh K.},
  title     = {Selective inhibition of miRNA 1 processing by a herpesvirus encoded miRNA},
  edition   = {accepted version},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-267862},
  year      = {2022},
  abstract  = {Herpesviruses have mastered host cell modulation and immune evasion to augment productive infection, life-long latency and reactivation thereof 1,2. A long appreciated, yet elusively defined relationship exists between the lytic-latent switch and viral non-coding RNAs 3,4. Here, we identify miRNA-mediated inhibition of miRNA processing as a thus far unknown cellular mechanism that human herpesvirus 6A (HHV-6A) exploits to disrupt mitochondrial architecture, evade intrinsic host defense and drive the lytic-latent switch. We demonstrate that virus-encoded miR-aU14 selectively inhibits the processing of multiple miR-30 family members by direct interaction with the respective pri-miRNA hairpin loops. Subsequent loss of miR-30 and activation of the miR-30/p53/Drp1 axis triggers a profound disruption of mitochondrial architecture. This impairs induction of type I interferons and is necessary for both productive infection and virus reactivation. Ectopic expression of miR-aU14 triggered virus reactivation from latency, identifying viral miR-aU14 as a readily drugable master regulator of the herpesvirus lytic-latent switch. Our results show that miRNA-mediated inhibition of miRNA processing represents a generalized cellular mechanism that can be exploited to selectively target individual members of miRNA families. We anticipate that targeting miR-aU14 provides exciting therapeutic options for preventing herpesvirus reactivations in HHV-6-associated disorders.},
  language  = {en}
}