Brenig, Bertram B.

[["dc.bibliographiccitation.firstpage","57"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","KLEINTIERPRAXIS"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Droegemueller, Cord"],["dc.contributor.author","Leeb, Tosso"],["dc.contributor.author","Scharfenstein, Melanie"],["dc.contributor.author","Brenig, Bertram"],["dc.date.accessioned","2018-11-07T09:13:33Z"],["dc.date.available","2018-11-07T09:13:33Z"],["dc.date.issued","2012"],["dc.description.abstract","Osteogenesis imperfecta in the dachshund Osteogenesis imperfecta (OI) in the Dachshund is due to a recessive mutation in the SERPINH1 gene (serpin H1, serinarginine-protease inhibitor, heat shock protein 47, collagen-binding protein 1). An alteration or loss of function of SERPINH1 results in a misfolding of collagen fibrils and consequently to an abnormal ossification. Homozygous mutant animals are nonviable and usually die shortly after birth with multiple bone fractures often already acquired during foetal development. In the present study, we analysed 591 Dachshunds for the presence of the SERPINH1 mutation and recorded the rate of stillborn puppies. The association between both parameters was recorded in male dogs with at least 15 registered litters. The allele frequency of the SERPINH1 mutation was calculated to be 8.86%. In litters of heterozygous male Dachshunds, the mortality rate was exceedingly significantly higher (p = 0.00002; n = 3299 puppies) than in dogs without this mutation (odds-ratio: 1.8). One affected homozygous Dachshund showed the typical clinic signs of OI with brittle bones, fractures, and translucent reddish teeth. In summary, we were able show that the causative OI mutation within the SERPINH1 gene in the Dachshund results in a significantly increased mortality rate among the offspring of carriers. Due to the relatively high allele frequency of the mutated allele and animal welfare issues involved, dogs that are used for breeding should be tested using the robust DNA-based assay described here. With a consistent implementation of DNA-based diagnosis, it should be possible to eliminate carriers gradually with preservation of the genetic diversity in the breeding population."],["dc.identifier.isi","000302201800001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27209"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","M H Schaper Gmbh Co Kg"],["dc.relation.issn","0023-2076"],["dc.title","Osteogenesis imperfecta in the dachshund"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Animal Genetics"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Leeb, Tosso"],["dc.contributor.author","Pfeiffer, I."],["dc.contributor.author","Brenig, Bertram"],["dc.date.accessioned","2018-11-07T09:18:19Z"],["dc.date.available","2018-11-07T09:18:19Z"],["dc.date.issued","2000"],["dc.format.extent","337"],["dc.identifier.doi","10.1046/j.1365-2052.2000.00659.x"],["dc.identifier.isi","000165797800013"],["dc.identifier.pmid","11105220"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28384"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.relation.issn","0268-9146"],["dc.title","Two highly polymorphic microsatellites between the canine DAG1 and BSN genes on CFA20q15.1-15.2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","166"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Animal Genetics"],["dc.bibliographiccitation.lastpage","167"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Spotter, A."],["dc.contributor.author","Kuiper, H."],["dc.contributor.author","Drogemuller, Cord"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Leeb, Tosso"],["dc.contributor.author","Distl, O."],["dc.date.accessioned","2018-11-07T10:30:43Z"],["dc.date.available","2018-11-07T10:30:43Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1046/j.1365-2052.2002.0831i.x"],["dc.identifier.isi","000174849800020"],["dc.identifier.pmid","12047239"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43932"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0268-9146"],["dc.title","Assignment of the porcine epidermal growth factor (EGF) gene to SSC8q2.3-q2.4 by fluorescence in situ hybridization and radiation hybrid mapping"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","216"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Spotter, A."],["dc.contributor.author","Drogemuller, Cord"],["dc.contributor.author","Kuiper, H."],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Leeb, Tosso"],["dc.contributor.author","Distl, O."],["dc.date.accessioned","2018-11-07T10:32:58Z"],["dc.date.available","2018-11-07T10:32:58Z"],["dc.date.issued","2002"],["dc.description.abstract","Leukemia inhibitory factor receptor (LIFR), epidermal growth factor receptor (EGFR), and their respective ligands have been implicated in regulating growth and development of the early pig conceptus. We isolated a PAC clone containing the porcine gene for LIFR and a BAC clone with the porcine EGFR gene, respectively. On each of these clones one microsatellite marker was identified by sequencing a collection of subclones. These gene-associated markers were evaluated by genotyping of 202 unrelated boars of four different breeds. Based on fluorescence in situ hybridization and radiation hybrid mapping, the porcine LIFR gene was assigned to SSC16q13 --> q14. The EGFR gene mapped to SSC9q26. Copyright (C) 2002 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000069816"],["dc.identifier.isi","000182472500015"],["dc.identifier.pmid","12698007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44483"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.title","Mapping and microsatellite marker development for the porcine leukemia inhibitory factor receptor (LIFR) and epidermal growth factor receptor (EGFR) genes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2307"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Haematologica"],["dc.bibliographiccitation.lastpage","2313"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Steingräber, Lilith"],["dc.contributor.author","Shan, Shuwen"],["dc.contributor.author","Xu, Fangzheng"],["dc.contributor.author","Hirschfeld, Marc"],["dc.contributor.author","Andag, Reiner"],["dc.contributor.author","Spengeler, Mirjam"],["dc.contributor.author","Dietschi, Elisabeth"],["dc.contributor.author","Mischke, Reinhard"],["dc.contributor.author","Leeb, Tosso"],["dc.date.accessioned","2020-12-10T18:44:18Z"],["dc.date.available","2020-12-10T18:44:18Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3324/haematol.2018.215426"],["dc.identifier.eissn","1592-8721"],["dc.identifier.issn","0390-6078"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78402"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Christmas disease in a Hovawart family resembling human hemophilia B Leyden is caused by a single nucleotide deletion in a highly conserved transcription factor binding site of the F9 gene promoter"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Animal Genetics"],["dc.bibliographiccitation.lastpage","336"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Leeb, Tosso"],["dc.contributor.author","Deppe, A."],["dc.contributor.author","Kriegesmann, B."],["dc.contributor.author","Brenig, Bertram"],["dc.date.accessioned","2018-11-07T09:17:52Z"],["dc.date.available","2018-11-07T09:17:52Z"],["dc.date.issued","2000"],["dc.identifier.doi","10.1046/j.1365-2052.2000.00656.x"],["dc.identifier.isi","000165797800011"],["dc.identifier.pmid","11105218"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28272"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.relation.issn","0268-9146"],["dc.title","Genomic structure and nucleotide polymorphisms of the porcine agouti signalling protein gene (ASIP)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","193"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","TIERAERZTLICHE PRAXIS AUSGABE KLEINTIERE HEIMTIERE"],["dc.bibliographiccitation.lastpage","199"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Kreuter, R."],["dc.contributor.author","Mueller, G."],["dc.contributor.author","Leeb, Tosso"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Moritz, Andreas"],["dc.contributor.author","Baumgaertner, Wolfgang"],["dc.date.accessioned","2018-11-07T11:07:38Z"],["dc.date.available","2018-11-07T11:07:38Z"],["dc.date.issued","2007"],["dc.description.abstract","Objective: GM(1)-gangliosidosis of the Alaskan Husky is an autosomal recessively inherited metabolic disease caused by a defect of the canine acid beta-galactosidase gene (GLBI). Clinically, affected animals display dwarfism and neurological deficits consisting of ataxia and dysmetria starting at six to eight weeks of age. To prevent the birth of affected pups it is important to identify carriers oft he genetic defect and to avoid matings between two carriers. Material and methods: Specificity and sensitivity of a recently described genetic test for direct detection of GM(1)-gangliosidosis of the Alaskan Husky was compared to the biochemical measurement of the enzyme activity of the beta-galactosidase in isolated skin fibroblasts, clinical and pathological findings as well as pedigree analysis. Results: The -galactosidase enzyme activities of carriers were lower on average than the enzyme activities of homozygous wild-type dogs. However, the individually measured values between the groups showed a considerable overlap. Therefore, it was not possible to identify carriers unambiguously. In contrast, genetic testing allowed the direct discrimination between homozygous wild-type dogs and carriers. Conclusion: Genetic testing is superior to biochemical testing. Clinical relevance: The phenotypically inconspicuous carriers can be identified unambiguously by genetic testing. Thus, matings of two carriers can be avoided and the occurrence of GM(1)-gangliosidosis can be prevented in the future."],["dc.identifier.isi","000247655200007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52608"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Schattauer Gmbh-verlag Medizin Naturwissenschaften"],["dc.relation.issn","1434-1239"],["dc.title","Genetic testing for GM1-gang liosidosis in the Alaskan husky"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Veterinary Record"],["dc.bibliographiccitation.volume","172"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Scharfenstein, Melanie"],["dc.contributor.author","Droegemueller, Cord"],["dc.contributor.author","Leeb, Tosso"],["dc.date.accessioned","2018-11-07T09:26:59Z"],["dc.date.available","2018-11-07T09:26:59Z"],["dc.date.issued","2013"],["dc.format.extent","319"],["dc.identifier.doi","10.1136/vr.f1823"],["dc.identifier.isi","000317893000024"],["dc.identifier.pmid","23525816"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30430"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","British Veterinary Assoc"],["dc.relation.issn","0042-4900"],["dc.title","Osteogenesis imperfecta in dachshunds"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","58"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Mammalian Genome"],["dc.bibliographiccitation.lastpage","66"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Drogemuller, Cord"],["dc.contributor.author","Giese, A."],["dc.contributor.author","Martins-Wess, F."],["dc.contributor.author","Wiedemann, S."],["dc.contributor.author","Andersson, L."],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Fries, R."],["dc.contributor.author","Leeb, Tosso"],["dc.date.accessioned","2018-11-07T10:38:10Z"],["dc.date.available","2018-11-07T10:38:10Z"],["dc.date.issued","2006"],["dc.description.abstract","The gene for agouti signaling protein ( ASIP) is centrally involved in the expression of coat color traits in animals. The Mangalitza pig breed is characterized by a black-and-tan phenotype with black dorsal pigmentation and yellow or white ventral pigmentation. We investigated a Mangalitza x Pietrain cross and observed a coat color segregation pattern in the F-2 generation that can be explained by virtue of two alleles at the MC1R locus and two alleles at the ASIP locus. Complete linkage of the black-and-tan phenotype to microsatellite alleles at the ASIP locus on SSC 17q21 was observed. Corroborated by the knowledge of similar mouse coat color mutants, it seems therefore conceivable that the black-and-tan pigmentation of Mangalitza pigs is caused by an ASIP allele a(t), which is recessive to the wild-type allele A. Toward positional cloning of the at mutation, a 200-kb genomic BAC/PAC contig of this chromosomal region has been constructed and subsequently sequenced. Full-length ASIP cDNAs obtained by RACE differed in their 5' untranslated regions, whereas they shared a common open reading frame. Comparative sequencing of all ASIP exons and ASIP cDNAs between Mangalitza and Pietrain pigs did not reveal any differences associated with the coat color phenotype. Relative qRT-PCR analyses showed different dorsoventral skin expression intensities of the five ASIP transcripts in black-and-tan Mangalitza. The a(t) mutation is therefore probably a regulatory ASIP mutation that alters its dorsoventral expression pattern."],["dc.identifier.doi","10.1007/s00335-005-0104-1"],["dc.identifier.isi","000234825800007"],["dc.identifier.pmid","16416091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45746"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0938-8990"],["dc.title","The mutation causing the black-and-tan pigmentation phenotype of Mangalitza pigs maps to the porcine ASIP locus but does not affect its coding sequence"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","190"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","CYTOGENETICS AND CELL GENETICS"],["dc.bibliographiccitation.lastpage","193"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Drogemuller, Cord"],["dc.contributor.author","Kuiper, H."],["dc.contributor.author","Voss-Nemitz, R."],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Distl, O."],["dc.contributor.author","Leeb, Tosso"],["dc.date.accessioned","2018-11-07T09:31:06Z"],["dc.date.available","2018-11-07T09:31:06Z"],["dc.date.issued","2001"],["dc.description.abstract","The COX7A1 gene encodes a heart- and muscle-specific isoform of the subunit VIIA of cvtochrome c oxidase, Which is the last component of the mitochondrial electron transfer chain, Cloning and characterization of the porcine COX7A1 gene revealed a highly conserved organization with respect to other mammalian COX7A1 orthologs. The porcine gene consists of four exons spanning approximately 1.5 kb and codes for a peptide of 80 amino acids. The COX7A1 gene showed no variation between pigs from different breeds. The gene was assigned by FISH and RH-mapping to SSC 6q1.1 --> q1.2 which is in agreement with previously established comparative maps. Copyright (C) 2002 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000048814"],["dc.identifier.isi","000174156400016"],["dc.identifier.pmid","11856879"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31461"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0301-0171"],["dc.title","Molecular characterization and chromosome assignment of the porcine gene COX7A1 coding for the muscle specific cytochrome c oxidase subunit VIIa-M"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]