Burfeind, Peter

[["dc.bibliographiccitation.firstpage","593"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Clinical Genetics"],["dc.bibliographiccitation.lastpage","597"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Auber, Bernd"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Thiels, C."],["dc.contributor.author","Alsat, E. A."],["dc.contributor.author","Shoukier, Moneef"],["dc.contributor.author","Liehr, Thomas"],["dc.contributor.author","Nelle, H."],["dc.contributor.author","Bartels, I."],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Laccone, Franco A."],["dc.date.accessioned","2018-11-07T08:42:29Z"],["dc.date.available","2018-11-07T08:42:29Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1111/j.1399-0004.2009.01363.x"],["dc.identifier.isi","000277523400012"],["dc.identifier.pmid","20236119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19711"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0009-9163"],["dc.title","An unbalanced translocation resulting in a duplication of Xq28 causes a Rett syndrome-like phenotype in a female patient"],["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","303"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Medical Genetics"],["dc.bibliographiccitation.lastpage","307"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Blanck, C."],["dc.contributor.author","Kohlhase, Juergen"],["dc.contributor.author","Engels, P."],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Bottani, A."],["dc.contributor.author","Patel, M. S."],["dc.contributor.author","Kroes, H. Y."],["dc.contributor.author","Cobben, J. M."],["dc.date.accessioned","2018-11-07T11:15:39Z"],["dc.date.available","2018-11-07T11:15:39Z"],["dc.date.issued","2000"],["dc.identifier.doi","10.1136/jmg.37.4.303"],["dc.identifier.isi","000086453000013"],["dc.identifier.pmid","10819639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54414"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","British Med Journal Publ Group"],["dc.relation.issn","0022-2593"],["dc.title","Three novel SALL1 mutations extend the mutational spectrum in Townes-Brocks syndrome"],["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.artnumber","10"],["dc.bibliographiccitation.journal","Molecular Cytogenetics"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Auber, Bernd"],["dc.contributor.author","Bruemmer, Verena"],["dc.contributor.author","Zoll, Barbara"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Boehm, Detlef"],["dc.contributor.author","Liehr, Thomas"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Wilichowski, Ekkehard"],["dc.contributor.author","Argyriou, Loukas"],["dc.contributor.author","Bartels, Iris"],["dc.date.accessioned","2018-11-07T08:35:08Z"],["dc.date.available","2018-11-07T08:35:08Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Submicroscopic imbalances in the subtelomeric regions of the chromosomes are considered to play an important role in the aetiology of mental retardation (MR). The aim of the study was to evaluate a quantitative PCR (qPCR) protocol established by Boehm et al. (2004) in the clinical routine of subtelomeric testing. Results: 296 patients with MR and a normal karyotype (500-550 bands) were screened for subtelomeric imbalances by using qPCR combined with SYBR green detection. In total, 17 patients (5.8%) with 20 subtelomeric imbalances were identified. Six of the aberrations (2%) were classified as causative for the symptoms, because they occurred either de novo in the patients (5 cases) or the aberration were be detected in the patient and an equally affected parent (1 case). The extent of the deletions ranged from 1.8 to approximately 10 Mb, duplications were 1.8 to approximately 5 Mb in size. In 6 patients, the copy number variations (CNVs) were rated as benign polymorphisms, and the clinical relevance of these CNVs remains unclear in 5 patients (1.7%). Therefore, the overall frequency of clinically relevant imbalances ranges between 2% and 3.7% in our cohort."],["dc.identifier.doi","10.1186/1755-8166-2-10"],["dc.identifier.isi","000208460900009"],["dc.identifier.pmid","19284615"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5765"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17987"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1755-8166"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Identification of subtelomeric genomic imbalances and breakpoint mapping with quantitative PCR in 296 individuals with congenital defects and/or mental retardation"],["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","543"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","552"],["dc.bibliographiccitation.volume","163"],["dc.contributor.author","Grzmil, M."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Voigt, S."],["dc.contributor.author","Mury, D."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T10:37:03Z"],["dc.date.available","2018-11-07T10:37:03Z"],["dc.date.issued","2003"],["dc.description.abstract","To analyze differential gene expression of putative prostate tumor markers we compared the expression levels of more than 400 cancer-related genes using the cDNA array technique in a set of capsule-invasive prostate tumor and matched normal prostate tissue. The overexpression. of Bax inhibitor-1 (BI-1) in prostate carcinoma and prostate cancer cell lines was confirmed by using Northern blot and Western blot analyses. Quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) on intact RNAs from 17 paired laser-captured microdissected epithelial tissue samples confirmed up-regulated BI-1 expression in 11 of 17 prostate tumors. In addition, it was demonstrated that BI-1 expression is down-regulated in stromal cells as. compared to matched normal epithelial cells of the prostate. In situ hybridization experiments on prostate sections also revealed that BI-1 expression is mainly restricted to epithelial cells. Furthermore, quantitative RT-PCR on RNAs derived from five benign prostate hyperplasia (BPH) samples showed no significant difference in BI-1 expression as compared to normal epithelial prostate tissue. To determine the function of BI-1 in vitro, human PC-3, LNCaP, and DU-145 prostate carcinoma cells were transfected with small interfering double-strand RNA (siRNA) oligonucleotides against the BI-1 gene leading to a specific down-regulation of BI-1 expression. Furthermore, transfection of PC-3, LNCaP, and DU-145 cells with BI-1 sequence-specific siRNAs caused a significant increase in spontaneous apoptosis in all cell lines. Taken together, our results indicate that the human BI-1 gene contains the potential to serve as a prostate cancer expression marker and as a potential target for developing therapeutic strategies for prostate cancer."],["dc.identifier.doi","10.1016/S0002-9440(10)63682-6"],["dc.identifier.isi","000184366400016"],["dc.identifier.pmid","12875974"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45473"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.title","Bax inhibitor-1 is overexpressed in prostate cancer and its specific down-regulation by RNA interference leads to cell death in human prostate carcinoma cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","65"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","70"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Schmidt, T."],["dc.contributor.author","Bartels, I."],["dc.contributor.author","Liehr, Thomas"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Zoll, Barbara"],["dc.contributor.author","Shoukier, Moneef"],["dc.date.accessioned","2018-11-07T09:30:55Z"],["dc.date.available","2018-11-07T09:30:55Z"],["dc.date.issued","2013"],["dc.description.abstract","Here, we report a 3-year-old boy with short stature, developmental delay and mild facial dysmorphic signs. Karyotype analysis and array-CGH revealed a pure duplication 5q22.1q23.2 with a length of 14.25 Mb. As demonstrated by multicolor-fluorescence in situ hybridization, the duplicated segment was orientated in an inverted tandem manner. One of the 2 older half-brothers of the index patient was intellectually disabled and showed short stature as well. The mother of the siblings was only 149 cm in height. The affected half-brother as well as the mother of the siblings were tested positive for the same duplication. Duplications of the long arm of chromosome 5 are rare. There are 16 reported cases of different 5q segments with a pure duplication and no additional chromosomal imbalance. In order to refine the 5q-duplication phenotype, reported cases were recently classified in 3 groups on the basis of clinical findings and the involved chromosome segments. However, our case does not fit in any of these groups but is placed in the interjacent chromosomal area between 2 of these groups. Overall, this is the second reported family with a duplication of 5q22.1q23.2 and both families share phenotypic features like short stature, facial dysmorphic signs and speech delay. The reported family provides further information for delineating phenotype-genotype correlations of pure duplications of the 5q region. Copyright (C) 2012 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000342914"],["dc.identifier.isi","000312004200010"],["dc.identifier.pmid","23051634"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31425"],["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","A Family with an Inverted Tandem Duplication 5q22.1q23.2"],["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.artnumber","7"],["dc.bibliographiccitation.journal","Molecular Cytogenetics"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schwaibold, Eva Maria Christina"],["dc.contributor.author","Bartels, Iris"],["dc.contributor.author","Kuester, Helmut"],["dc.contributor.author","Lorenz, Michael"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Adam, Ronja"],["dc.contributor.author","Zoll, Barbara"],["dc.date.accessioned","2018-11-07T09:45:02Z"],["dc.date.available","2018-11-07T09:45:02Z"],["dc.date.issued","2014"],["dc.description.abstract","Reported cases of \"pure\" duplication of the entire short arm of chromosome 16 (16p) are rare, with only 7 patients described in the literature. We report on a female infant with de novo 16p duplication localized to the short arm of chromosome 6, detected by chromosomal analysis and characterized by array CGH and fluorescence in situ hybridization. This baby girl presented with clinical symptoms characteristic of patients with duplications of the short arm of chromosome 16: psychomotor retardation, constitutional growth delay and specific dysmorphic features, including proximally placed hypoplastic thumbs. In addition, she exhibited evidence of neonatal hemochromatosis as shown by direct hyperbilirubinemia, iron overload and elevated liver enzyme levels. To our knowledge, this is the first report of signs of neonatal hemochromatosis in a patient with 16p duplication."],["dc.identifier.doi","10.1186/1755-8166-7-7"],["dc.identifier.isi","000331553800001"],["dc.identifier.pmid","24456940"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9752"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34529"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1755-8166"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","De novo duplication of chromosome 16p in a female infant with signs of neonatal hemochromatosis"],["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","454"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinical Genetics"],["dc.bibliographiccitation.lastpage","459"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Auber, Bernd"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Herold, Sylvia"],["dc.contributor.author","Schoner, K."],["dc.contributor.author","Simson, G."],["dc.contributor.author","Rauskolb, R."],["dc.contributor.author","Rehder, H."],["dc.date.accessioned","2018-11-07T10:55:51Z"],["dc.date.available","2018-11-07T10:55:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Meckel-Gruber syndrome (MKS) is an autosomal recessive disorder causing severe defects in the developing central nervous system and other organs. Recently, mutations in the MKS1 gene have been identified as disease causing in individuals of Finnish MKS families. The primary aim of the present study was to assess the frequency of the 'Finnish founder mutation' (29 bp IVS15-7_35) in the MKS1 gene in 20 aborted fetuses with a diagnosis of MKS. The secondary aim was to screen for novel mutations in the coding sequence of the MKS1 gene of MKS fetuses and to obtain genotype-phenotype correlations where possible. Furthermore, we evaluated the carrier rate of a deletion of 29 bp in intron 15 of the MKS1 gene in a German population. To identify and characterize mutations in the MKS1 gene, sequence analyses and quantitative real time polymerase chain reaction studies were performed. We could identify the same type of mutation, a deletion of 29 bp in intron 15 of the MKS1 gene, in 8 out of the 20 cases studied. Six out of the eight cases with such a mutation displayed the campomelic variant of MKS. The carrier frequency among 519 healthy German individuals was 1:260. This deletion in the MKS1 gene is highly associated with a distinct subtype of the MKS, namely the campomelic variant. In individuals of European origin suffering from the campomelic MKS variant, the described deletion is highly likely to be causative. Regarding the results of our study, the incidence of MKS in Germany can be estimated as 1:135,000. In families with a known mutation in the MKS1 gene, it is now possible to offer an early prenatal testing, for example with chorionic villus sampling and mutation analysis."],["dc.identifier.doi","10.1111/j.1399-0004.2007.00880.x"],["dc.identifier.isi","000250145000011"],["dc.identifier.pmid","17935508"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49880"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0009-9163"],["dc.title","A disease causing deletion of 29 base pairs in intron 15 in the MKS1 gene is highly associated with the campomelic variant of the Meckel-Gruber syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","59"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics Part A"],["dc.bibliographiccitation.lastpage","64"],["dc.bibliographiccitation.volume","137A"],["dc.contributor.author","von Beust, G."],["dc.contributor.author","Sauter, Simone M."],["dc.contributor.author","Liehr, Thomas"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Bartels, I."],["dc.contributor.author","Stark, Holger"],["dc.contributor.author","von Eggeling, F."],["dc.contributor.author","Zoll, Barbara"],["dc.date.accessioned","2018-11-07T10:56:47Z"],["dc.date.available","2018-11-07T10:56:47Z"],["dc.date.issued","2005"],["dc.description.abstract","We report on a girl with mosaicism. (65%) of a de novo supernumerary ring chromosome 7. The main clinical features were delayed psychomotor development, congenital heart defect, facial dysmorphisms, and long hands, fingers, feet and toes. Molecular cytogenetic analysis revealed that the ring chromosome was duplicated in 20% of the analyzed metaphases with marker chromosome and quadruplicated in 5% thereof. Uniparental disomy (UPD) of the two normal sister chromosomes 7 was excluded. This is, to our knowledge, the first report of a partial tetrasomy to hexasomy due to a ring chromosome 7. Additionally, the ring evolution could be reconstructed according to the FISH-results. (c) 2005 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/ajmg.a.30835"],["dc.identifier.isi","000231009900011"],["dc.identifier.pmid","16007665"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50099"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1552-4825"],["dc.title","Molecular cytogenetic characterization of a De Novo supernumerary ring chromosome 7 resulting in partial trisomy, tetrasomy, and hexasomy in a child with dysmorphic signs, congenital heart defect, and developmental delay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2626"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","2633"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Stettner, Mark"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T10:58:18Z"],["dc.date.available","2018-11-07T10:58:18Z"],["dc.date.issued","2007"],["dc.description.abstract","In the prostate, estrogen receptor beta (ER beta), the preferred receptor for phytoestrogens, has features of a tumor suppressor. To investigate the mechanisms underlying the beneficial effects on prostate cancer of histone deacetylase inhibitor valproic acid (VPA) and phytoestrogen tectorigenin, we analyzed the expression of ER after tectorigenin or VPA treatment. For further functional analysis, we knocked down ER beta expression by RNA interference. LNCaP prostate cancer cells were treated with 5 mmol/L VPA or 100 mu mol/L tectorigenin and transfected with small interfering RNA (siRNA) against ER beta. Control transfections were done with luciferase (LUC) siRNA. Expression of ER beta was assessed by Western blot. mRNA expression was quantitated by real-time reverse transcription-PCR. Expression of ER beta mRNA and protein markedly increased after VPA or tectorigenin treatment. When ER beta was knocked down by siRNA, the expression of prostate-derived Ets factor, prostate-specific antigen, prostate cancer-specific indicator gene DD3(PCA3), insulin-like growth factor-1 receptor, the catalytic subunit of the telomerase, and ER beta was up-regulated and the tectorigenin effects were abrogated. ER beta levels were diminished in prostate cancer and loss of ER beta was associated with proliferation. Here, we show that siRNA-mediated knockdown of ER beta increases the expression of genes highly relevant to tumor cell proliferation. In addition, we show that one prominent result of treatment with VPA or tectorigenin is the up-regulation of ER beta resulting in antiproliferative effects. Thus, these drugs, by restoring the regulatory function of ER in tumor cells, could become useful in the intervention of prostate cancer."],["dc.identifier.doi","10.1158/1535-7163.MCT-07-0197"],["dc.identifier.isi","000250252100003"],["dc.identifier.pmid","17913855"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50445"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1535-7163"],["dc.title","The relevance of estrogen receptor-beta expression to the antiproliferative effects observed with histone deacetylase inhibitors and phytoestrogens in prostate cancer treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1123"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","MHR Basic science of reproductive medicine"],["dc.bibliographiccitation.lastpage","1131"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Tascou, S."],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Trappe, Ralf"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:22:05Z"],["dc.date.available","2018-11-07T11:22:05Z"],["dc.date.issued","2001"],["dc.description.abstract","In an attempt to determine the susceptibility of spermatocytes to malignant transformation by simian virus 40 (SV40) large tumour antigen (TAg), transgenic mice harbouring a chimeric gene composed of the SV40 TAg gene fused to the 1.4 kb promoter sequence of the human phosphoglycerate kinase 2 (PGK2) gene were generated. Northern blot analysis on RNA from different tissues indicated a specific transcription of TAg in the testis of PGK2-TAg transgenic mice. Reverse transcription-polymerase chain reaction and Western blot analysis on testes at different stages of development revealed that transcription and translation of the TAg gene starts in 12-day-old testis, which coincides with the appearance of pre-leptotene spermatocytes. Germ cells of transgenic mice showed no tendency toward transformation, but in testes of both 18- and 25-day-old transgenic mice, a significantly enhanced number of spermatocytes was found. In contrast, in 42-day-old transgenic mice no differences in the number of spermatocytes and spermatids were observed. The number of Sertoli cells was determined to be equal in transgenic and wild type mice. In-situ end labelling of fragmented DNA revealed a higher rate of apoptosis in testes of 18-day-old transgenic mice as compared with wild type mice. These results indicate that germ cell homeostasis in transgenic mice is maintained by an apoptotic mechanism."],["dc.identifier.doi","10.1093/molehr/7.12.1123"],["dc.identifier.isi","000172625800004"],["dc.identifier.pmid","11719589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55922"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1360-9947"],["dc.title","Targeted expression of SV40 large tumour antigen (TAg) induces a transient enhancement of spermatocyte proliferation and apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]