Small conductance calcium-activated potassium channel protein 1, also known as KCNN1, is encoded by the gene KCNN1,which is mapped to the chromosome 19p13.1. KCNN1 is a member of the KCNN family of potassium channels. As an integral membrane protein, KCNN1 contains 6 putative transmembrane domains and pore region. It also forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits.
|Basic Information of KCNN1|
|Protein Name||Small conductance calcium-activated potassium channel protein 1|
|Aliases||KCa2.1, SK1, SKCa 1, SKCa1|
|Organism||Homo sapiens (Human)|
The basic function of KCNN1 is regarded as a voltage-independent potassium channel which is activated by intracellular calcium. It is activated by an afterhyperpolarization (AHP) and regulates neuronal excitability by contributing to the slow component of synaptic AHP. Activation of KCNN1 is usually followed by membrane hyperpolarization. KCNN1 is also important regulators of many biological processes, including chemical synaptic transmission and potassium ion transport. In recent studies, KCNN1 is shown to play an important role in the pathophysiology of pain following nerve injury. It is reported to be blocked by apamin.
Fig.1 Mitochondrial K+ cycle. (Charles, 2017)
In this article, the authors suggest a possible role in the tuning of SK1 channel function via the evolutionary conservation of this complex transcription pattern.
This article figures out the gene structure of KCNN1 and its localization by the method of radiation hybrid mapping to chromosome 19p13.1.
The results in this article are agreed with a model in which Mtb inhibits both the activation and phagosomal translocation of SK1 and in further blocks the localized Ca2+ transients required for phagosome maturation.
This article suggests that the recombinant strain has the potential to be applied in microbial indigo production.
In this article, they find that decreased retrograde transport of neurotrophic factors in injured sensory neurons may thus reduce expression of ion channels and increase excitability. Selective potassium channel openers are likely to represent novel therapies for pain following nerve injury.
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