Guan, Kaomei

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Weninger, Gunnar"],["dc.contributor.author","Pochechueva, Tatiana"],["dc.contributor.author","El Chami, Dana"],["dc.contributor.author","Luo, Xiaojing"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Brandenburg, Sören"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Lehnart, Stephan Elmar"],["dc.date.accessioned","2022-07-01T07:34:53Z"],["dc.date.available","2022-07-01T07:34:53Z"],["dc.date.issued","2022"],["dc.description.abstract","Calpains are calcium-activated neutral proteases involved in the regulation of key signaling pathways. Junctophilin-2 (JP2) is a Calpain-specific proteolytic target and essential structural protein inside Ca 2+ release units required for excitation-contraction coupling in cardiomyocytes. While downregulation of JP2 by Calpain cleavage in heart failure has been reported, the precise molecular identity of the Calpain cleavage sites and the (patho-)physiological roles of the JP2 proteolytic products remain controversial. We systematically analyzed the JP2 cleavage fragments as function of Calpain-1 versus Calpain-2 proteolytic activities, revealing that both Calpain isoforms preferentially cleave mouse JP2 at R565, but subsequently at three additional secondary Calpain cleavage sites. Moreover, we identified the Calpain-specific primary cleavage products for the first time in human iPSC-derived cardiomyocytes. Knockout of RyR2 in hiPSC-cardiomyocytes destabilized JP2 resulting in an increase of the Calpain-specific cleavage fragments. The primary N-terminal cleavage product NT 1 accumulated in the nucleus of mouse and human cardiomyocytes in a Ca 2+ -dependent manner, closely associated with euchromatic chromosomal regions, where NT 1 is proposed to function as a cardio-protective transcriptional regulator in heart failure. Taken together, our data suggest that stabilizing NT 1 by preventing secondary cleavage events by Calpain and other proteases could be an important therapeutic target for future studies."],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship"," Deutsches Zentrum für Herz-Kreislaufforschung http://dx.doi.org/10.13039/100010447"],["dc.description.sponsorship","Herzzentrum Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1038/s41598-022-14320-9"],["dc.identifier.pii","14320"],["dc.identifier.pmid","35725601"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112032"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/179"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/508"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/435"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P03: Erhaltung und funktionelle Kopplung von ER-Kontakten mit der Plasmamembran"],["dc.relation","SFB 1190 | Z02: Massenspektrometrie-basierte Proteomanalyse"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A09: Lokale molekulare Nanodomänen-Regulation der kardialen Ryanodin-Rezeptor-Funktion"],["dc.relation.eissn","2045-2322"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Calpain cleavage of Junctophilin-2 generates a spectrum of calcium-dependent cleavage products and DNA-rich NT1-fragment domains in cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","139"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Vlasov, Alla"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Yin, Dongjiao"],["dc.contributor.author","Nayernia, Karim"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2017-09-07T11:47:33Z"],["dc.date.available","2017-09-07T11:47:33Z"],["dc.date.issued","2009"],["dc.description.abstract","Recently, we reported the successful establishment of multipotent adult germ-Line stem cells (maGSCs) from cultured adult mouse spermatogonial stem cells. Similar to embryonic stem cells, maGSCs are able to self-renew and differentiate into derivatives of all three germ Layers. These properties make maGSCs a potential cell source for the treatment of neural degenerative diseases. In this study, we describe the generation of maGSC-derived proliferating neural precursor cells using growth factor-mediated neural Lineage induction. The neural precursors were positive for nestin and Sox1 and could be continuously expanded. Upon further differentiation, they formed functional neurons and glial cells, as demonstrated by expression of lineage-restricted genes and proteins and by electrophysiological properties. Characterization of maGSC-derived neurons revealed the generation of specific subtypes, including GABAergic, glutamatergic, serotonergic, and dopaminergic neurons. Electrophysiological analysis revealed passive and active membrane properties and postsynaptic currents, indicating their functional maturation. Functional networks formed at later stages of differentiation, as evidenced by synaptic transmission of spontaneous neuronal activity. In conclusion, our data demonstrate that maGSCs may be used as a new stem cell source for basic research and biomedical. applications. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.scr.2008.09.001"],["dc.identifier.gro","3143148"],["dc.identifier.isi","000272224500006"],["dc.identifier.pmid","19383419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/630"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-5061"],["dc.title","Generation of functional neurons and glia from multipotent adult mouse germ-line stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","975"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","991"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Guessoum, Celina I."],["dc.contributor.author","Lam, Tuan-Dinh D."],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Huber, Mia A."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lüscher, Thomas F."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2018-04-23T11:48:11Z"],["dc.date.available","2018-04-23T11:48:11Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Takotsubo syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-threating complications in the acute phase. The underlying disease mechanism in TTS is still unknown. A genetic basis has been suggested to be involved in the pathogenesis. Objectives The aims of the study were to establish an in vitro induced pluripotent stem cell (iPSC) model of TTS, to test the hypothesis of altered β-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), and to explore whether genetic susceptibility underlies the pathophysiology of TTS. Methods Somatic cells of patients with TTS and control subjects were reprogrammed to iPSCs and differentiated into CMs. Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overstimulation. We investigated β-adrenergic signaling and TTS cardiomyocyte function. Results Enhanced β-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosphate levels; and cyclic adenosine monophosphate–dependent protein kinase A–mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24, and Cav1.2-S1928, and leads to a reduced calcium time to transient 50% decay. These cellular catecholamine-dependent responses were mainly mediated by β1-adrenoceptor signaling in TTS. Engineered heart muscles from TTS-iPSC-CMs showed an impaired force of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control subjects. In addition, altered electrical activity and increased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed by differentially expressed lipid transporters CD36 and CPT1C. Furthermore, we uncovered genetic variants in different key regulators of cardiac function. Conclusions Enhanced β-adrenergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechanisms associated with the TTS phenotype."],["dc.identifier.doi","10.1016/j.jacc.2017.06.061"],["dc.identifier.gro","3142333"],["dc.identifier.pmid","28818208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13468"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/204"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","267"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Heart Rhythm"],["dc.bibliographiccitation.lastpage","276"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Ben Jehuda, Ronen"],["dc.contributor.author","Eisen, Binyamin"],["dc.contributor.author","Shemer, Yuval"],["dc.contributor.author","Mekies, Lucy N."],["dc.contributor.author","Szantai, Agnes"],["dc.contributor.author","Reiter, Irina"],["dc.contributor.author","Cui, Huanhuan"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Haron-Khun, Shiraz"],["dc.contributor.author","Freimark, Dov"],["dc.contributor.author","Sperling, Silke R."],["dc.contributor.author","Gherghiceanu, Mihaela"],["dc.contributor.author","Arad, Michael"],["dc.contributor.author","Binah, Ofer"],["dc.date.accessioned","2020-12-10T14:24:24Z"],["dc.date.available","2020-12-10T14:24:24Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.hrthm.2017.09.024"],["dc.identifier.issn","1547-5271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72243"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","CRISPR correction of the PRKAG2 gene mutation in the patient's induced pluripotent stem cell-derived cardiomyocytes eliminates electrophysiological and structural abnormalities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","76"],["dc.bibliographiccitation.journal","Cellular Signalling"],["dc.bibliographiccitation.lastpage","84"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Weber, Silvio"],["dc.contributor.author","Zeller, Miriam"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Wunder, Frank"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2019-02-27T15:40:20Z"],["dc.date.available","2019-02-27T15:40:20Z"],["dc.date.issued","2017"],["dc.description.abstract","The cyclic nucleotides cAMP and cGMP are central second messengers in cardiac cells and critical regulators of cardiac physiology as well as pathophysiology. Consequently, subcellular compartmentalization allows for spatiotemporal control of cAMP/cGMP metabolism and subsequent regulation of their respective effector kinases PKA or PKG is most important for cardiac function in health and disease. While acute cAMP-mediated signalling is a mandatory prerequisite for the physiological fight-or-flight response and enhanced cardiac contractility and relaxation, sustained activation of this pathway may lead to the progression of heart failure. In contrast, acute as well as sustained cGMP-mediated signalling can foster beneficial features, e.g. anti-hypertrophic and vasodilatory effects and thus blunting some of the aforementioned cAMP-mediated effects. Although these two signalling pathways seem to be intuitively counteracting, there is increasing evidence for a functionally relevant crosstalk between cAMP and cGMP signalling pathways on the level of cyclic nucleotide hydrolysing phosphodiesterases (PDEs). Among this diverse group of enzymes, PDE2 fulfils a unique integrator role. Equipped with dual substrate specificity for cAMP as well as for cGMP, it is the only cAMP hydrolysing PDE, which is allosterically activated by cGMP. Recent studies have revealed strongly remodelled cAMP/cGMP microdomains and subcellular concentration profiles in different cardiac pathologies, leading to a putatively enhanced involvement of PDE2 in cAMP/cGMP breakdown and crosstalk compared to the other cardiac PDEs. This review sums up the current knowledge about molecular properties and regulation of PDE2 and explains the complex signalling network encompassing PDE2 in order to better understand the functional role of PDE2 in distinct cell types in cardiac health and disease. Moreover, this review gives an outlook in which way PDE2 may serve as a therapeutic target to treat cardiac diseases."],["dc.identifier.doi","10.1016/j.cellsig.2017.06.020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57652"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/172"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation.issn","1873-3913"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.title","PDE2 at the crossway between cAMP and cGMP signalling in the heart"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","30967"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Veerman, Christiaan C."],["dc.contributor.author","Mengarelli, Isabella"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Barc, Julien"],["dc.contributor.author","Tan, Hanno L."],["dc.contributor.author","Wilde, Arthur A. M."],["dc.contributor.author","Verkerk, Arie O."],["dc.contributor.author","Bezzina, Connie R."],["dc.date.accessioned","2018-11-07T10:10:20Z"],["dc.date.available","2018-11-07T10:10:20Z"],["dc.date.issued","2016"],["dc.description.abstract","Brugada syndrome (BrS) is a rare cardiac rhythm disorder associated with sudden cardiac death. Mutations in the sodium channel gene SCN5A are found in similar to 20% of cases while mutations in other genes collectively account for <5%. In the remaining patients the genetic defect and the underlying pathogenic mechanism remain obscure. To provide insight into the mechanism of BrS in individuals without identified mutations, we here studied electrophysiological properties of cardiomyocytes (CMs) generated from human induced pluripotent stem cells (hiPSCs) from 3 BrS patients who tested negative for mutations in the known BrS-associated genes. Patch clamp studies revealed no differences in sodium current (I-Na) in hiPSC-CMs from the 3 BrS patients compared to 2 unrelated controls. Moreover, action potential upstroke velocity (V-max), reflecting INa, was not different between hiPSC-CMs from the BrS patients and the controls. hiPSC-CMs harboring the BrS-associated SCN5A-1795insD mutation exhibited a reduction in both I-Na and V-max, demonstrating our ability to detect reduced sodium channel function. hiPSC-CMs from one of the BrS lines demonstrated a mildly reduced action potential duration, however, the transient outward potassium current (I-to) and the L-type calcium current (I-Ca,I-L), both implicated in BrS, were not different compared to the controls. Our findings indicate that ion channel dysfunction, in particular in the cardiac sodium channel, may not be a prerequisite for BrS."],["dc.identifier.doi","10.1038/srep30967"],["dc.identifier.isi","000380637700001"],["dc.identifier.pmid","27485484"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13667"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39835"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/322"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","hiPSC-derived cardiomyocytes from Brugada Syndrome patients without identified mutations do not exhibit clear cellular electrophysiological abnormalities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","128"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","138"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Chuykin, Ilya"],["dc.contributor.author","Schulz, Herbert"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Bader, Michael"],["dc.date.accessioned","2018-11-07T09:30:11Z"],["dc.date.available","2018-11-07T09:30:11Z"],["dc.date.issued","2013"],["dc.description.abstract","During early mammalian development, primitive endoderm (PrE) is specified and segregated away from the pluripotent epiblast. At a later developmental stage, PrE forms motile parietal endoderm (PE) lying proximal to the trophectoderm, and visceral endoderm (VE) that contacts the developing epiblast and extraembryonic ectoderm. Mouse extraembryonic endoderm (XEN) cells were isolated and became widely used to study signals governing lineage specification. Rat XEN cell lines have also been derived, but were distinguished from mouse by expression of SSEA1 and Oct4. We showed here that rat XEN cells grown in the presence of a GSK3 inhibitor or overexpressing beta-catenin exhibited enhanced formation of cell contacts and decreased motility. Rat XEN cells treated with BMP4 revealed similar morphological changes. Furthermore, we observed that rat XEN cells cultured with GSK3 inhibitor formed adhesion and tight junctions, and acquired bottom-top polarity, indicating the formation of VE cells. In contrast, forskolin, an activator of the cAMP pathway, induced the disruption of cell contacts in rat XEN cells. Treatment with forskolin induced PE formation and epithelial-mesenchymal transition (EMT) in rat XEN cells. Using microarray and real-time PCR assays, we found that VE versus PE formation of rat XEN cells was correlated with change in expression levels of VE or PE marker genes. Similar to forskolin, EMT was prompted upon treatment of rat XEN cells with recombinant parathyroid hormone related peptide (PTHRP), an activator of the cAMP pathway in vivo. Taken together, our data suggest that rat XEN cells are PrE-like cells. The activation of Wnt or BMP4 pathways in rat XEN cells leads to the acquisition of VE characteristics, whereas the activation of the PTHRP/cAMP pathway leads to EMT and the formation of PE."],["dc.identifier.doi","10.1242/jcs.110239"],["dc.identifier.isi","000316460800014"],["dc.identifier.pmid","23038778"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31241"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Company Of Biologists Ltd"],["dc.relation.issn","0021-9533"],["dc.title","Activation of the PTHRP/adenylate cyclase pathway promotes differentiation of rat XEN cells into parietal endoderm, whereas Wnt/beta-catenin signaling promotes differentiation into visceral endoderm"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Schreiter, Jessica"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Nayemia, Karim"],["dc.contributor.author","Chapuy, Bjoem"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T08:57:49Z"],["dc.date.available","2018-11-07T08:57:49Z"],["dc.date.issued","2006"],["dc.format.extent","480A"],["dc.identifier.isi","000242440002204"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23491"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0006-4971"],["dc.title","Hematopoietic and endothelial progenitor cells from mouse adult testis derived stem cell lines."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Tissue Antigens"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Hamann, Carina"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:38:32Z"],["dc.date.available","2018-11-07T09:38:32Z"],["dc.date.issued","2014"],["dc.format.extent","5"],["dc.identifier.isi","000337546000002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","1399-0039"],["dc.relation.issn","0001-2815"],["dc.title","PLURIPOTENT STEM CELLS VARYING IN A SINGLE MINOR HISTOCOMPATIBILITY ANTIGEN ELICIT CELLULAR AND HUMORAL IMMUNE RESPONSES THAT CAN MEDIATE GRAFT REJECTION"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Fischer, C."],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Perret, A."],["dc.contributor.author","Oezcelic, C."],["dc.contributor.author","Wagner, S."],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2018-11-07T09:37:39Z"],["dc.date.available","2018-11-07T09:37:39Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1093/cvr/cvu083.2"],["dc.identifier.isi","000343730100211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32886"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","RBM20-dependent regulation of organized myofilament structure and titin splicing in induced pluripotent stem cell-derived cardiomyocytes from patients with dilative cardiomyopathy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]