| Characterization of the HCN Interaction Partner TRIP8b/PEX5R in the Intracardiac Nervous System of TRIP8b-Deficient and Wild-Type Mice. | Characterization of the HCN Interaction Partner TRIP8b/PEX5R in the Intracardiac Nervous System of TRIP8b-Deficient and Wild-Type Mice.
Scherschel K, Bräuninger H, Mölders A, Erlenhardt N, Amin E, Jungen C, Pape U, Lindner D, Chetkovich DM, Klöcker N, Meyer C., Free PMC Article | 05/29/2021 |
| loss of TRIP8b phosphorylation may affect HCN channel properties during epileptogenesis. | Phosphorylation of the HCN channel auxiliary subunit TRIP8b is altered in an animal model of temporal lobe epilepsy and modulates channel function.
Foote KM, Lyman KA, Han Y, Michailidis IE, Heuermann RJ, Mandikian D, Trimmer JS, Swanson GT, Chetkovich DM., Free PMC Article | 06/6/2020 |
| This study found that global loss of TRIP8b, a necessary subunit for proper HCN channel localization in pyramidal cells, led to active coping behavior in numerous assays specific to coping style. | HCN channels in the hippocampus regulate active coping behavior.
Fisher DW, Han Y, Lyman KA, Heuermann RJ, Bean LA, Ybarra N, Foote KM, Dong H, Nicholson DA, Chetkovich DM., Free PMC Article | 06/29/2019 |
| This study demonstrated that Hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels have important functions in controlling neuronal excitability and generating rhythmic oscillatory activity. The role of tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b) in regulation of hyperpolarization-activated inward current, I h, in the thalamocortical system and its functional relevance | Modulation of thalamocortical oscillations by TRIP8b, an auxiliary subunit for HCN channels.
Zobeiri M, Chaudhary R, Datunashvili M, Heuermann RJ, Lüttjohann A, Narayanan V, Balfanz S, Meuth P, Chetkovich DM, Pape HC, Baumann A, van Luijtelaar G, Budde T., Free PMC Article | 03/2/2019 |
| Study characterized the effects of deletion of the HCN channel auxiliary subunit TRIP8b in the mouse thalamus and cortex, focusing on electrophysiological changes and their role in promoting absence epilepsy | Reduction of thalamic and cortical Ih by deletion of TRIP8b produces a mouse model of human absence epilepsy.
Heuermann RJ, Jaramillo TC, Ying SW, Suter BA, Lyman KA, Han Y, Lewis AS, Hampton TG, Shepherd GMG, Goldstein PA, Chetkovich DM., Free PMC Article | 09/24/2016 |
| We conclude that TRIP8b in the retina is needed to achieve maximal expression of HCN1. | TRIP8b is required for maximal expression of HCN1 in the mouse retina.
Pan Y, Bhattarai S, Modestou M, Drack AV, Chetkovich DM, Baker SA., Free PMC Article | 09/20/2014 |
| TRIP8b deletion is not restricted to the integrative properties of neurons but also includes both synaptic and intrinsic plasticity | Short- and long-term plasticity in CA1 neurons from mice lacking h-channel auxiliary subunit TRIP8b.
Brager DH, Lewis AS, Chetkovich DM, Johnston D., Free PMC Article | 07/5/2014 |
| TRIP8b isoforms are important regulators of HCN1 trafficking in entorhinal neurons. | Regulation of axonal HCN1 trafficking in perforant path involves expression of specific TRIP8b isoforms.
Wilkars W, Liu Z, Lewis AS, Stoub TR, Ramos EM, Brandt N, Nicholson DA, Chetkovich DM, Bender RA., Free PMC Article | 06/30/2012 |
| Study links elevated MMP-2/PEX2 to ischemia and poor wound healing. | Elevation of hemopexin-like fragment of matrix metalloproteinase-2 tissue levels inhibits ischemic wound healing and angiogenesis.
Nedeau AE, Gallagher KA, Liu ZJ, Velazquez OC., Free PMC Article | 12/17/2011 |
| increasing cAMP levels in cells antagonized the up-regulation of HCN1 channels mediated by a TRIP8b construct binding the CNBD exclusively. | 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.
Han Y, Noam Y, Lewis AS, Gallagher JJ, Wadman WJ, Baram TZ, Chetkovich DM., Free PMC Article | 08/6/2011 |
| Mice lacking TRIP8b demonstrate motor learning deficits and enhanced resistance to multiple tasks of behavioral despair with high predictive validity for antidepressant efficacy. | Deletion of the hyperpolarization-activated cyclic nucleotide-gated channel auxiliary subunit TRIP8b impairs hippocampal Ih localization and function and promotes antidepressant behavior in mice.
Lewis AS, Vaidya SP, Blaiss CA, Liu Z, Stoub TR, Brager DH, Chen X, Bender RA, Estep CM, Popov AB, Kang CE, Van Veldhoven PP, Bayliss DA, Nicholson DA, Powell CM, Johnston D, Chetkovich DM., Free PMC Article | 07/23/2011 |
| This study demonstrated that TRIP8b splice isoforms are necessary for the proper trafficking of HCN1 channels to the surface membrane of CA1 pyramidal neurons and for the proper targeting of the channels to the distal dendritic compartment. | TRIP8b splice forms act in concert to regulate the localization and expression of HCN1 channels in CA1 pyramidal neurons.
Piskorowski R, Santoro B, Siegelbaum SA., Free PMC Article | 07/16/2011 |
| The results suggested that all TRIP8b isoforms inhibit channel opening by shifting activation to more negative potentials. Its functions as an auxiliary subunit that provides a mechanism for the dynamic regulation of HCN1 channel expression and function. | TRIP8b splice variants form a family of auxiliary subunits that regulate gating and trafficking of HCN channels in the brain.
Santoro B, Piskorowski RA, Pian P, Hu L, Liu H, Siegelbaum SA., Free PMC Article | 01/21/2010 |
| Both untreated and bile acid-fed PEX2(-/-) mice accumulated high levels of predominantly unconjugated bile acids in plasma because of altered expression of hepatocyte bile acid transporters. | Bile acid treatment alters hepatic disease and bile acid transport in peroxisome-deficient PEX2 Zellweger mice.
Keane MH, Overmars H, Wikander TM, Ferdinandusse S, Duran M, Wanders RJ, Faust PL. | 01/21/2010 |
| These data suggest a possible role for TRIP8b in regulating HCN channel density in the plasma membrane. [TRIP8b] | Regulation of HCN channel surface expression by a novel C-terminal protein-protein interaction.
Santoro B, Wainger BJ, Siegelbaum SA., Free PMC Article | 01/21/2010 |