Burk, Katja

[["dc.bibliographiccitation.artnumber","eaav1483"],["dc.bibliographiccitation.issue","6422"],["dc.bibliographiccitation.journal","Science (New York, N.Y.)"],["dc.bibliographiccitation.volume","363"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Shinoda, Yo"],["dc.contributor.author","Nitzan, Noam"],["dc.contributor.author","Heukamp, Alina"],["dc.contributor.author","Rannio, Sabine"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Wang, Yu Tian"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-31T13:02:46Z"],["dc.date.available","2019-07-31T13:02:46Z"],["dc.date.issued","2019"],["dc.description.abstract","Forgetting is important. Without it, the relative importance of acquired memories in a changing environment is lost. We discovered that synaptotagmin-3 (Syt3) localizes to postsynaptic endocytic zones and removes AMPA receptors from synaptic plasma membranes in response to stimulation. AMPA receptor internalization, long-term depression (LTD), and decay of long-term potentiation (LTP) of synaptic strength required calcium-sensing by Syt3 and were abolished through Syt3 knockout. In spatial memory tasks, mice in which Syt3 was knocked out learned normally but exhibited a lack of forgetting. Disrupting Syt3:GluA2 binding in a wild-type background mimicked the lack of LTP decay and lack of forgetting, and these effects were occluded in the Syt3 knockout background. Our findings provide evidence for a molecular mechanism in which Syt3 internalizes AMPA receptors to depress synaptic strength and promote forgetting."],["dc.identifier.doi","10.1126/science.aav1483"],["dc.identifier.pmid","30545844"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62245"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.issn","1095-9203"],["dc.title","Synaptotagmin-3 drives AMPA receptor endocytosis, depression of synapse strength, and forgetting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2118"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cell reports"],["dc.bibliographiccitation.lastpage","2133"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Siebrecht, Michael"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Reissner, Carsten"],["dc.contributor.author","Kohansal-Nodehi, Mahdokht"],["dc.contributor.author","Steubler, Vicky"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Ting, Jonathan T"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-09T11:44:43Z"],["dc.date.available","2019-07-09T11:44:43Z"],["dc.date.issued","2017-11-21"],["dc.description.abstract","Delivery of neurotrophins and neuropeptides via long-range trafficking of dense core vesicles (DCVs) from the cell soma to nerve terminals is essential for synapse modulation and circuit function. But the mechanism by which transiting DCVs are captured at specific sites is unknown. Here, we discovered that Synaptotagmin-4 (Syt4) regulates the capture and spatial distribution of DCVs in hippocampal neurons. We found that DCVs are highly mobile and undergo long-range translocation but switch directions only at the distal ends of axons, revealing a circular trafficking pattern. Phosphorylation of serine 135 of Syt4 by JNK steers DCV trafficking by destabilizing Syt4-Kif1A interaction, leading to a transition from microtubule-dependent DCV trafficking to capture at en passant presynaptic boutons by actin. Furthermore, neuronal activity increased DCV capture via JNK-dependent phosphorylation of the S135 site of Syt4. Our data reveal a mechanism that ensures rapid, site-specific delivery of DCVs to synapses."],["dc.identifier.doi","10.1016/j.celrep.2017.10.084"],["dc.identifier.pmid","29166604"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59077"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/260916/EU//SYT ACTIVITY"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","612"],["dc.title","Capture of Dense Core Vesicles at Synapses by JNK-Dependent Phosphorylation of Synaptotagmin-4."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2149"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific reports"],["dc.bibliographiccitation.lastpage","19"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Murdoch, John D"],["dc.contributor.author","Koenig, Melanie"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Markworth, Ronja"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-01-09T14:36:50Z"],["dc.date.available","2018-01-09T14:36:50Z"],["dc.date.issued","2017-05-19"],["dc.description.abstract","The sorting of activated receptors into distinct endosomal compartments is essential to activate specific signaling cascades and cellular events including growth and survival. However, the proteins involved in this sorting are not well understood. We discovered a novel role of EndophilinAs in sorting of activated BDNF-TrkB receptors into late endosomal compartments. Mice lacking all three EndophilinAs accumulate Rab7-positive late endosomes. Moreover, EndophilinAs are differentially localized to, co-traffic with, and tubulate, distinct endosomal compartments: In response to BDNF, EndophilinA2 is recruited to both early and late endosomes, EndophilinA3 is recruited to Lamp1-positive late endosomes, and co-trafficks with Rab5 and Rab7 in both the presence and absence of BDNF, while EndophilinA1 colocalizes at lower levels with endosomes. The absence of all three EndophilinAs caused TrkB to accumulate in EEA1 and Rab7-positive endosomes, and impaired BDNF-TrkB-dependent survival signaling cascades. In addition, EndophilinA triple knockout neurons exhibited increased cell death which could not be rescued by exogenous BDNF, in a neurotrophin-dependent survival assay. Thus, EndophilinAs differentially regulate activated receptor sorting via distinct endosomal compartments to promote BDNF-dependent cell survival."],["dc.identifier.doi","10.1038/s41598-017-02202-4"],["dc.identifier.pmid","28526875"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14709"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11603"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","EndophilinAs regulate endosomal sorting of BDNF-TrkB to mediate survival signaling in hippocampal neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5842"],["dc.bibliographiccitation.issue","30"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","5860"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Markworth, Ronja"],["dc.contributor.author","Adolfs, Youri"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Steinbeck, Lars M."],["dc.contributor.author","Lizé, Muriel"],["dc.contributor.author","Pasterkamp, R. Jeroen"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Burk, Katja"],["dc.date.accessioned","2020-12-10T18:42:33Z"],["dc.date.available","2020-12-10T18:42:33Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1523/JNEUROSCI.0027-19.2019"],["dc.identifier.eissn","1529-2401"],["dc.identifier.issn","0270-6474"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78005"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Sensory Axon Growth Requires Spatiotemporal Integration of CaSR and TrkB Signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1087"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cerebral Cortex"],["dc.bibliographiccitation.lastpage","1104"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Hurtado-Zavala, Joaquin I"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Faram, Ruth"],["dc.contributor.author","Ahmad, Hamid"],["dc.contributor.author","Swaminathan, Aarti"],["dc.contributor.author","McIlhinney, Jeffrey"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Perestenko, Pavel"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-01-09T14:34:30Z"],["dc.date.available","2018-01-09T14:34:30Z"],["dc.date.issued","2017"],["dc.description.abstract","Dendritic spines compartmentalize information in the brain, and their morphological characteristics are thought to underly synaptic plasticity. Here we identify copine-6 as a novel modulator of dendritic spine morphology. We found that brain-derived neurotrophic factor (BDNF) - a molecule essential for long-term potentiation of synaptic strength - upregulated and recruited copine-6 to dendritic spines in hippocampal neurons. Overexpression of copine-6 increased mushroom spine number and decreased filopodia number, while copine-6 knockdown had the opposite effect and dramatically increased the number of filopodia, which lacked PSD95. Functionally, manipulation of post-synaptic copine-6 levels affected miniature excitatory post-synaptic current (mEPSC) kinetics and evoked synaptic vesicle recycling in contacting boutons, and post-synaptic knockdown of copine-6 reduced hippocampal LTP and increased LTD. Mechanistically, copine-6 promotes BDNF-TrkB signaling and recycling of activated TrkB receptors back to the plasma membrane surface, and is necessary for BDNF-induced increases in mushroom spines in hippocampal neurons. Thus copine-6 regulates BDNF-dependent changes in dendritic spine morphology to promote synaptic plasticity."],["dc.identifier.doi","10.1093/cercor/bhx009"],["dc.identifier.pmid","28158493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11602"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1460-2199"],["dc.title","Regulation of Dendritic Spine Morphology in Hippocampal Neurons by Copine-6"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]