Decalmodulation of Cav1 channels by CaBPs

Ca2+-dependent inactivation (CDI) is a negative feedback regulation of voltage-gated Cav1 and Cav2 channels that is mediated by the Ca2+ sensing protein, calmodulin (CaM), binding to the pore-forming Cav α1 subunit. David Yue and his colleagues made seminal contributions to our understanding of this process, as well as factors that regulate CDI. Important in this regard are members of a family of Ca2+ binding proteins (CaBPs) that are related to calmodulin. CaBPs are expressed mainly in neural tissues and can antagonize CaM-dependent CDI for Cav1 L-type channels. This review will focus on the roles of CaBPs as Cav1-interacting proteins, and the significance of these interactions for vision, hearing, and neuronal Ca2+ signaling events.

• Publication year

  2015

• Venue

  Channels

• Publication date

  2015-07-08

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.1080/19336950.2015.1051273PMID 26155893PMCID 4802809
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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