| Differential brain expression pattern of Sez6 alternative splicing isoform with deleted transmembrane domain. | Differential brain expression pattern of Sez6 alternative splicing isoform with deleted transmembrane domain.
Hidaka C, Mitsui S, Osako Y, Takahashi K, Tanaka K, Yuri K. | 11/26/2022 |
| BACE inhibitor treatment of mice induces hyperactivity in a Seizure-related gene 6 family dependent manner without altering learning and memory. | BACE inhibitor treatment of mice induces hyperactivity in a Seizure-related gene 6 family dependent manner without altering learning and memory.
Nash A, Gijsen HJM, Hrupka BJ, Teng KS, Lichtenthaler SF, Takeshima H, Gunnersen JM, Munro KM., Free PMC Article | 11/6/2021 |
| Lack of Sez6 Family Proteins Impairs Motor Functions, Short-Term Memory, and Cognitive Flexibility and Alters Dendritic Spine Properties. | Lack of Sez6 Family Proteins Impairs Motor Functions, Short-Term Memory, and Cognitive Flexibility and Alters Dendritic Spine Properties.
Nash A, Aumann TD, Pigoni M, Lichtenthaler SF, Takeshima H, Munro KM, Gunnersen JM. | 08/21/2021 |
| Seizure protein 6 controls glycosylation and trafficking of kainate receptor subunits GluK2 and GluK3. | Seizure protein 6 controls glycosylation and trafficking of kainate receptor subunits GluK2 and GluK3.
Pigoni M, Hsia HE, Hartmann J, Rudan Njavro J, Shmueli MD, Müller SA, Güner G, Tüshaus J, Kuhn PH, Kumar R, Gao P, Tran ML, Ramazanov B, Blank B, Hipgrave Ederveen AL, Von Blume J, Mulle C, Gunnersen JM, Wuhrer M, Rammes G, Busche MA, Koeglsperger T, Lichtenthaler SF., Free PMC Article | 04/13/2021 |
| Results show that NPC1 loss-of-function in a mouse model of Niemann-Pick type C disease leads to enhanced cleavage of BACE1 substrates Sez6 and Sez6L, in addition to APP, and that this effect most likely involves altered trafficking of BACE1 and of its substrates within the endolysosomal system. Efficacy of Sez6 cleavage by BACE1 may be spatiotemporally differently regulated in contrast to the cleavage of Sez6L. | BACE1-cleavage of Sez6 and Sez6L is elevated in Niemann-Pick type C disease mouse brains.
Causevic M, Dominko K, Malnar M, Vidatic L, Cermak S, Pigoni M, Kuhn PH, Colombo A, Havas D, Flunkert S, McDonald J, Gunnersen JM, Hutter-Paier B, Tahirovic S, Windisch M, Krainc D, Lichtenthaler SF, Hecimovic S., Free PMC Article | 01/19/2019 |
| study demonstrates that SEZ6 and SEZ6L are physiological BACE1 substrates in the murine brain and suggests that sSEZ6 and sSEZ6L levels in CSF are suitable markers to monitor BACE1 inhibition in mice | Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons.
Pigoni M, Wanngren J, Kuhn PH, Munro KM, Gunnersen JM, Takeshima H, Feederle R, Voytyuk I, De Strooper B, Levasseur MD, Hrupka BJ, Müller SA, Lichtenthaler SF., Free PMC Article | 11/11/2017 |
| results indicate that N-glycosylation regulates cell morphology through modulating the cell surface distribution of sez-6 protein | N-Glycosylation modulates filopodia-like protrusions induced by sez-6 through regulating the distribution of this protein on the cell surface.
Hidaka C, Mitsui S. | 08/29/2015 |
| co-expression of sez-6 with motopsin restored the effect of motopsin at the basal level, while sez-6 expression alone showed no effects on cell morphology. Our results suggest that the interaction of motopsin and sez-6 modulates neuronal cell morphology | A mental retardation gene, motopsin/prss12, modulates cell morphology by interaction with seizure-related gene 6.
Mitsui S, Hidaka C, Furihata M, Osako Y, Yuri K. | 10/26/2013 |
| Spatiotemporal alterations of the regional and intracellular distribution of Sez-6 suggest its multiple functions during the postnatal development of the forebrain. | The distribution of the seizure-related gene 6 (Sez-6) protein during postnatal development of the mouse forebrain suggests multiple functions for this protein: an analysis using a new antibody.
Osaki G, Mitsui S, Yuri K. | 03/17/2012 |
| Retinal morphology, ganglion cell dendritic branching and ERG waveforms appeared normal in the Sez-6 knockout mouse suggesting that, in spite of widespread expression of Sez-6, retinal function in the absence of Sez-6 is not affected | Seizure-related gene 6 (Sez-6) in amacrine cells of the rodent retina and the consequence of gene deletion.
Gunnersen JM, Kuek A, Phipps JA, Hammond VE, Puthussery T, Fletcher EL, Tan SS., Free PMC Article | 01/25/2010 |
| In conclusion, cell-surface protein complexes involving Sez-6 help to sculpt the dendritic arbor, in turn enhancing synaptic connectivity. | Sez-6 proteins affect dendritic arborization patterns and excitability of cortical pyramidal neurons.
Gunnersen JM, Kim MH, Fuller SJ, De Silva M, Britto JM, Hammond VE, Davies PJ, Petrou S, Faber ES, Sah P, Tan SS. | 01/21/2010 |
| the pattern of SEZ-6 expression is closely tied with the emergence of the neocortical layers and hippocampus, and implies a forebrain-specific role for this gene during development | Localized expression of the seizure-related gene SEZ-6 in developing and adult forebrains.
Kim MH, Gunnersen JM, Tan SS. | 01/21/2010 |