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| http://purl.uniprot.org/citations/15564593 | http://www.w3.org/2000/01/rdf-schema#comment | "Hyperpolarization-activated cation currents (I(h)) are carried by channels encoded by a family of four genes (HCN1-4) that are differentially expressed within the brain in specific cellular and subcellular compartments. HCN1 shows a high level of expression in apical dendrites of cortical pyramidal neurons and in presynaptic terminals of cerebellar basket cells, structures with a high density of I(h). Expression of I(h) is also regulated by neuronal activity. To isolate proteins that may control HCN channel expression or function, we performed yeast two-hybrid screens using the C-terminal cytoplasmic tails of the HCN proteins as bait. We identified a brain-specific protein, which has been previously termed TRIP8b (for TPR-containing Rab8b interacting protein) and PEX5Rp (for Pex5p-related protein), that specifically interacts with all four HCN channels through a conserved sequence in their C-terminal tails. In situ hybridization and immunohistochemistry show that TRIP8b and HCN1 are colocalized, particularly within dendritic arbors of hippocampal CA1 and neocortical layer V pyramidal neurons. The dendritic expression of TRIP8b in layer V pyramidal neurons is disrupted after deletion of HCN1 through homologous recombination, demonstrating a key in vivo interaction between HCN1 and TRIP8b. TRIP8b dramatically alters the trafficking of HCN channels heterologously expressed in Xenopus oocytes and human embryonic kidney 293 cells, causing a specific decrease in surface expression of HCN protein and I(h) density, with a pronounced intracellular accumulation of HCN protein that is colocalized in discrete cytoplasmic clusters with TRIP8b. Finally, TRIP8b expression in cultured pyramidal neurons markedly decreases native I(h) density. These data suggest a possible role for TRIP8b in regulating HCN channel density in the plasma membrane."xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.org/dc/terms/identifier | "doi:10.1523/jneurosci.3300-04.2004"xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/author | "Wainger B.J."xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/author | "Siegelbaum S.A."xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/author | "Santoro B."xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/name | "J Neurosci"xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/pages | "10750-10762"xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/title | "Regulation of HCN channel surface expression by a novel C-terminal protein-protein interaction."xsd:string |
| http://purl.uniprot.org/citations/15564593 | http://purl.uniprot.org/core/volume | "24"xsd:string |
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