Mohamed, Belal A.

[["dc.bibliographiccitation.artnumber","149"],["dc.bibliographiccitation.journal","Journal of Translational Medicine"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Qasim, Mohamed"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2017-09-07T11:44:53Z"],["dc.date.available","2017-09-07T11:44:53Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Hemodynamic load leads to cardiac hypertrophy and heart failure. While afterload (pressure overload) induces concentric hypertrophy, elevation of preload (volume overload) yields eccentric hypertrophy and is associated with a better outcome. Here we analysed the proteomic pattern of mice subjected to short-term preload. Methods and Results: Female FVB/N mice were subjected to aortocaval shunt-induced volume overload that leads to an eccentric hypertrophy (left ventricular weight/tibia length +31 %) with sustained systolic heart function at 1 week after operation. Two-dimensional gel electrophoresis (2-DE) followed by mass spectrometric analysis showed alteration in the expression of 25 protein spots representing 21 different proteins. 64 % of these protein spots were up-regulated and 36 % of the protein spots were consistently down-regulated. Interestingly, alpha-1-antitrypsin was down-regulated, indicating higher elastin degradation and possibly contributing to the early dilatation. In addition to contractile and mitochondrial proteins, polymerase I and transcript release factor protein (PTRF) was also up-regulated, possibly contributing to the preload-induced signal transduction. Conclusions: Our findings reveal the proteomic changes of early-stage eccentric myocardial remodeling after volume overload. Induced expression of some of the respiratory chain enzymes suggests a metabolic shift towards an oxidative phosphorylation that might contribute to the favorable remodeling seen in early VO. Down-regulation of alpha-1-antitrypsin might contribute to extracellular matrix remodeling and left ventricular dilatation. We also identified PTRF as a potential signaling regulator of volume overload-induced cardiac hypertrophy."],["dc.identifier.doi","10.1186/s12967-016-0898-5"],["dc.identifier.gro","3141681"],["dc.identifier.isi","000377182700001"],["dc.identifier.pmid","27234427"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8784"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation [SFB1002]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1479-5876"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Proteomic analysis of short-term preload-induced eccentric cardiac hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4655"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Endocrinology"],["dc.bibliographiccitation.lastpage","4665"],["dc.bibliographiccitation.volume","153"],["dc.contributor.author","Burnicka-Turek, Ozanna"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Shirneshan, Katayoon"],["dc.contributor.author","Thanasupawat, Thatchawan"],["dc.contributor.author","Hombach-Klonisch, Sabine"],["dc.contributor.author","Klonisch, Thomas"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T09:05:20Z"],["dc.date.available","2018-11-07T09:05:20Z"],["dc.date.issued","2012"],["dc.description.abstract","Insulin-like factor 5 (INSL5), a member of the insulin superfamily, is expressed in the colorectum and hypothalamus. To facilitate studies into the role of INSL5, we generated Insl5(-/-) mice by gene targeting. Insl5(-/-) mice were born in the expected Mendelian ratio, reached normal body weight, but displayed impaired male and female fertility that are due to marked reduction in sperm motility and irregular length of the estrous cycle. Furthermore, Insl5(-/-) mice showed impairment in glucose homeostasis with characteristic elevation of serum glucose levels at an advanced age. Glucose and insulin tolerance tests revealed that the increased blood glucose in Insl5(-/-) mice was due to glucose intolerance resulting from reduced insulin secretion. Morphometric and immunohistological analyses revealed that the Insl5(-/-) mice had markedly reduced average islets area and beta-cell numbers. Furthermore, immunohistochemistry showed the expression of INSL5 in enteroendocrine cells in the colorectal epithelium and the presence of its putative receptor relaxin family peptide receptor 4 in pancreatic islet cells. These results suggest the potential role of INSL5 signaling in the regulation of insulin secretion and beta-cell homeostasis. (Endocrinology 153: 4655-4665, 2012)"],["dc.identifier.doi","10.1210/en.2012-1161"],["dc.identifier.isi","000309210200008"],["dc.identifier.pmid","22822165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25294"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0013-7227"],["dc.title","INSL5-Deficient Mice Display an Alteration in Glucose Homeostasis and an Impaired Fertility"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","9889"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Buchholz, Eric"],["dc.contributor.author","Koszewa, Sabrina"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2019-08-06T11:25:13Z"],["dc.date.available","2019-08-06T11:25:13Z"],["dc.date.issued","2019"],["dc.description.abstract","Calcium/calmodulin-dependent protein kinase type II delta (CaMKIIδ), the predominant CaMKII isoform expressed in the heart, has been implicated in the progression of myocardial infarction- and pressure overload-induced pathological remodeling. However, the role of CaMKIIδ in volume overload (VO) has not been explored. We have previously reported an activation of CaMKII during transition to HF in long-term VO. Here, we address whether CaMKIIδ is critically involved in the mortality, myocardial remodeling, and heart failure (HF) progression in response to VO. CaMKIIδ knockout (δ-KO) and wild-type (WT) littermates were exposed to aortocaval shunt-induced VO, and the progression of adverse myocardial remodeling was assessed by serial echocardiography, histological and molecular analyses. The mortality rates during 10 weeks of VO were similar in δ-KO and WT mice. Both genotypes displayed comparable eccentric myocardial hypertrophy, altered left ventricle geometry, perturbed systolic and diastolic functions after shunt. Additionally, cardiomyocytes hypertrophy, augmented myocyte apoptosis, and up-regulation of hypertrophic genes were also not significantly different in δ-KO versus WT hearts after shunt. Therefore, CaMKIIδ signaling seems to be dispensable for the progression of VO-induced maladaptive cardiac remodeling. Accordingly, we hypothesize that CaMKIIδ-inhibition as a therapeutic approach might not be helpful in the context of VO-triggered HF."],["dc.identifier.doi","10.1038/s41598-019-46332-3"],["dc.identifier.pmid","31285482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16358"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62306"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/281"],["dc.language.iso","en"],["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 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","2045-2322"],["dc.relation.issn","2045-2322"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genetic deletion of calcium/calmodulin-dependent protein kinase type II delta does not mitigate adverse myocardial remodeling in volume-overloaded hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Nicolas, Jan-David"],["dc.contributor.author","Khan, Amara"],["dc.contributor.author","Markus, Andrea"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Salditt, Tim"],["dc.date.accessioned","2021-04-14T08:31:46Z"],["dc.date.available","2021-04-14T08:31:46Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41598-020-76163-6"],["dc.identifier.pmid","33168890"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17813"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83706"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/102"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","2045-2322"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Salditt (Structure of Biomolecular Assemblies and X-Ray Physics)"],["dc.relation.workinggroup","RG Alves (Translationale Molekulare Bildgebung)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.gro","x-ray imaging"],["dc.subject.gro","x-ray scattering"],["dc.subject.gro","biomedical tomography"],["dc.title","X-ray diffraction and second harmonic imaging reveal new insights into structural alterations caused by pressure-overload in murine hearts"],["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","235"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Neef, S."],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2018-11-07T09:57:24Z"],["dc.date.available","2018-11-07T09:57:24Z"],["dc.date.issued","2015"],["dc.identifier.isi","000366200402357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37149"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Does leaky ryanodine receptors play any role in maladaptive remodeling after chronic mechanical stress in mice?"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4285"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","4296"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zhu, Wuqiang"],["dc.contributor.author","Hünlich, Mark"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Reuter, Sean P."],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Ramanujam, Deepak"],["dc.contributor.author","Engelhardt, Stefan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2021-06-01T10:47:52Z"],["dc.date.available","2021-06-01T10:47:52Z"],["dc.date.issued","2017"],["dc.description.abstract","Induction of the cell cycle is emerging as an intervention to treat heart failure. Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cyclin D2 would be beneficial during hemodynamic overload. We induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2–expressing and WT mice. Although cyclin D2 expression dramatically improved survival following TAC, it did not confer a survival advantage to mice following aortocaval shunt. Cardiac function decreased following TAC in WT mice, but was preserved in cyclin D2–expressing mice. On the other hand, cardiac structure and function were compromised in response to aortocaval shunt in both WT and cyclin D2–expressing mice. The preserved function and improved survival in cyclin D2–expressing mice after TAC was associated with an approximately 50% increase in cardiomyocyte number and exaggerated cardiac hypertrophy, as indicated by increased septum thickness. Aortocaval shunt did not further impact cardiomyocyte number in mice expressing cyclin D2. Following TAC, cyclin D2 expression attenuated cardiomyocyte hypertrophy, reduced cardiomyocyte apoptosis, fibrosis, calcium/calmodulin–dependent protein kinase IIδ phosphorylation, brain natriuretic peptide expression, and sustained capillarization. Thus, we show that cyclin D2–induced cardiomyocyte renewal reduced myocardial remodeling and dysfunction after pressure overload but not after volume overload."],["dc.identifier.doi","10.1172/JCI81870"],["dc.identifier.gro","3142324"],["dc.identifier.pmid","29083322"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85743"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/192"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["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 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Schäfer (Translationale Vaskuläre Biologie)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.title","Cardiomyocyte proliferation prevents failure in pressure overload but not volume overload"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","817"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Journal of Respiratory Cell and Molecular Biology"],["dc.bibliographiccitation.lastpage","824"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Barakat, Amal Z."],["dc.contributor.author","Held, Torsten"],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Muehlfeld, Christian"],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T09:41:50Z"],["dc.date.available","2018-11-07T09:41:50Z"],["dc.date.issued","2014"],["dc.description.abstract","Heat shock proteins HSPA4L and HSPA4 are closely related members of the HSP110 family and act as cochaperones. We generated Hspa4l(-1-) Hspa4(-1-) mice to investigate a functional complementarity between HSPA4L and HSPA4 during embryonic development. Hspa4l(-1-) Hspa4(-1-) 2 embryos exhibited marked pulmonary hypoplasia and neonatal death. Compared with lungs of wild- type, Hspa4l(-1-) , and Hspa4(-1-) embryos, Hspa4l(-1-) Hspa4(-1-) lungs were characterized by diminished saccular spaces and increased mesenchymal septa. Mesenchymal hypercellularity was determined to be due to an increased cell proliferation index and decreased cell death. A significant increase in expression levels of prosurvival protein B cell leukemia/ lymphoma 2 may be the cause for inhibition of apoptotic process in lungs of Hspa4(-1-) Hspa4l(-1-) embryos. Accumulation of glycogen and diminished expression of surfactant protein B, prosurfactant protein C, and aquaporin 5 in saccular epithelium suggested impaired maturation of type II and type I pneumocytes in the Hspa4l(-1-) Hspa4(-1-) lungs. Further experiments showed a significant accumulation of ubiquitinated proteins in the lungs of Hspa4l(-1-) Hspa4(-1-) embryos, indicating an impaired chaperone activity. Our study demonstrates that HSPA4L and HSPA4 collaborate in embryonic lung maturation, which is necessary for adaptation to air breathing at birth."],["dc.identifier.doi","10.1165/rcmb.2013-0132OC"],["dc.identifier.isi","000334403900016"],["dc.identifier.pmid","23980576"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33820"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Thoracic Soc"],["dc.relation.issn","1535-4989"],["dc.relation.issn","1044-1549"],["dc.title","Respiratory Distress and Early Neonatal Lethality in Hspa4l/Hspa4 Double-Mutant Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Lbik, D."],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Halder, R."],["dc.contributor.author","Fischer, A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2018-11-07T10:15:52Z"],["dc.date.available","2018-11-07T10:15:52Z"],["dc.date.issued","2016"],["dc.format.extent","S51"],["dc.identifier.isi","000375417500098"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40906"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Maximal resolution of the heart transcriptome with cell type specific profiling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","362"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","371"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Herwig, Melissa"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2017-09-07T11:54:33Z"],["dc.date.available","2017-09-07T11:54:33Z"],["dc.date.issued","2016"],["dc.description.abstract","AimWe have previously reported that early phase (1week) of experimental volume overload (VO) has an adaptive phenotype while wall stress-matched pressure overload (PO) is maladaptive. Here we investigate the transition from adaptation to heart failure (HF) in long-term VO. Methods and resultsFVB/N wild-type mice were subjected to VO induced by aortocaval shunt, and were followed by serial echocardiography until in vivo left ventricular ejection fraction was below <50% (13535days). Heart failure was evident from increased lung and liver weight and increased mortality compared with sham. Maladaptive remodelling resulted in significantly reduced sarcomeric titin phosphorylation (causing increased sarcomeric stiffness), whereas interstitial fibrosis was not increased. This was paralleled by re-expression of the fetal gene program, activation of calcium/calmodulin-dependent protein kinase II (CaMKII), decreased protein kinase B (Akt) phosphorylation, high oxidative stress, and increased apoptosis. Consistently, development of HF and mortality were significantly aggravated in Akt-deficient mice. ConclusionTransition to HF in VO is associated with decreased Akt and increased CaMKII signalling pathways together with increased oxidative stress and apoptosis. Lack of interstitial fibrosis together with sarcomeric titin hypophosphorylation indicates an increased stiffness at the sarcomeric but not matrix level in VO-induced HF (in contrast to PO). Transition to HF may result from myocyte loss and myocyte dysfunction owing to increased stiffness."],["dc.identifier.doi","10.1002/ejhf.465"],["dc.identifier.gro","3141701"],["dc.identifier.isi","000374308700005"],["dc.identifier.pmid","26694078"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/102"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation DFG [SFB 1002, IRTG1816]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A08: Translationale und posttranslationale Kontrolle trunkierter Titinproteine in Kardiomyozyten von Patienten mit dilatativer Kardiomyopathie"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.eissn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Molecular and structural transition mechanisms in long-term volume overload"],["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","133"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","REPRODUCTION"],["dc.bibliographiccitation.lastpage","144"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Held, Torsten"],["dc.contributor.author","Barakat, Amal Z."],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Paprotta, Ilona"],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T08:54:40Z"],["dc.date.available","2018-11-07T08:54:40Z"],["dc.date.issued","2011"],["dc.description.abstract","Heat-shock protein 110 (HSP110) family members act as nucleotide exchange factors (NEF) of mammalian and yeast HSP70 chaperones during the ATP hydrolysis cycle. In this study, we describe the expression pattern of murine HSPA4, a member of the HSP110 family, during testis development and the consequence of HSPA4 deficiency on male fertility. HSPA4 is ubiquitously expressed in all the examined tissues. During prenatal and postnatal development of gonad, HSPA4 is expressed in both somatic and germ cells; however, expression was much higher in germ cells of prenatal gonads. Analyses of Hspa4-deficient mice revealed that all homozygous mice on the hybrid C57BL/6Jx129/Sv genetic background were apparently healthy. Although HSPA4 is expressed as early as E13.5 in male gonad, a lack of histological differences between Hspa4(-/-) and control littermates suggests that Hspa4 deficiency does not impair the gonocytes or their development to spermatogonia. Remarkably, an increased number of the Hspa4-deficient males displayed impaired fertility, whereas females were fertile. The total number of spermatozoa and their motility were drastically reduced in infertile Hspa4-deficient mice compared with wild-type littermates. The majority of pachytene spermatocytes in the juvenile Hspa4(-/-) mice failed to complete the first meiotic prophase and became apoptotic. Furthermore, down-regulation of transcription levels of genes known to be expressed in spermatocytes at late stages of prophase I and post-meiotic spermatids leads to suggest that the development of most spermatogenic cells is arrested at late stages of meiotic prophase I. These results provide evidence that HSPA4 is required for normal spermatogenesis. Reproduction (2011) 142 133-144"],["dc.description.sponsorship","DAAD [A/07/80490]"],["dc.identifier.doi","10.1530/REP-11-0023"],["dc.identifier.isi","000292731400012"],["dc.identifier.pmid","21487003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22722"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bioscientifica Ltd"],["dc.relation.issn","1470-1626"],["dc.title","Heat-shock protein HSPA4 is required for progression of spermatogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]