Functions of the different electrically silent Kv subunits
| KvS subunit | Tissue | Function |
| Kv5.1 | Cortex | Kv5.1 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| Kv5.1 may play a role in cognitive functions but not in sensorimotor functions. | ||
| Urinary bladder | Kv2/Kv5.1 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv6.1 | Cortex | Kv6.1 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| Kv6.1 may play a role in cognitive functions but not in sensorimotor functions. | ||
| DRG neurons | Kv2.1/Kv6.1 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Hippocampus | Kv6.1 may be involved in epilepsy; Kv6.1 contributes to epileptic seizures but not to the spatially protective effects produced by early life conditioning seizures. | |
| Urinary bladder | Kv2/Kv6.1 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv6.2 | Urinary bladder | Kv2/Kv6.2 heterotetramers may contribute to IK in DSMs of the urinary bladder. |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv6.3 | Urinary bladder | Kv2/Kv6.3 heterotetramers may contribute to IK in DSMs of the urinary bladder. |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| VSMCs | Kv6.3 subunits contribute to the Kv current in mesenteric VSMCs during hypertension; de novo expression of Kv6.3 mRNA is found in mesenteric VSMCs obtained from a hypertensive mice strain. | |
| Kv6.4 | Central nervous system | Kv6.4 is involved in migraine; the L360P missense mutation in the Kv6.4 gene was found only in migraine patients. |
| Fast motor neurons | Kv6.4 expression is regulated by Notch ligand Dlk1 in fast motor neurons where an excess of Kv6.4 increased firing threshold, increased firing frequency, and shortened the duration of firing periods, shifting the neuronal biophysical properties of late-gestation chick motor neurons toward that of a typical fast motor neuron. | |
| Urinary bladder | Kv2/Kv6.4 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv8.1 | DRG neurons | Kv2.1/Kv8.1 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. |
| Hippocampus | Hippocampal CA3 pyramidal cells express a current, IK(slow), with properties that resemble those of the currents seen when Kv2/Kv8.1 subunits are expressed in mammalian cells. | |
| Kv8.1 may contribute to the pathologic mechanisms involved in epileptogenesis. | ||
| Kv8.2 | Eye | Kv2.1/Kv8.2 heterotetramers contribute to IK in amphibian photoreceptors. |
| Several mutations in Kv8.2 are known to cause the retinal disorder CDSR. | ||
| Hippocampus | Kv8.2 is involved in epilepsy; the Kv8.2 mRNA level was threefold higher in the hippocampus of the susceptible SJL/J mouse strain than in that of the resistant C57BL/6J mouse strain, and the two unique nonsynonymous Kv8.2 coding variants R7K and M285R are involved in human epilepsy. | |
| Urinary bladder | Kv2/Kv8.2 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv9.1 | Cortex | Kv9.1 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| DRG neurons | Kv2.1/Kv9.1 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Kv9.1 is involved in pain sensation; Kv9.1 down-regulation reduced the mechanical pain threshold in rats, and two Kv9.1 SNPs were associated with pain. | ||
| Cochlear nucleus | The preferential expression of Kv9.1 in the DCN may provide some flexibility to DCN neurons. | |
| Urinary bladder | Kv2/Kv9.1 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv9.2 | Cortex | Kv9.2 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| DRG neurons | Kv2.1/Kv9.2 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Urinary bladder | Kv2/Kv9.2 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv9.3 | Cancer cells | Kv9.3 plays a role in cell-cycle progression and cell proliferation in cancer cells; stable down-regulation of Kv9.3 reduced tumor growth in mouse xenografts. |
| Cerebral arteries | Kv2.1/Kv9.3 channels underlie the ScTx-1–sensitive current that constitutes approximately 60% of the Kv current in RMCAs. | |
| Kv2.1/Kv9.3 channels contribute to controlling RMCA diameter. | ||
| Cortex | Kv9.3 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. | |
| Kv9.3 is involved in schizophrenia; Kv9.3 is found in the parvalbumin-expressing GABA neurons from which the transmission appears to be altered in schizophrenic subjects, and lower Kv9.3 mRNA levels are found in schizophrenic subjects compared with controls. | ||
| Cochlear nucleus | Kv9.3 is preferentially expressed in the AVCN, indicating that Kv9.3 may play a role in spherical bushy cells that are found mainly in the AVCN and carry the information that is used to localize sounds. | |
| DRG neurons | Kv2.1/Kv9.3 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Lung | Kv2.1/Kv9.3 complexes are involved in hypoxia-induced vasoconstriction of resistance PASMCs; Kv2.1/Kv9.3 currents are reversibly inhibited by hypoxia in the voltage range of the resting membrane potential of PASMCs, and chronic hypoxia causes a decrease in Kv2.1 and Kv9.3 abundance in these cells. | |
| Kv9.3 gene abundance affects lung function; SNPs of the Kv9.3 gene were associated with increased values of forced expiratory volume in the first second, one of the parameters used to determine lung function. | ||
| Kv9.3 has been proposed to be involved in airway hyperresponsiveness; an observed association between two SNPs of the Kv9.3 gene and airway hyperresponsiveness has been revealed. | ||
| Placenta | Kv2.1/Kv9.3 channels have been proposed to be involved in hypoxic fetoplacental vasoconstriction; the U46619-induced contraction of chorionic plate arteries was enhanced by the relatively specific Kv2/Kv9.3 blocker ScTx-1, and Kv9.3 is present in the arteries and veins of the chorionic plate. | |
| Urinary bladder | Kv2/Kv9.3 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. |
| KvS subunit | Tissue | Function |
| Kv5.1 | Cortex | Kv5.1 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| Kv5.1 may play a role in cognitive functions but not in sensorimotor functions. | ||
| Urinary bladder | Kv2/Kv5.1 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv6.1 | Cortex | Kv6.1 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| Kv6.1 may play a role in cognitive functions but not in sensorimotor functions. | ||
| DRG neurons | Kv2.1/Kv6.1 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Hippocampus | Kv6.1 may be involved in epilepsy; Kv6.1 contributes to epileptic seizures but not to the spatially protective effects produced by early life conditioning seizures. | |
| Urinary bladder | Kv2/Kv6.1 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv6.2 | Urinary bladder | Kv2/Kv6.2 heterotetramers may contribute to IK in DSMs of the urinary bladder. |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv6.3 | Urinary bladder | Kv2/Kv6.3 heterotetramers may contribute to IK in DSMs of the urinary bladder. |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| VSMCs | Kv6.3 subunits contribute to the Kv current in mesenteric VSMCs during hypertension; de novo expression of Kv6.3 mRNA is found in mesenteric VSMCs obtained from a hypertensive mice strain. | |
| Kv6.4 | Central nervous system | Kv6.4 is involved in migraine; the L360P missense mutation in the Kv6.4 gene was found only in migraine patients. |
| Fast motor neurons | Kv6.4 expression is regulated by Notch ligand Dlk1 in fast motor neurons where an excess of Kv6.4 increased firing threshold, increased firing frequency, and shortened the duration of firing periods, shifting the neuronal biophysical properties of late-gestation chick motor neurons toward that of a typical fast motor neuron. | |
| Urinary bladder | Kv2/Kv6.4 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv8.1 | DRG neurons | Kv2.1/Kv8.1 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. |
| Hippocampus | Hippocampal CA3 pyramidal cells express a current, IK(slow), with properties that resemble those of the currents seen when Kv2/Kv8.1 subunits are expressed in mammalian cells. | |
| Kv8.1 may contribute to the pathologic mechanisms involved in epileptogenesis. | ||
| Kv8.2 | Eye | Kv2.1/Kv8.2 heterotetramers contribute to IK in amphibian photoreceptors. |
| Several mutations in Kv8.2 are known to cause the retinal disorder CDSR. | ||
| Hippocampus | Kv8.2 is involved in epilepsy; the Kv8.2 mRNA level was threefold higher in the hippocampus of the susceptible SJL/J mouse strain than in that of the resistant C57BL/6J mouse strain, and the two unique nonsynonymous Kv8.2 coding variants R7K and M285R are involved in human epilepsy. | |
| Urinary bladder | Kv2/Kv8.2 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv9.1 | Cortex | Kv9.1 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| DRG neurons | Kv2.1/Kv9.1 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Kv9.1 is involved in pain sensation; Kv9.1 down-regulation reduced the mechanical pain threshold in rats, and two Kv9.1 SNPs were associated with pain. | ||
| Cochlear nucleus | The preferential expression of Kv9.1 in the DCN may provide some flexibility to DCN neurons. | |
| Urinary bladder | Kv2/Kv9.1 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv9.2 | Cortex | Kv9.2 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. |
| DRG neurons | Kv2.1/Kv9.2 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Urinary bladder | Kv2/Kv9.2 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. | ||
| Kv9.3 | Cancer cells | Kv9.3 plays a role in cell-cycle progression and cell proliferation in cancer cells; stable down-regulation of Kv9.3 reduced tumor growth in mouse xenografts. |
| Cerebral arteries | Kv2.1/Kv9.3 channels underlie the ScTx-1–sensitive current that constitutes approximately 60% of the Kv current in RMCAs. | |
| Kv2.1/Kv9.3 channels contribute to controlling RMCA diameter. | ||
| Cortex | Kv9.3 may cause the shift in hyperpolarized direction in the voltage dependence of inactivation that the Kv2-mediated current in neocortical pyramidal neurons shows. | |
| Kv9.3 is involved in schizophrenia; Kv9.3 is found in the parvalbumin-expressing GABA neurons from which the transmission appears to be altered in schizophrenic subjects, and lower Kv9.3 mRNA levels are found in schizophrenic subjects compared with controls. | ||
| Cochlear nucleus | Kv9.3 is preferentially expressed in the AVCN, indicating that Kv9.3 may play a role in spherical bushy cells that are found mainly in the AVCN and carry the information that is used to localize sounds. | |
| DRG neurons | Kv2.1/Kv9.3 heterotetramers may contribute to the outward delayed rectifier K+ current in small DRG neurons. | |
| Lung | Kv2.1/Kv9.3 complexes are involved in hypoxia-induced vasoconstriction of resistance PASMCs; Kv2.1/Kv9.3 currents are reversibly inhibited by hypoxia in the voltage range of the resting membrane potential of PASMCs, and chronic hypoxia causes a decrease in Kv2.1 and Kv9.3 abundance in these cells. | |
| Kv9.3 gene abundance affects lung function; SNPs of the Kv9.3 gene were associated with increased values of forced expiratory volume in the first second, one of the parameters used to determine lung function. | ||
| Kv9.3 has been proposed to be involved in airway hyperresponsiveness; an observed association between two SNPs of the Kv9.3 gene and airway hyperresponsiveness has been revealed. | ||
| Placenta | Kv2.1/Kv9.3 channels have been proposed to be involved in hypoxic fetoplacental vasoconstriction; the U46619-induced contraction of chorionic plate arteries was enhanced by the relatively specific Kv2/Kv9.3 blocker ScTx-1, and Kv9.3 is present in the arteries and veins of the chorionic plate. | |
| Urinary bladder | Kv2/Kv9.3 heterotetramers may contribute to IK in DSMs of the urinary bladder. | |
| ScTx-1–sensitive Kv2-containing channels are key regulators of the excitability and contractility of rat, guinea pig, and human DSMs of the urinary bladder. |