Raimundo, Nuno

[["dc.bibliographiccitation.artnumber","54"],["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Raimundo, Nuno"],["dc.contributor.author","Krisko, Anita"],["dc.date.accessioned","2019-07-09T11:51:27Z"],["dc.date.available","2019-07-09T11:51:27Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3389/fcell.2019.00054"],["dc.identifier.pmid","31032256"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16125"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59946"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/337327/EU//MITOPEXLYSONETWORK"],["dc.relation.eissn","2296-634X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Editorial: Mitochondrial Communication in Physiology, Disease and Aging"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","editorial_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","552"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Stem Cell Reports"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Simão, Daniel"],["dc.contributor.author","Silva, Marta M."],["dc.contributor.author","Terrasso, Ana P."],["dc.contributor.author","Arez, Francisca"],["dc.contributor.author","Sousa, Marcos F.Q."],["dc.contributor.author","Mehrjardi, Narges Z."],["dc.contributor.author","Šarić, Tomo"],["dc.contributor.author","Gomes-Alves, Patrícia"],["dc.contributor.author","Raimundo, Nuno"],["dc.contributor.author","Alves, Paula M."],["dc.contributor.author","Brito, Catarina"],["dc.date.accessioned","2020-12-10T15:21:30Z"],["dc.date.available","2020-12-10T15:21:30Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.stemcr.2018.06.020"],["dc.identifier.issn","2213-6711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73044"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Recapitulation of Human Neural Microenvironment Signatures in iPSC-Derived NPC 3D Differentiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2407"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Aging"],["dc.bibliographiccitation.lastpage","2427"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Musa, Marina"],["dc.contributor.author","Perić, Matea"],["dc.contributor.author","Bou Dib, Peter"],["dc.contributor.author","Sobočanec, Sandra"],["dc.contributor.author","Šarić, Ana"],["dc.contributor.author","Lovrić, Anita"],["dc.contributor.author","Rudan, Marina"],["dc.contributor.author","Nikolić, Andrea"],["dc.contributor.author","Milosević, Ira"],["dc.contributor.author","Vlahoviček, Kristian"],["dc.contributor.author","Raimundo, Nuno"],["dc.contributor.author","Kriško, Anita"],["dc.date.accessioned","2020-12-10T18:42:49Z"],["dc.date.available","2020-12-10T18:42:49Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.18632/aging.v10i9"],["dc.identifier.eissn","1945-4589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78101"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Heat-induced longevity in budding yeast requires respiratory metabolism and glutathione recycling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Sathyanarayanan, Udhayabhaskar"],["dc.contributor.author","Musa, Marina"],["dc.contributor.author","Bou Dib, Peter"],["dc.contributor.author","Raimundo, Nuno"],["dc.contributor.author","Milosevic, Ira"],["dc.contributor.author","Krisko, Anita"],["dc.date.accessioned","2021-04-14T08:31:49Z"],["dc.date.available","2021-04-14T08:31:49Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41467-020-19104-1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83720"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2041-1723"],["dc.relation.orgunit","Abteilung Experimentelle Neurodegeneration"],["dc.rights","CC BY 4.0"],["dc.title","ATP hydrolysis by yeast Hsp104 determines protein aggregate dissolution and size in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","45076"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Fernandez-Mosquera, Lorena"],["dc.contributor.author","Diogo, Catia V."],["dc.contributor.author","Yambire, King Faisal"],["dc.contributor.author","Santos, Gabriela L."],["dc.contributor.author","Luna Sanchez, Marta"],["dc.contributor.author","Benit, Paule"],["dc.contributor.author","Rustin, Pierre"],["dc.contributor.author","Carlos Lopez, Luis"],["dc.contributor.author","Milosevic, Ira"],["dc.contributor.author","Raimundo, Nuno"],["dc.date.accessioned","2018-11-07T10:26:02Z"],["dc.date.available","2018-11-07T10:26:02Z"],["dc.date.issued","2017"],["dc.description.abstract","Mitochondria are key cellular signaling platforms, affecting fundamental processes such as cell proliferation, differentiation and death. However, it remains unclear how mitochondrial signaling affects other organelles, particularly lysosomes. Here, we demonstrate that mitochondrial respiratory chain (RC) impairments elicit a stress signaling pathway that regulates lysosomal biogenesis via the microphtalmia transcription factor family. Interestingly, the effect of mitochondrial stress over lysosomal biogenesis depends on the timeframe of the stress elicited: while RC inhibition with rotenone or uncoupling with CCCP initially triggers lysosomal biogenesis, the effect peaks after few hours and returns to baseline. Long-term RC inhibition by long-term treatment with rotenone, or patient mutations in fibroblasts and in a mouse model result in repression of lysosomal biogenesis. The induction of lysosomal biogenesis by short-term mitochondrial stress is dependent on TFEB and MITF, requires AMPK signaling and is independent of calcineurin signaling. These results reveal an integrated view of how mitochondrial signaling affects lysosomes, which is essential to fully comprehend the consequences of mitochondrial malfunction, particularly in the context of mitochondrial diseases."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1038/srep45076"],["dc.identifier.isi","000397760800001"],["dc.identifier.pmid","28345620"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14396"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42963"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Acute and chronic mitochondrial respiratory chain deficiency differentially regulate lysosomal biogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Yambire, King Faisal"],["dc.contributor.author","Rostosky, Christine"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Pacheu-Grau, David"],["dc.contributor.author","Torres-Odio, Sylvia"],["dc.contributor.author","Sanchez-Guerrero, Angela"],["dc.contributor.author","Senderovich, Ola"],["dc.contributor.author","Meyron-Holtz, Esther G"],["dc.contributor.author","Milosevic, Ira"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","West, A Phillip"],["dc.contributor.author","Raimundo, Nuno"],["dc.date.accessioned","2020-12-10T18:48:09Z"],["dc.date.available","2020-12-10T18:48:09Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.7554/eLife.51031"],["dc.identifier.pmid","31793879"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17114"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/79035"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/104"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P02: Charakterisierung der ER-Mitochondrien-Kontakte und ihre Rolle in der Signalweiterleitung"],["dc.relation.workinggroup","RG Milosevic (Synaptic Vesicle Dynamics)"],["dc.relation.workinggroup","RG Raimundo"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Impaired lysosomal acidification triggers iron deficiency and inflammation in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","87"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","500"],["dc.contributor.author","Diogo, Cátia V."],["dc.contributor.author","Yambire, King Faisal"],["dc.contributor.author","Fernández Mosquera, Lorena"],["dc.contributor.author","Branco F., Tiago"],["dc.contributor.author","Raimundo, Nuno"],["dc.date.accessioned","2020-12-10T14:22:35Z"],["dc.date.available","2020-12-10T14:22:35Z"],["dc.date.issued","2018"],["dc.description.abstract","Mitochondria are constantly communicating with the rest of the cell. Defects in mitochondria underlie severe pathologies, whose mechanisms remain poorly understood. It is becoming increasingly evident that mitochondrial malfunction resonates in other organelles, perturbing their function and their biogenesis. In this manuscript, we review the current knowledge on the cross-talk between mitochondria and other organelles, particularly lysosomes, peroxisomes and the endoplasmic reticulum. Several organelle interactions are mediated by transcriptional programs, and other signaling mechanisms are likely mediating organelle dysfunction downstream of mitochondrial impairments. Many of these organelle crosstalk pathways are likely to have a role in pathological processes."],["dc.identifier.doi","10.1016/j.bbrc.2017.04.124"],["dc.identifier.pmid","28456629"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71662"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/23"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P02: Charakterisierung der ER-Mitochondrien-Kontakte und ihre Rolle in der Signalweiterleitung"],["dc.relation.workinggroup","RG Raimundo"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Mitochondrial adventures at the organelle society"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","overview_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5590"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Aging"],["dc.bibliographiccitation.lastpage","5611"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zhao, Jingjing"],["dc.contributor.author","Li, Gen"],["dc.contributor.author","Zhao, Xuan"],["dc.contributor.author","Lin, Xin"],["dc.contributor.author","Gao, Yunge"],["dc.contributor.author","Raimundo, Nuno"],["dc.contributor.author","Li, Geng-Lin"],["dc.contributor.author","Shang, Wei"],["dc.contributor.author","Wu, Hao"],["dc.contributor.author","Song, Lei"],["dc.date.accessioned","2021-04-14T08:26:28Z"],["dc.date.available","2021-04-14T08:26:28Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.18632/aging.102977"],["dc.identifier.eissn","1945-4589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81954"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1945-4589"],["dc.title","Down-regulation of AMPK signaling pathway rescues hearing loss in TFB1 transgenic mice and delays age-related hearing loss"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","71"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Trends in Molecular Medicine"],["dc.bibliographiccitation.lastpage","88"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Deus, Cláudia M."],["dc.contributor.author","Yambire, King Faisal"],["dc.contributor.author","Oliveira, Paulo J."],["dc.contributor.author","Raimundo, Nuno"],["dc.date.accessioned","2020-12-10T15:20:23Z"],["dc.date.available","2020-12-10T15:20:23Z"],["dc.date.issued","2020"],["dc.description.abstract","Cellular function requires coordination between different organelles and metabolic cues. Mitochondria and lysosomes are essential for cellular metabolism as major contributors of chemical energy and building blocks. It is therefore pivotal for cellular function to coordinate the metabolic roles of mitochondria and lysosomes. However, these organelles do more than metabolism, given their function as fundamental signaling platforms in the cell that regulate many key processes such as autophagy, proliferation, and cell death. Mechanisms of crosstalk between mitochondria and lysosomes are discussed, both under physiological conditions and in diseases that affect these organelles."],["dc.identifier.doi","10.1016/j.molmed.2019.10.009"],["dc.identifier.pmid","31791731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72652"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/100"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P02: Charakterisierung der ER-Mitochondrien-Kontakte und ihre Rolle in der Signalweiterleitung"],["dc.relation.workinggroup","RG Raimundo"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Mitochondria–Lysosome Crosstalk: From Physiology to Neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","overview_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","994"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Aging Cell"],["dc.bibliographiccitation.lastpage","1005"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Perić, Matea"],["dc.contributor.author","Lovrić, Anita"],["dc.contributor.author","Šarić, Ana"],["dc.contributor.author","Musa, Marina"],["dc.contributor.author","Bou Dib, Peter"],["dc.contributor.author","Rudan, Marina"],["dc.contributor.author","Nikolić, Andrea"],["dc.contributor.author","Sobočanec, Sandra"],["dc.contributor.author","Mikecin, Ana-Matea"],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Milošević, Ira"],["dc.contributor.author","Vlahoviček, Kristian"],["dc.contributor.author","Raimundo, Nuno"],["dc.contributor.author","Kriško, Anita"],["dc.date.accessioned","2019-07-09T11:44:59Z"],["dc.date.available","2019-07-09T11:44:59Z"],["dc.date.issued","2017"],["dc.description.abstract","Protein quality control mechanisms, required for normal cellular functioning, encompass multiple functions related to protein production and maintenance. However, the existence of communication between proteostasis and metabolic networks and its underlying mechanisms remain elusive. Here, we report that enhanced chaperone activity and consequent improved proteostasis are sensed by TORC1 via the activity of Hsp82. Chaperone enrichment decreases the level of Hsp82, which deactivates TORC1 and leads to activation of Snf1/AMPK, regardless of glucose availability. This mechanism culminates in the extension of yeast replicative lifespan (RLS) that is fully reliant on both TORC1 deactivation and Snf1/AMPK activation. Specifically, we identify oxygen consumption increase as the downstream effect of Snf1 activation responsible for the entire RLS extension. Our results set a novel paradigm for the role of proteostasis in aging: modulation of the misfolded protein level can affect cellular metabolic features as well as mitochondrial activity and consequently modify lifespan. The described mechanism is expected to open new avenues for research of aging and age-related diseases."],["dc.identifier.doi","10.1111/acel.12623"],["dc.identifier.pmid","28613034"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14988"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59133"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","315997"],["dc.relation","316289"],["dc.relation","337327"],["dc.relation.issn","1474-9726"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","612"],["dc.title","TORC1-mediated sensing of chaperone activity alters glucose metabolism and extends lifespan."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]