Toward an understanding of cochlear homeostasis: The impact of location and the role of OCP1 and OCP2

Ruediger Thalmann, Michael T. Henzl, Richard Killick, Elena G. Ignatova, Isolde Thalmann

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


The central role of the supporting cell population, or epithelial support complex (ESC), in cochlear homeostasis has gained general acceptance. That the details of this role may vary markedly with location, however, remains poorly appreciated. For example, the K+ recirculation pathway may well be dictated by position along the cochlear axis: a perilymphatic route near the apex and a transcellular one near the base. The ESC expresses very high levels of OCP1 and OCP2, now known to be components of a novel, organ of Corti (OC)-specific SCF ubiquitin ligase (SCFOCP1). In the SCFOCP1 complex, OCP1 presumably binds selected protein targets, positioning them for ubiquitination. The recent demonstration that recombinant OCP1 interacts non-covalently with Cx26 suggests that the connexins may be target proteins for SCFOCP1. Although ubiquitination has classically been viewed as a signal for subsequent destruction by the 26S proteasome, the energy-limited state of the OC prompts consideration of alternative fates, e.g. reversible internalization. The ESC also expresses several components of the Wingless/Wnt signaling pathway. Significantly, two of the gap-junction proteins expressed in the OC, Cx43 and Cx30, are known targets of the Wnt pathway. On the basis of these observations, a working hypothesis is proposed wherein the Wnt pathway activates connexin expression, while OCP1 regulates its degradation.

Original languageEnglish
Pages (from-to)203-208
Number of pages6
JournalActa Oto-Laryngologica
Issue number2
StatePublished - 2003


  • Cochlear homeostasis
  • Connexin
  • Epithelial gap junctions
  • K recycling
  • OCP1
  • OCP2
  • Wnt signaling


Dive into the research topics of 'Toward an understanding of cochlear homeostasis: The impact of location and the role of OCP1 and OCP2'. Together they form a unique fingerprint.

Cite this