KCNK13: Difference between revisions
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'''KCNK13''' is a | == KCNK13 == | ||
[[File:Two-pore_domain_potassium_channel_K2P13.jpg|thumb|right|Diagram of the KCNK13 channel structure]] | |||
'''KCNK13''' is a member of the [[two-pore domain potassium channel]] family, which are integral membrane proteins that contribute to the regulation of the resting membrane potential in cells. These channels are characterized by having two pore-forming domains and are known for their role in setting the background potassium conductance in various tissues. | |||
== Structure == | |||
KCNK13, like other members of the [[K2P channel]] family, contains four transmembrane segments and two pore-forming domains. This unique structure allows the channel to conduct potassium ions across the cell membrane, contributing to the maintenance of the cell's resting potential. The channel is thought to form dimers, with each subunit contributing to the formation of the pore. | |||
== Function == | == Function == | ||
The primary function of KCNK13 is to facilitate the passive flow of [[potassium ions]] across the cell membrane. This flow is crucial for maintaining the [[resting membrane potential]] and for the regulation of [[neuronal excitability]]. KCNK13 channels are also involved in various physiological processes, including [[cell volume regulation]] and [[apoptosis]]. | |||
The [[ | |||
== Expression == | |||
KCNK13 is expressed in a variety of tissues, with notable expression in the [[central nervous system]]. Its expression pattern suggests a role in modulating neuronal activity and maintaining the excitability of neurons. The channel is also found in other tissues, indicating potential roles in non-neuronal physiological processes. | |||
== Clinical Significance == | == Clinical Significance == | ||
Alterations in the function or expression of KCNK13 have been implicated in several pathological conditions. Dysregulation of KCNK13 activity can affect neuronal excitability, potentially contributing to [[neurological disorders]] such as [[epilepsy]] and [[depression]]. Research is ongoing to better understand the role of KCNK13 in these and other conditions. | |||
[[Category: | == Related pages == | ||
* [[Potassium channel]] | |||
* [[Ion channel]] | |||
* [[Resting membrane potential]] | |||
* [[Neuronal excitability]] | |||
{{Ion channels}} | |||
[[Category:Ion channels]] | |||
[[Category:Potassium channels]] | [[Category:Potassium channels]] | ||
Latest revision as of 16:25, 16 February 2025
KCNK13[edit]

KCNK13 is a member of the two-pore domain potassium channel family, which are integral membrane proteins that contribute to the regulation of the resting membrane potential in cells. These channels are characterized by having two pore-forming domains and are known for their role in setting the background potassium conductance in various tissues.
Structure[edit]
KCNK13, like other members of the K2P channel family, contains four transmembrane segments and two pore-forming domains. This unique structure allows the channel to conduct potassium ions across the cell membrane, contributing to the maintenance of the cell's resting potential. The channel is thought to form dimers, with each subunit contributing to the formation of the pore.
Function[edit]
The primary function of KCNK13 is to facilitate the passive flow of potassium ions across the cell membrane. This flow is crucial for maintaining the resting membrane potential and for the regulation of neuronal excitability. KCNK13 channels are also involved in various physiological processes, including cell volume regulation and apoptosis.
Expression[edit]
KCNK13 is expressed in a variety of tissues, with notable expression in the central nervous system. Its expression pattern suggests a role in modulating neuronal activity and maintaining the excitability of neurons. The channel is also found in other tissues, indicating potential roles in non-neuronal physiological processes.
Clinical Significance[edit]
Alterations in the function or expression of KCNK13 have been implicated in several pathological conditions. Dysregulation of KCNK13 activity can affect neuronal excitability, potentially contributing to neurological disorders such as epilepsy and depression. Research is ongoing to better understand the role of KCNK13 in these and other conditions.
Related pages[edit]