TRIP8b splice variants form a family of auxiliary subunits that regulate gating and trafficking of HCN channels in the brain.
about
Searching for new targets for treatment of pediatric epilepsyCortical HCN channels: function, trafficking and plasticityStructure and stoichiometry of an accessory subunit TRIP8b interaction with hyperpolarization-activated cyclic nucleotide-gated channelsDifferential expression of HCN subunits alters voltage-dependent gating of h-channels in CA1 pyramidal neurons from dorsal and ventral hippocampusTrafficking and surface expression of hyperpolarization-activated cyclic nucleotide-gated channels in hippocampal neuronsStructures of the Human HCN1 Hyperpolarization-Activated ChannelIdentification of Small-Molecule Inhibitors of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels.Deletion of the hyperpolarization-activated cyclic nucleotide-gated channel auxiliary subunit TRIP8b impairs hippocampal Ih localization and function and promotes antidepressant behavior in mice.Homeostatic regulation of synaptic excitability: tonic GABA(A) receptor currents replace I(h) in cortical pyramidal neurons of HCN1 knock-out mice.Distinct perinatal features of the hyperpolarization-activated non-selective cation current I(h) in the rat cortical plate.Restoring visual function to blind mice with a photoswitch that exploits electrophysiological remodeling of retinal ganglion cells.Reduction of thalamic and cortical Ih by deletion of TRIP8b produces a mouse model of human absence epilepsy.TRIP8b-independent trafficking and plasticity of adult cortical presynaptic HCN1 channels.Dendritic ion channel trafficking and plasticity.Regulation of axonal HCN1 trafficking in perforant path involves expression of specific TRIP8b isoforms.The latrophilins, "split-personality" receptors.Reelin signaling specifies the molecular identity of the pyramidal neuron distal dendritic compartment.Targeted deletion of Kcne2 impairs HCN channel function in mouse thalamocortical circuits.Dynamic measurements for funny channels.Structural basis for the mutual antagonism of cAMP and TRIP8b in regulating HCN channel function.Ion channel gradients in the apical tuft region of CA1 pyramidal neuronsCalcium store depletion induces persistent perisomatic increases in the functional density of h channels in hippocampal pyramidal neurons.HCN Channel Targets for Novel Antidepressant Treatment.HCN channels in behavior and neurological disease: too hyper or not active enough?Mechanisms and function of dendritic exocytosis.A di-arginine ER retention signal regulates trafficking of HCN1 channels from the early secretory pathway to the plasma membrane.Trafficking and gating of hyperpolarization-activated cyclic nucleotide-gated channels are regulated by interaction with tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b) and cyclic AMP at distinct sites.TRIP8b is required for maximal expression of HCN1 in the mouse retinaThe fast and slow ups and downs of HCN channel regulation.cAMP control of HCN2 channel Mg2+ block reveals loose coupling between the cyclic nucleotide-gating ring and the pore.Corticospinal-specific HCN expression in mouse motor cortex: I(h)-dependent synaptic integration as a candidate microcircuit mechanism involved in motor controlHCN channelopathies: pathophysiology in genetic epilepsy and therapeutic implicationsAn N-terminal deletion variant of HCN1 in the epileptic WAG/Rij strain modulates HCN current densities.Cellular context and multiple channel domains determine cAMP sensitivity of HCN4 channels: ligand-independent relief of autoinhibition in HCN4.Binding of the auxiliary subunit TRIP8b to HCN channels shifts the mode of action of cAMPShort- and long-term plasticity in CA1 neurons from mice lacking h-channel auxiliary subunit TRIP8b.HCN-channel dendritic targeting requires bipartite interaction with TRIP8b and regulates antidepressant-like behavioral effects.Filamin A promotes dynamin-dependent internalization of hyperpolarization-activated cyclic nucleotide-gated type 1 (HCN1) channels and restricts Ih in hippocampal neurons.Towards an integrated view of HCN channel role in epilepsy.Exploring HCN channels as novel drug targets.
P2860
Q27014368-3D4511E6-9E63-49BB-95FA-015D9CBB3EC9Q27027165-2DBCACA2-DFCF-47D2-9497-902D1B466165Q27678862-1872CE0A-36EA-4F6D-AA29-AF3075F74F43Q28564312-43E8CA79-AAD5-4BD6-B357-D99D72DC7A49Q28572166-F2466D0E-D900-49AE-9D17-71800B4061C8Q28975760-25FCAF08-3150-4890-AC56-22C46184C3B0Q30373260-21A2FD1B-58C8-4401-BB24-6C58CDA5C20EQ30429700-CD249705-8704-4C51-B66E-51ECECE689DCQ30435045-87AC4669-E7EB-4B66-87C7-45AF1481F84EQ30529629-46A68A34-1954-4DF9-A6A2-F9C864FDB501Q30572674-DFAF107C-77C6-4692-9F8D-24BBECD3475FQ30691989-D59CAA1F-95D1-4B5E-894E-BE3EE2DEA143Q33924152-F8190683-903F-4AB8-B278-22C829971AD4Q33987823-32419518-7F19-4671-96A4-7C9449E6CDFAQ34171697-D963AE7C-4B8C-4237-85C6-67CECB22C056Q34187817-291C9317-EB78-4256-9B50-887DBE3B3898Q34280023-4E125C08-0533-4978-8D66-638A1105B2DFQ34374682-8BD799A2-FB76-48D8-9FCD-85998DC130EDQ34407387-A1E640FE-83B3-46BE-A517-543238E8C4C0Q34407624-2F432F97-CCFF-41B6-AE30-72EFEBF857C9Q34441790-FB60F15C-2CE4-4664-A094-C18E732E5138Q34508404-9EF8088A-0D10-4257-B1D1-93ADB97D828FQ34557298-7F7AE99C-3E69-4DCD-B9E1-5551967D4C66Q34777401-94A74DE6-6FA9-4EE9-B8B2-D745AEF76B6AQ34778354-83D32DB0-3D1B-43E3-900A-18A5D03D02D8Q35024706-CEFAA373-9C52-4A1C-BF44-9436AD6F1ADDQ35063427-F3E5E5F3-424D-49B3-BFF5-49C0CA647712Q35084850-B04F7D44-CE1D-4F41-A668-0480C12D87C4Q35147010-BA9CB485-6967-49A7-A9FB-558FBEA5836DQ35199062-891AEF1C-23A6-4DEC-9E35-B2B38BEA3695Q35543931-008536F8-6A28-4B0E-8991-BD9D60A297CBQ35657898-202B6066-A8DD-43E3-9E48-15A10F93D5E9Q35844665-E033DA06-3BFB-49F0-B811-AA7C3E230DB7Q36353470-89144168-03CF-424B-80EC-3040C8B9EFB6Q37343871-F390DD79-2086-4B5B-B093-524A083A6FFDQ37346231-C566E343-207E-4FD2-B962-41CF0B0A4D58Q37583999-4D7EA157-F4DA-4424-9991-8AE93F76F25FQ37608503-CCAF487C-5C75-45E6-9CE5-F92C12D8B9DFQ37904129-D465E920-DB5C-42E7-B326-009612104F17Q37957655-2703E813-65AB-48F1-AF93-2F571336279C
P2860
TRIP8b splice variants form a family of auxiliary subunits that regulate gating and trafficking of HCN channels in the brain.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on June 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
TRIP8b splice variants form a ...... of HCN channels in the brain.
@en
TRIP8b splice variants form a ...... of HCN channels in the brain.
@nl
type
label
TRIP8b splice variants form a ...... of HCN channels in the brain.
@en
TRIP8b splice variants form a ...... of HCN channels in the brain.
@nl
prefLabel
TRIP8b splice variants form a ...... of HCN channels in the brain.
@en
TRIP8b splice variants form a ...... of HCN channels in the brain.
@nl
P2093
P2860
P1433
P1476
TRIP8b splice variants form a ...... g of HCN channels in the brain
@en
P2093
Bina Santoro
Haiying Liu
Phillip Pian
Steven A Siegelbaum
P2860
P304
P356
10.1016/J.NEURON.2009.05.009
P407
P577
2009-06-01T00:00:00Z