Stühmer, Walter

[["dc.bibliographiccitation.artnumber","6672"],["dc.bibliographiccitation.journal","Nature communications"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Lörinczi, Éva"],["dc.contributor.author","Gómez-Posada, Juan Camilo"],["dc.contributor.author","de la Peña, Pilar"],["dc.contributor.author","Tomczak, Adam P"],["dc.contributor.author","Fernández-Trillo, Jorge"],["dc.contributor.author","Leipscher, Ulrike"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Barros, Francisco"],["dc.contributor.author","Pardo, Luis A"],["dc.date.accessioned","2019-07-09T11:42:35Z"],["dc.date.available","2019-07-09T11:42:35Z"],["dc.date.issued","2015"],["dc.description.abstract","Voltage-gated channels open paths for ion permeation upon changes in membrane potential, but how voltage changes are coupled to gating is not entirely understood. Two modules can be recognized in voltage-gated potassium channels, one responsible for voltage sensing (transmembrane segments S1 to S4), the other for permeation (S5 and S6). It is generally assumed that the conversion of a conformational change in the voltage sensor into channel gating occurs through the intracellular S4-S5 linker that provides physical continuity between the two regions. Using the pathophysiologically relevant KCNH family, we show that truncated proteins interrupted at, or lacking the S4-S5 linker produce voltage-gated channels in a heterologous model that recapitulate both the voltage-sensing and permeation properties of the complete protein. These observations indicate that voltage sensing by the S4 segment is transduced to the channel gate in the absence of physical continuity between the modules."],["dc.identifier.doi","10.1038/ncomms7672"],["dc.identifier.pmid","25818916"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58702"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Ether-A-Go-Go Potassium Channels"],["dc.subject.mesh","Immunoblotting"],["dc.subject.mesh","Immunoprecipitation"],["dc.subject.mesh","Oocytes"],["dc.subject.mesh","Patch-Clamp Techniques"],["dc.subject.mesh","Potassium Channels, Voltage-Gated"],["dc.subject.mesh","Protein Structure, Tertiary"],["dc.subject.mesh","Xenopus laevis"],["dc.title","Voltage-dependent gating of KCNH potassium channels lacking a covalent link between voltage-sensing and pore domains."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","755"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Neoplasia (New York, N.Y.)"],["dc.bibliographiccitation.lastpage","765"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Missbach-Guentner, Jeannine"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Zientkowska, Marta"],["dc.contributor.author","Domeyer-Missbach, Melanie"],["dc.contributor.author","Kimmina, Sarah"],["dc.contributor.author","Obenauer, Silvia"],["dc.contributor.author","Kauer, Fritz"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Grabbe, Eckhardt"],["dc.contributor.author","Vogel, Wolfgang F."],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2019-07-10T08:11:50Z"],["dc.date.available","2019-07-10T08:11:50Z"],["dc.date.issued","2007-09-01"],["dc.description.abstract","Skeletal metastasis is an important cause of mortality in patients with breast cancer. Hence, animal models, in combination with various imaging techniques, are in high demand for preclinical assessment of novel therapies. We evaluated the applicability of flat-panel volume computed tomography (fpVCT) to noninvasive detection of osteolytic bone metastases that develop in severe immunodeficient mice after intracardial injection of MDA-MB-231 breast cancer cells. A single fpVCT scan at 200-microm isotropic resolution was employed to detect osteolysis within the entire skeleton. Osteolytic lesions identified by fpVCT correlated with Faxitron X-ray analysis and were subsequently confirmed by histopathological examination. Isotropic three-dimensional image data sets obtained by fpVCT were the basis for the precise visualization of the extent of the lesion within the cortical bone and for the measurement of bone loss. Furthermore, fpVCT imaging allows continuous monitoring of growth kinetics for each metastatic site and visualization of lesions in more complex regions of the skeleton, such as the skull. Our findings suggest that fpVCT is a powerful tool that can be used to monitor the occurrence and progression of osteolytic lesions in vivo and can be further developed to monitor responses to antimetastatic therapies over the course of the disease."],["dc.identifier.pmid","17898871"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60807"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1476-5586"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.subject.mesh","Adenocarcinoma"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Bone Neoplasms"],["dc.subject.mesh","Breast Neoplasms"],["dc.subject.mesh","Disease Progression"],["dc.subject.mesh","Female"],["dc.subject.mesh","Femoral Neoplasms"],["dc.subject.mesh","Humerus"],["dc.subject.mesh","Imaging, Three-Dimensional"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, SCID"],["dc.subject.mesh","Models, Animal"],["dc.subject.mesh","Osteolysis"],["dc.subject.mesh","Skull Neoplasms"],["dc.subject.mesh","Specific Pathogen-Free Organisms"],["dc.subject.mesh","Tibia"],["dc.subject.mesh","Tomography, X-Ray Computed"],["dc.subject.mesh","Tumor Burden"],["dc.title","Flat-panel detector-based volume computed tomography: a novel 3D imaging technique to monitor osteolytic bone lesions in a mouse tumor metastasis model."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Neural Circuits"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","El Hady, Ahmed"],["dc.contributor.author","Afshar, Ghazaleh"],["dc.contributor.author","Bröking, Kai"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Geisel, Theo"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Wolf, Fred"],["dc.date.accessioned","2017-09-07T11:45:38Z"],["dc.date.available","2017-09-07T11:45:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Synchronized bursting is found in many brain areas and has also been implicated in the pathophysiology of neuropsychiatric disorders such as epilepsy, Parkinson’s disease, and schizophrenia. Despite extensive studies of network burst synchronization, it is insufficiently understood how this type of network wide synchronization can be strengthened, reduced, or even abolished. We combined electrical recording using multi-electrode array with optical stimulation of cultured channelrhodopsin-2 transducted hippocampal neurons to study and manipulate network burst synchronization. We found low frequency photo-stimulation protocols that are sufficient to induce potentiation of network bursting, modifying bursting dynamics, and increasing interneuronal synchronization. Surprisingly, slowly fading-in light stimulation, which substantially delayed and reduced light-driven spiking, was at least as effective in reorganizing network dynamics as much stronger pulsed light stimulation. Our study shows that mild stimulation protocols that do not enforce particular activity patterns onto the network can be highly effective inducers of network-level plasticity."],["dc.identifier.doi","10.3389/fncir.2013.00167"],["dc.identifier.fs","599562"],["dc.identifier.gro","3151828"],["dc.identifier.pmid","24155695"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8658"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","1662-5110"],["dc.relation.orgunit","Fakultät für Physik"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Action Potentials"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Hippocampus"],["dc.subject.mesh","Models, Neurological"],["dc.subject.mesh","Nerve Net"],["dc.subject.mesh","Neurons"],["dc.subject.mesh","Optogenetics"],["dc.subject.mesh","Rats"],["dc.subject.mesh","Rats, Wistar"],["dc.title","Optogenetic stimulation effectively enhances intrinsically generated network synchrony"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]