Männer, Jörg

[["dc.bibliographiccitation.artnumber","2959"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Demal, Till Joscha"],["dc.contributor.author","Heise, Melina"],["dc.contributor.author","Reiz, Benedikt"],["dc.contributor.author","Dogra, Deepika"],["dc.contributor.author","Brænne, Ingrid"],["dc.contributor.author","Reichenspurner, Hermann"],["dc.contributor.author","Männer, Jörg"],["dc.contributor.author","Aherrahrou, Zouhair"],["dc.contributor.author","Schunkert, Heribert"],["dc.contributor.author","Erdmann, Jeanette"],["dc.contributor.author","Abdelilah-Seyfried, Salim"],["dc.date.accessioned","2019-07-09T11:50:35Z"],["dc.date.available","2019-07-09T11:50:35Z"],["dc.date.issued","2019"],["dc.description.abstract","The genetics of many congenital heart diseases (CHDs) can only unsatisfactorily be explained by known chromosomal or Mendelian syndromes. Here, we present sequencing data of a family with a potentially multigenic origin of CHD. Twelve of nineteen family members carry a familial mutation [NM_004329.2:c.1328 G > A (p.R443H)] which encodes a predicted deleterious variant of BMPR1A. This mutation co-segregates with a linkage region on chromosome 1 that associates with the emergence of severe CHDs including Ebstein's anomaly, atrioventricular septal defect, and others. We show that the continuous overexpression of the zebrafish homologous mutation bmpr1aap.R438H within endocardium causes a reduced AV valve area, a downregulation of Wnt/ß-catenin signalling at the AV canal, and growth of additional tissue mass in adult zebrafish hearts. This finding opens the possibility of testing genetic interactions between BMPR1A and other candidate genes within linkage region 1 which may provide a first step towards unravelling more complex genetic patterns in cardiovascular disease aetiology."],["dc.identifier.doi","10.1038/s41598-019-39648-7"],["dc.identifier.pmid","30814609"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59803"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","A familial congenital heart disease with a possible multigenic origin involving a mutation in BMPR1A"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","096007"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Biomedical Optics"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Happel, Christoph M."],["dc.contributor.author","Thommes, Jan"],["dc.contributor.author","Thrane, Lars"],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Ortmaier, Tobias"],["dc.contributor.author","Heimann, Bodo"],["dc.contributor.author","Yelbuz, Talat Mesud"],["dc.date.accessioned","2018-11-07T08:52:01Z"],["dc.date.available","2018-11-07T08:52:01Z"],["dc.date.issued","2011"],["dc.description.abstract","We introduce a new method of rotational image acquisition for four-dimensional (4D) optical coherence tomography (OCT) of beating embryonic chick hearts. The rotational axis and the central A-scan of the OCT are identical. An out-of-phase image sequence covering multiple heartbeats is acquired at every angle of an incremental rotation of the deflection mirrors of the OCT system. Image acquisition is accomplished after a rotation of 180 degrees. Comparison of a displayed live M-mode of the central A-scan with a reference M-mode allows instant detection of translational movements of the embryo. For calculation of 4D data sets, we apply an image-based retrospective gating algorithm using the phase information of the common central A-scan present in all acquired images. This leads to cylindrical three-dimensional data sets for every time step of the cardiac cycle that can be used for 4D visualization. We demonstrate this approach and provide a video of a beating Hamburger and Hamilton stage 16 embryonic chick heart generated from a 4D OCT data set using rotational image acquisition. (C) 2011 Society of Photo-Optical Instrumentation Engineers (SPIE). [DOI: 10.1117/1.3622491]"],["dc.identifier.doi","10.1117/1.3622491"],["dc.identifier.isi","000296707100017"],["dc.identifier.pmid","21950921"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8152"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22071"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spie-soc Photo-optical Instrumentation Engineers"],["dc.relation.issn","1083-3668"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Rotationally acquired four-dimensional optical coherence tomography of embryonic chick hearts using retrospective gating on the common central A-scan"],["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.firstpage","3264"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Erhart, Philipp; 1Department of Vascular and Endovascular Surgery, University Hospital of Heidelberg, 69120 Heidelberg, Germany; daniel.koerfer@med.uni-heidelberg.de (D.K.); susanne.dihlmann@med.uni-heidelberg.de (S.D.); jiaiu.qiao@stud.uni-heidelberg.de (J.-L.Q.); caspar.grond-ginsbach@med.uni-heidelberg.de (C.G.-G.); dittmar.boeckler@med.uni-heidelberg.de (D.B.)"],["dc.contributor.affiliation","Körfer, Daniel; 1Department of Vascular and Endovascular Surgery, University Hospital of Heidelberg, 69120 Heidelberg, Germany; daniel.koerfer@med.uni-heidelberg.de (D.K.); susanne.dihlmann@med.uni-heidelberg.de (S.D.); jiaiu.qiao@stud.uni-heidelberg.de (J.-L.Q.); caspar.grond-ginsbach@med.uni-heidelberg.de (C.G.-G.); dittmar.boeckler@med.uni-heidelberg.de (D.B.)"],["dc.contributor.affiliation","Dihlmann, Susanne; 1Department of Vascular and Endovascular Surgery, University Hospital of Heidelberg, 69120 Heidelberg, Germany; daniel.koerfer@med.uni-heidelberg.de (D.K.); susanne.dihlmann@med.uni-heidelberg.de (S.D.); jiaiu.qiao@stud.uni-heidelberg.de (J.-L.Q.); caspar.grond-ginsbach@med.uni-heidelberg.de (C.G.-G.); dittmar.boeckler@med.uni-heidelberg.de (D.B.)"],["dc.contributor.affiliation","Qiao, Jia-Lu; 1Department of Vascular and Endovascular Surgery, University Hospital of Heidelberg, 69120 Heidelberg, Germany; daniel.koerfer@med.uni-heidelberg.de (D.K.); susanne.dihlmann@med.uni-heidelberg.de (S.D.); jiaiu.qiao@stud.uni-heidelberg.de (J.-L.Q.); caspar.grond-ginsbach@med.uni-heidelberg.de (C.G.-G.); dittmar.boeckler@med.uni-heidelberg.de (D.B.)"],["dc.contributor.affiliation","Hausser, Ingrid; 2Institute of Pathology, University Hospital of Heidelberg, 69120 Heidelberg, Germany; ingrid.hausser-siller@med.uni-heidelberg.de"],["dc.contributor.affiliation","Ringleb, Peter; 3Department of Neurology, University Hospital of Heidelberg, 69120 Heidelberg, Germany; peter.arthur.ringleb@med.uni-heidelberg.de"],["dc.contributor.affiliation","Männer, Jörg; 4Institute of Anatomy and Embryology, UMG, University of Göttingen, 37075 Göttingen, Germany; jmaenne@gwdg.de"],["dc.contributor.affiliation","Dikow, Nicola; 5Institute of Human Genetics, Heidelberg University, 69120 Heidelberg, Germany; nicola.dikow@med.uni-heidelberg.de (N.D.); christian.schaaf@med.uni-heidelberg.de (C.P.S.)"],["dc.contributor.affiliation","Schaaf, Christian P.; 5Institute of Human Genetics, Heidelberg University, 69120 Heidelberg, Germany; nicola.dikow@med.uni-heidelberg.de (N.D.); christian.schaaf@med.uni-heidelberg.de (C.P.S.)"],["dc.contributor.affiliation","Grond-Ginsbach, Caspar; 1Department of Vascular and Endovascular Surgery, University Hospital of Heidelberg, 69120 Heidelberg, Germany; daniel.koerfer@med.uni-heidelberg.de (D.K.); susanne.dihlmann@med.uni-heidelberg.de (S.D.); jiaiu.qiao@stud.uni-heidelberg.de (J.-L.Q.); caspar.grond-ginsbach@med.uni-heidelberg.de (C.G.-G.); dittmar.boeckler@med.uni-heidelberg.de (D.B.)"],["dc.contributor.affiliation","Böckler, Dittmar; 1Department of Vascular and Endovascular Surgery, University Hospital of Heidelberg, 69120 Heidelberg, Germany; daniel.koerfer@med.uni-heidelberg.de (D.K.); susanne.dihlmann@med.uni-heidelberg.de (S.D.); jiaiu.qiao@stud.uni-heidelberg.de (J.-L.Q.); caspar.grond-ginsbach@med.uni-heidelberg.de (C.G.-G.); dittmar.boeckler@med.uni-heidelberg.de (D.B.)"],["dc.contributor.author","Erhart, Philipp"],["dc.contributor.author","Körfer, Daniel"],["dc.contributor.author","Dihlmann, Susanne"],["dc.contributor.author","Qiao, Jia-Lu"],["dc.contributor.author","Hausser, Ingrid"],["dc.contributor.author","Ringleb, Peter"],["dc.contributor.author","Männer, Jörg"],["dc.contributor.author","Dikow, Nicola"],["dc.contributor.author","Schaaf, Christian P."],["dc.contributor.author","Grond-Ginsbach, Caspar"],["dc.contributor.author","Böckler, Dittmar"],["dc.date.accessioned","2022-07-01T07:35:32Z"],["dc.date.available","2022-07-01T07:35:32Z"],["dc.date.issued","2022"],["dc.date.updated","2022-07-08T10:41:22Z"],["dc.description.abstract","Background: Although patients with multiple arterial dissections in distinct arterial regions rarely present with known connective tissue syndromes, we hypothesized that mild connective tissue abnormalities are common findings in these patients. Methods: From a consecutive register of 322 patients with cervical artery dissection (CeAD), we identified and analyzed 4 patients with a history of additional dissections in other vascular beds. In three patients, dermal connective tissue was examined by electron microscopy. DNA from all four patients was studied by whole-exome sequencing and copy number variation (CNV) analysis. Results: The collagen fibers of dermal biopsies were pathologic in all three analyzed patients. One patient carried a CNV disrupting the COL3A1 and COL5A2 genes (vascular or hypermobility type of Ehlers–Danlos syndrome), and another patient a CNV in MYH11 (familial thoracic aortic aneurysms and dissections). The third patient carried a missense substitution in COL5A2. Conclusion: Three patients showed morphologic alterations of the dermal connective tissue, and two patients carried pathogenic variants in genes associated with arterial connective tissue dysfunction. The findings suggest that genetic testing should be recommended after recurrent arterial dissections, independently of apparent phenotypical signs of connective tissue disorders."],["dc.description.sponsorship","Heidelberger Stiftung Chirurgie"],["dc.identifier.doi","10.3390/jcm11123264"],["dc.identifier.pii","jcm11123264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112197"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112414"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2077-0383"],["dc.rights","CC BY 4.0"],["dc.title","Multiple Arterial Dissections and Connective Tissue Abnormalities"],["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","12"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cardiovascular Development and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Männer, Jörg"],["dc.contributor.author","Yelbuz, Talat Mesud"],["dc.date.accessioned","2020-12-10T18:47:10Z"],["dc.date.available","2020-12-10T18:47:10Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3390/jcdd6010012"],["dc.identifier.eissn","2308-3425"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78670"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","MDPI"],["dc.relation.eissn","2308-3425"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Functional Morphology of the Cardiac Jelly in the Tubular Heart of Vertebrate Embryos"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP 112"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Bayraktar, Meriç"],["dc.contributor.author","Männer, Jörg"],["dc.date.accessioned","2018-11-07T09:41:21Z"],["dc.date.available","2018-11-07T09:41:21Z"],["dc.date.issued","2014"],["dc.description.abstract","The transformation of the straight embryonic heart tube into a helically wound loop is named cardiac looping. Such looping is regarded as an essential process in cardiac morphogenesis since it brings the building blocks of the developing heart into an approximation of their definitive topographical relationships. During the past two decades, a large number of genes have been identified which play important roles in cardiac looping. However, how genetic information is physically translated into the dynamic form changes of the looping heart is still poorly understood. The oldest hypothesis of cardiac looping mechanics attributes the form changes of the heart loop (ventral bending -> simple helical coiling -> complex helical coiling) to compressive loads resulting from growth differences between the heart and the pericardial cavity. In the present study, we have tested the physical plausibility of this hypothesis, which we call the growth-induced buckling hypothesis, for the first time. Using a physical simulation model, we show that growth-induced buckling of a straight elastic rod within the confined space of a hemispherical cavity can generate the same sequence of form changes as observed in the looping embryonic heart. Our simulation experiments have furthermore shown that, under bilaterally symmetric conditions, growth-induced buckling generates left- and right-handed helices (D-/Lloops) in a 1:1 ratio, while even subtle left- or rightward displacements of the caudal end of the elastic rod at the pre-buckling state are sufficient to direct the buckling process toward the generation of only D- or L-loops, respectively. Our data are discussed with respect to observations made in biological \"models.\" We conclude that compressive loads resulting from unequal growth of the heart and pericardial cavity play important roles in cardiac looping. Asymmetric positioning of the venous heart pole may direct these forces toward a biased generation of D- or Lloops."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.3389/fphys.2014.00112"],["dc.identifier.isi","000347031600001"],["dc.identifier.pmid","24772086"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33710"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Cardiac looping may be driven by compressive loads resulting from unequal growth of the heart and pericardial cavity. Observations on a physical simulation model"],["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.firstpage","40"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cardiovascular Development and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Männer, Jörg"],["dc.date.accessioned","2020-12-10T18:47:10Z"],["dc.date.available","2020-12-10T18:47:10Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3390/jcdd6040040"],["dc.identifier.eissn","2308-3425"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78671"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2308-3425"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Spontaneous Left Cardiac Isomerism in Chick Embryos: Case Report, Review of the Literature, and Possible Significance for the Understanding of Ventricular Non-Compaction Cardiomyopathy in the Setting of Human Heterotaxy Syndromes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","19"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cardiovascular Development and Disease"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hiermeier, Florian"],["dc.contributor.author","Männer, Jörg"],["dc.date.accessioned","2020-12-10T18:47:10Z"],["dc.date.available","2020-12-10T18:47:10Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.3390/jcdd4040019"],["dc.identifier.eissn","2308-3425"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78669"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","MDPI"],["dc.relation.eissn","2308-3425"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Kinking and Torsion Can Significantly Improve the Efficiency of Valveless Pumping in Periodically Compressed Tubular Conduits. Implications for Understanding of the Form-Function Relationship of Embryonic Heart Tubes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Developmental Biology"],["dc.bibliographiccitation.lastpage","63"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Männer, Jörg"],["dc.date.accessioned","2019-07-09T11:40:20Z"],["dc.date.available","2019-07-09T11:40:20Z"],["dc.date.issued","2013"],["dc.description.abstract","The epicardium is the outer skin of the mature vertebrate heart. Its embryonic origin and its possible roles in the developing and mature heart did not receive much recognition during the 19th and most of the 20th century. During the past 25 years, however, the epicardium came into the focus of developmental biology and regenerative medicine. Clinical researchers usually prefer genetically modified mouse models when they want to gain insight into developmental or pathological processes. The story of research on the embryonic epicardium, however, nicely demonstrates the value of non-mammalian species, namely avian species, for elucidating fundamental processes in embryonic and fetal development. Studies on chick and quail embryos have not only led to the identification of the primarily extracardiac source of the epicardium􀂲presently called the proepicardium (PE)􀂲they have also significantly contributed to our current knowledge about the developmental significance of the embryonic epicardium. In this review article, I describe three 􀂳classical􀂴 microsurgical experiments that have been developed for studying the developmental significance of the PE/epicardium in avian embryos (mechanical PE-blocking, PE-photoablation, orthotopic PE-grafting). Furthermore, I show how these microsurgical experiments have contributed to our current knowledge about the roles of the PE/epicardium in cardiac development. There are still some unsolved aspects in the physiology of the developing epicardium, which may be clarified with the aid of these 􀂳classical􀂴 microsurgical experiments."],["dc.identifier.doi","10.3390/jdb1010047"],["dc.identifier.fs","598786"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10940"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58150"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2221-3759"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Microsurgical Procedures for Studying the Developmental Significance of the Proepicardium and Epicardium in Avian Embryos: PE-Blocking, PE-Photoablation, and PE-Grafting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E561"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","E564"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Happel, Christoph M."],["dc.contributor.author","Klose, Christian D."],["dc.contributor.author","Witton, Gabriele"],["dc.contributor.author","Angrisani, Gian L."],["dc.contributor.author","Wienecke, Soenke"],["dc.contributor.author","Groos, Stephanie"],["dc.contributor.author","Bach, Friedrich-Wilhelm"],["dc.contributor.author","Bormann, Dirk"],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Yelbuz, Talat Mesud"],["dc.date.accessioned","2018-11-07T08:36:36Z"],["dc.date.available","2018-11-07T08:36:36Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.110.977884"],["dc.identifier.isi","000284691700001"],["dc.identifier.pmid","21147724"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6294"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18356"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Non-Destructive, High-Resolution 3-Dimensional Visualization of a Cardiac Defect in the Chick Embryo Resembling Complex Heart Defect in Humans Using Micro-Computed Tomography Double Outlet Right Ventricle With Left Juxtaposition of Atrial Appendages"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","88"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","95"],["dc.bibliographiccitation.volume","121"],["dc.contributor.author","Goering, Wolfgang"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Pasche, B."],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Ochs, Matthias"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Zoll, Barbara"],["dc.date.accessioned","2018-11-07T11:19:46Z"],["dc.date.available","2018-11-07T11:19:46Z"],["dc.date.issued","2008"],["dc.description.abstract","The mouse Foxq1 gene, also known as Hfh1, encodes a winged helix/forkhead transcription factor. In adult mice, Foxq1 is highly expressed in kidney and stomach. Here, we report that Foxq1 is expressed during prenatal and postnatal stomach development and the transcripts are restricted to acid secreting parietal cells. Mice homozygous for a deletion of the Foxq1 locus on a 129/Sv x C57BL/6J hybrid genetic background display variable phenotypes consistent with requirement of the gene during embryogenesis. Approximately 50% of Foxq1(-/-) embryos die in utero. Surviving homozygous mutants are normal and fertile, and have a silky shiny coat. Although the parietal cell development is not affected in the absence of Foxq1, there is a lack of gastric acid secretion in response to various secretagogue stimuli. Ultrastructural analysis suggests that the gastric acid secretion defect in Foxq1-deficient mice might be due to impairment in the fusion of cytoplasmic tubulovesicles to the apical membrane of secretory canaliculi. Copyright (C) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000125833"],["dc.identifier.isi","000256880300002"],["dc.identifier.pmid","18544931"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55367"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Impairment of gastric acid secretion and increase of embryonic lethality in Foxq1-deficient mice"],["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"]]