What is SK channel
SK channels (Small conductance calcium-activated K (potassium) channels) are a subfamily of Ca2+-activated K+ channels.[1] SK channels are a type of ion channel allowing potassium cations to cross the cell membrane and are activated (opened) by an increase in the concentration of intracellular calcium. Their activation limits the firing frequency of action potentials and are important for regulating afterhyperpolarization in central neurons and other types of electrically excitable cells.[2] SK channels are thought to be involved in synaptic plasticity and therefore play important roles in memory and learning.
Tags: Integral membrane proteins, Ion channels, Membrane proteins, Proteins, Transmembrane proteins
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Channel blockers are chemical substances, ranging from ions to complex organic molecules, that bind inside the pore of an ion channel and block the flow of ions through that channel. A subset of channel blockers, known as "open channel blockers" have access to their intra-channel binding site only when the channel is in the open configuration (i.e. in the configuration that conducts transmembrane ion flux). Open channel block is characterized by "flickery closings" in single-channel recordings.
The T-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the ?1 subunit is the one that determines most of the channel's properties.
Along with sodium "funny current," the T-type calcium channel produces the pacemaker potential in the SA node of the heart.
T-type calcium channel blockers are used primarily as antiepileptics.
A Calcium channel is an ion channel which displays selective permeabiltiy to calcium ions. It is sometimes synonymous as voltage-dependent calcium channel,[1] although there are also ligand-gated calcium channels.[2]
A Calcium channel is an ion channel which displays selective permeabiltiy to calcium ions. It is sometimes synonymous as voltage-dependent calcium channel,[1] although there are also ligand-gated calcium channels.[2]
Roderick MacKinnon commissioned "Birth of an Idea", a 5' (1.50 m) tall sculpture based on the KcsA potassium channel. The artwork contains a wire object representing the pore liner with a blown glass object representing the main cavity of the channel structure.
Potassium channel, subfamily K, member 2, also known as KCNK2, is a human gene.[1]
This gene encodes K2P2.1, one of the members of the two-pore-domain background potassium channel protein family. This type of potassium channel is formed by two homodimers that create a channel that leaks potassium out of the cell to control resting membrane potential. The channel can be opened, however, by certain anesthetics, membrane stretching, intracellular acidosis, and heat. Three transcript variants encoding different isoforms have been found for this gene.
Chloride channel 6, also known as CLCN6, is a human gene.[1]
The CLCN family of voltage-dependent chloride channel genes comprises nine members (CLCN1-7, Ka and Kb) which demonstrate quite diverse functional characteristics while sharing significant sequence homology. Chloride channel 6 and 7 belong to a subbranch of this family. Chloride channel 6 has four different alternatively spliced transcript variants. This gene is in close vicinity to two other kidney-specific chloride channel genes, CLCNKA and CLCNKB.[1]
The L-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the ?1 subunit is the one that determines most of the channel's properties.
L-type calcium channel blocker drugs are used as cardiac antiarrhythmics or antihypertensives, depending on whether the drugs has higher affinity to the heart, the phenylalkylamines (like verapamil) or to the vessels, the dihydropyridines (nifedipine).
L-type channels are selectively blocked by benzothiazepines (like diltiazem).
Potassium channel, subfamily K, member 17, also known as KCNK17, is a human gene.[1]
This gene encodes K2P17.1, one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. This open channel, primarily expressed in the pancreas, is activated at alkaline pH.
Voltage-gated sodium channels normally consist of an alpha subunit which forms the ion conduction pore and one to two beta subunits which have several functions including modulation of channel gating.[4] Expression of the alpha subunit alone is sufficient to produce a functional channel.
Potassium channel, subfamily K, member 3, also known as KCNK3, is a human gene.[1]
This gene encodes K2P3.1, one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. K2P3.1 is an outwardly rectifying channel that is sensitive to changes in extracellular pH and is inhibited by extracellular acidification. Also referred to as an acid-sensitive potassium channel, it is activated by the anesthetics halothane and isoflurane. Although three transcripts are detected in northern blots, there is currently no sequence available to confirm transcript variants for this gene.
The SK channel family contains 4 members - SK1, SK2, SK3, and SK4.
The Q-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the ?1 subunit is the one that determines most of the channel's properties.
They are poorly understood, but like R-type calcium channels, they appear to be present in cerebellar granule cells. They have a high threshold of activation and relatively slow kinetics.
The R-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the ?1 subunit is the one that determines most of the channel's properties.
They are poorly understood, but like Q-type calcium channels, they appear to be present in cerebellar granule cells. They have a high threshold of activation and relatively slow kinetics.
Potassium channel, subfamily K, member 9, also known as KCNK9, is a human gene.[1]
This gene encodes K2P9.1, one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. This open channel is highly expressed in the cerebellum. It is inhibited by extracellular acidification and arachidonic acid, and strongly inhibited by phorbol 12-myristate 13-acetate.
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